• No results found

A Study on Association between Anthropometric and Lipid Parameters in Newly Diagnosed Type 2 Diabetes Mellitus Patients

N/A
N/A
Protected

Academic year: 2019

Share "A Study on Association between Anthropometric and Lipid Parameters in Newly Diagnosed Type 2 Diabetes Mellitus Patients"

Copied!
112
0
0

Loading.... (view fulltext now)

Full text

(1)

A Dissertation on

A STUDY ON ASSOCIATION BETWEEN ANTHROPOMETRIC

AND LIPID PARAMETERS IN NEWLY DIAGNOSED TYPE 2

DIABETES MELLITUS PATIENTS

Dissertation Submitted to

THE TAMILNADU Dr.M.G.R. MEDICAL UNIVERSITY

CHENNAI - 600 032

With partial fulfillment of the regulations For the award of the degree of

M.D. GENERAL MEDICINE BRANCH-I

COIMBATORE MEDICAL COLLEGE COIMBATORE

(2)
(3)

CERTIFICATE

Certified that this is the bonafide dissertation done by Dr. D.MANOJ and

submitted in partial fulfilment of the requirements for the Degree of M.D.,

General Medicine, Branch I of The Tamilnadu Dr.M.G.R. Medical University,

Chennai.

Date: GUIDE & PROFESSOR 3RD UNIT

DR. M.RAVEENDRAN M.D

Date:

HOD & PROFESSOR

DR. KUMAR NATARAJAN M.D

Date: THE DEAN

DR.S.ASOKAN M.S., M.Ch

(4)

DECLARATION

I solemnly declare that the dissertation titled ―A STUDY ON ASSOCIATION

BETWEEN ANTHROPOMETRIC AND LIPID PARAMETERS IN

NEWLY DIAGNOSED TYPE 2 DIABETES MELLITUS PATIENTS”

was done by me from JUNE 2017 to JUNE 2018 under the guidance and

supervision of Professor DR.M.RAVEENDRAN M.D. This dissertation is

submitted to The Tamilnadu Dr.M.G.R. Medical University towards the

partial fulfilment of the requirement for the award of MD Degree in General

Medicine (Branch I).

Place: Coimbatore Dr. D. MANOJ

(5)

ACKNOWLEDGEMENT

I wish to express my sincere thanks to our respected Dean Dr. B. ASOKAN

M.S., MCH for having allowed me to conduct this study in our hospital.

I express my heartfelt thanks and deep gratitude to the Head of the Department

of Medicine Professor. Dr. KUMAR NATARAJAN, M.D. for his generous

help and guidance in the course of the study.

I express my heartfelt thanks and deep gratitude to my guide

PROF.DR.M.RAVEENDRAN.M.D for her support and guidance for the

study.

I sincerely thank all professors and Asst. Professors- Dr. P.S. MANSHUR,

Dr.P. SANBAKASREE, Dr. K. SANGEETHA for their guidance and kind

help.

My sincere thanks to Department of BIOCHEMISTRY for their help. My

sincere thanks to all my friends and post-graduate colleagues for their whole

hearted support and companionship during my studies.

I thank all my PATIENTS, who formed the backbone of this study without

whom this study would not have been possible.

Lastly, I am ever grateful to the ALMIGHTY GOD for always showering His

blessings on me and my family.

(6)

CERTIFICATE – II

This is to certify that this dissertation work titled ―A STUDY ON

ASSOCIATION BETWEEN ANTHROPOMETRIC AND LIPID

PARAMETERS IN NEWLY DIAGNOSED TYPE 2 DIABETES

MELLITUS PATIENTS” of the candidate DR.D.MANOJ with registration

Number 201611306 for the award of M.D in the branch of General Medicine I

personally verified the urkund.com website for the purpose of plagiarism

check. I found that the uploaded thesis file contains from introduction to

conclusion pages and result shows 7%of plagiarism in the dissertation.

(7)
(8)

TABLE OF CONTENTS

S. No. CONTENT Page No.

1 AIMS AND OBJECTIVES 1

2 INTRODUCTION 2

3 REVIEW OF LITERATURE 4

4 LIST OF ABBREVIATIONS 33

5 MATERIALS AND METHODS 34

6 OBSERVATIONS AND RESULTS 36

7 DISCUSSION 77

8 SUMMARY 81

9 CONCLUSION 82

10 BIBLIOGRAPHY 83

11 ANNEXURES

I. PROFORMA

II. MASTER CHART

III. KEY TO MASTER CHART

IV. CONSENT FORM

88

90

94

(9)

LIST OF TABLES

SL.NO TABLE TITLE PAGE

NO

1 AGE DISTRIBUTION 36

2 SEX DISTRIBUTION 37

3 LIPID PROFILE 38

4 MEAN CHOLESTEROL BASED ON SEX 39

5 MEAN TRIGLYCERIDE BASED ON SEX 40

6 MEAN HDL-CHOLESTEROL BASED ON SEX 41

7 MEAN LDL-CHOLESTEROL BASED ON SEX 42

8 DISTRIBUTION BASED ON BODY WEIGHT 43

9 COMPARISON BETWEEN BMI AND TOTAL

CHOLESTEROL

44

10 COMPARISON BETWEEN BMI AND

TRIGLYCERIDE

45

11 COMPARISON BETWEEN BMI AND

HDL-CHOLESTEROL

46

12 COMPARISON BETWEEN BMI AND

LDL-CHOLESTEROL

47

13 DISTRIBUTION BASED ON WAIST

CIRCUMFERENCE

48

14

COMPARISON BETWEEN WAIST CIRCUMFERENCE AND TOTAL CHOLESTEROL

(10)

15 COMPARISON BETWEEN WAIST

CIRCUMFERENCE AND TRIGLYCERIDE

50

16

COMPARISON BETWEEN WAIST CIRCUMFERENCE AND HDL- CHOLESTEROL

51

17

COMPARISON BETWEEN WAIST CIRCUMFERENCE AND LDL- CHOLESTEROL

52

18 DISTRIBUTION OF WAIST HIP RATIO 53

19 COMPARISON OF WAIST HIP RATIO AND

TOTAL CHOLESTEROL

54

20 COMPARISON OF WAIST HIP RATIO AND

TRIGLYCERIDE

55

21 COMPARISON OF WAIST HIP RATIO AND

HDL-CHOLESTEROL

56

22 COMPARISON OF WAIST HIP RATIO AND

LDL-CHOLESTEROL

57

23 COMPARISON BETWEEN FASTING BLOOD

SUGAR AND SYSTOLIC BP

58

24 COMPARISON BETWEEN POSTPRANDIAL

BLOOD SUGAR AND SYSTOLIC BP

59

25 COMPARISON BETWEEN FASTING BLOOD

SUGAR AND DIASTOLIC BP

60

26 COMPARISON BETWEEN POSTPRANDIAL

BLOOD SUGAR AND DIASTOLIC BP

(11)

27

COMPARISON BETWEEN WAIST

CIRCUMFERENCE AND FASTING BLOOD SUGAR

62

28

COMPARISON BETWEEN WAIST

CIRCUMFERENCE AND POSTPRANDIAL BLOOD SUGAR

63

29 COMPARISON BETWEEN WAIST HIP

RATIO AND FASTING BLOOD SUGAR

64

30 COMPARISON BETWEEN WAIST HIP RAIO

AND POSTPRANDIAL BLOOD SUGAR

65

31

COMPARISON BETWEEN TOTAL

CHOLESTEROL AND FASTING BLOOD SUGAR

66

32

COMPARISON BETWEEN TOTAL CHOLESTEROL AND POSTPRANDIAL BLOOD SUGAR

67

33 COMPARISON BETWEEN TRIGLYCERIDE

AND FASTING BLOOD SUGAR

68

34 COMPARISON BETWEEN TRIGLYCERIDE

AND POST PRANDIAL BLOOD SUGAR

69

35

COMPARISON BETWEEN

HDL-CHOLESTEROL AND FASTING BLOOD SUGAR

70

36

COMPARISON BETWEEN

HDL-CHOLESTEROL AND POST PRANDIAL BLOOD SUGAR

(12)

37

COMPARISON BETWEEN

LDL-CHOLESTEROL AND FASTING BLOOD SUGAR

72

38

COMPARISON BETWEEN

LDL-CHOLESTEROL AND POST PRANDIAL BLOOD SUGAR

73

39 COMPARISON BETWEEN BODY MASS

INDEX AND FASTING BLOOD SUGAR

74

40

COMPARISON BETWEEN BODY MASS INDEX AND POST PRANDIAL BLOOD SUGAR

(13)

LIST OF CHARTS

SL.NO CHART TITLE PAGE

NO

1 AGE DISTRIBUTION 36

2 SEX DISTRIBUTION 37

3 LIPID PROFILE 38

4 MEAN CHOLESTEROL BASED ON SEX 39

5 MEAN TRIGLYCERIDE BASED ON SEX 40

6 MEAN HDL-CHOLESTEROL BASED ON SEX 41

7 MEAN LDL-CHOLESTEROL BASED ON SEX 42

8 DISTRIBUTION BASED ON BODY WEIGHT 43

9 COMPARISON BETWEEN BMI AND TOTAL

CHOLESTEROL

44

10 COMPARISON BETWEEN BMI AND

TRIGLYCERIDE

45

11 COMPARISON BETWEEN BMI AND

HDL-CHOLESTEROL

46

12 COMPARISON BETWEEN BMI AND

LDL-CHOLESTEROL

47

13 DISTRIBUTION BASED ON WAIST

CIRCUMFERENCE

48

14

COMPARISON BETWEEN WAIST CIRCUMFERENCE AND TOTAL CHOLESTEROL

(14)

15 COMPARISON BETWEEN WAIST

CIRCUMFERENCE AND TRIGLYCERIDE

50

16

COMPARISON BETWEEN WAIST CIRCUMFERENCE AND HDL- CHOLESTEROL

51

17

COMPARISON BETWEEN WAIST CIRCUMFERENCE AND LDL- CHOLESTEROL

52

18 DISTRIBUTION OF WAIST HIP RATIO 53

19 COMPARISON OF WAIST HIP RATIO AND

TOTAL CHOLESTEROL

54

20 COMPARISON OF WAIST HIP RATIO AND

TRIGLYCERIDE

55

21 COMPARISON OF WAIST HIP RATIO AND

HDL-CHOLESTEROL

56

22 COMPARISON OF WAIST HIP RATIO AND

LDL-CHOLESTEROL

57

23 COMPARISON BETWEEN FASTING BLOOD

SUGAR AND SYSTOLIC BP

58

24 COMPARISON BETWEEN POSTPRANDIAL

BLOOD SUGAR AND SYSTOLIC BP

59

25 COMPARISON BETWEEN FASTING BLOOD

SUGAR AND DIASTOLIC BP

60

26 COMPARISON BETWEEN POSTPRANDIAL

BLOOD SUGAR AND DIASTOLIC BP

(15)

27 COMPARISON BETWEEN WAIST

CIRCUMFERENCE AND FASTING SUGAR

62

28

COMPARISON BETWEEN WAIST

CIRCUMFERENCE AND POSTPRANDIAL BLOOD SUGAR

63

29 COMPARISON BETWEEN WAIST HIP

RATIO AND FASTING BLOOD SUGAR

64

30 COMPARISON BETWEEN WAIST HIP RAIO

AND POSTPRANDIAL BLOOD SUGAR

65

31

COMPARISON BETWEEN TOTAL

CHOLESTEROL AND FASTING BLOOD SUGAR

66

32

COMPARISON BETWEEN TOTAL CHOLESTEROL AND POSTPRANDIAL BLOOD SUGAR

67

33 COMPARISON BETWEEN TRIGLYCERIDE

AND FASTING BLOOD SUGAR

68

34 COMPARISON BETWEEN TRIGLYCERIDE

AND POST PRANDIAL BLOOD SUGAR

69

35

COMPARISON BETWEEN

HDL-CHOLESTEROL AND FASTING BLOOD SUGAR

70

36

COMPARISON BETWEEN

HDL-CHOLESTEROL AND POST PRANDIAL BLOOD SUGAR

(16)

37

COMPARISON BETWEEN

LDL-CHOLESTEROL AND FASTING BLOOD SUGAR

72

38

COMPARISON BETWEEN

LDL-CHOLESTEROL AND POST PRANDIAL BLOOD SUGAR

73

39 COMPARISON BETWEEN BODY MASS

INDEX AND FASTING BLOOD SUGAR

74

40

COMPARISON BETWEEN BODY MASS INDEX AND POST PRANDIAL BLOOD SUGAR

(17)

1

AIMS AND OBJECTIVES OF STUDY

1.

To study the occurrence of dyslipidaemia in newly detected type2

diabetes mellitus

2.

To study the pattern of dyslipidaemia in this group

3.

To assess the relationship between anthropometric measurements and

(18)

2

INTRODUCTION

Diabetes Mellitus (DM) is a chronic disease and a silent epidemic.

Recent estimates show that by 2030, number of people with diabetes will

increase to more than 366 million which is twice the number in 2000. Diabetes

is more prevalent in developing countries and India is becoming the diabetic

capital in the world with prevalence range next to China. India has around 69.1

million people with diabetes. The increased prevalence is attributed to ageing

of the population and obesity. Type 2 diabetes being a chronic disease is

characterized by hyperglycaemia and dyslipidaemia due to underlying insulin

resistance. As the disease progresses it leads to micro vascular and macro

vascular complications. Obesity and particularly abdominal obesity are

strongly associated with insulin resistance. The aetiology of diabetes is

attributed to environmental and genetic factors. The modifiable risk factors like

abdominal obesity and physical inactivity are major contributors to the disease.

Rapid lifestyle changes, other non-communicable diseases like hypertension,

dyslipidaemia are also major etiologic factors for the rising incidence of type 2

diabetes around the globe. The Body Mass Index (BMI), Waist to Hip Ratio

(WHR), and the Waist Circumference (WC) are three main anthropometric

parameters to evaluate body fat and fat distribution in adults. These parameters

vary between the different ethnic populations. Previous studies have shown that

BMI and WHR can predict outcome of diabetes and WC correlates better with

intraabdominal fat than WHR. In Indian population central obesity is more

(19)

3

complications gains importance. So Waist Circumference and Waist Hip Ratio

are better predictors of obesity than Body Mass Index in Indian population.

Patients with type 2 diabetes mellitus-associated dyslipidaemia have a high risk

of cardiovascular diseases and its complications. The lipid parameters serum

Cholesterol, serum Triglyceride, serum Low Density Lipoprotein (LDL), serum

High Density Lipoprotein(HDL) are correlated with blood sugar levels in this

study. An understanding of the complex interplay of how treating

dyslipidaemia reduces the risk for CVD events in patients with type 2 diabetes

mellitus and an ability to assess at-risk patients is necessary to ensure the most

appropriate treatment strategies are implemented. The aim of this study was to

quantify the association between three anthropometric measurements (body

mass index, waist to hip ratio, waist circumference) and lipid profilein newly

(20)

4

REVIEW OF LITERATURE

Diabetes mellitus is a disease which affects all age group and is a

vascular disease that affects the endothelium all over the body. Diabetes

mellitus is recognized as a syndrome, a collection of disorders that have

hyperglycemia and glucose intolerance as their hallmark which can be due

either to insulin deficiency or to impaired effectiveness of insulin’s action or

both.

Etiological Classification of Hyperglycaemia (WHO 1999): (1)

Type 1 Diabetes mellitus (β-cell destruction, usually leading to absolute

insulin deficiency)

Autoimmune

Idiopathic

Type 2 Diabetes mellitus (may range from predominantly insulin resistance with relative insulin deficiency to a predominantly secretory defect with or

without insulin resistance)

Other specific types

 Genetic defects of β-cell function

 Genetic defects in insulin action

 Diseases of the exocrine pancreas

 Endocrinopathies

(21)

5

 Infections

 Uncommon forms of immune-mediated diabetes

 Other genetic syndromes sometimes associated with diabetes

Gestational diabetes

The terms insulin-dependent diabetes mellitus and non-insulin dependent

diabetes mellitus were removed from classification of diabetes because it

classified based on age and treatment given only and pathogenesis of the

disease was not considered. The current classification retains the terms ―type 1‖

and ―type 2‖ diabetes mellitus (Arabic numerals are used). Type 1 diabetes

mellitus occurs due to autoimmune process leading to β-cell destruction but the

pathogenesis and etiology are not known. The conditions like e.g. cystic

fibrosis; mitochondrial defects which have specific etiologies for beta cell

dysfunction are not classified as type 1diabetes. Type 2 diabetes mellitus is due

to defective insulin secretion and/or from insulin resistance or combination of

both. Malnutrition related diabetes (MRDM) is removed from the WHO

classification (2). It has two subtypes. One of which is protein-deficient

pancreatic diabetes needs a better definition. Next is fibrocalculous pancreatic

diabetes (FCPD) which is classified as a disease of the exocrine pancreas and

(22)

6

Other Specific Types of Diabetes: (3)

Genetic defects of 𝛃-cell function

HNF1A MODY HNF4A MODY HNF1B MODY GCK MODY

MtDNA 3243 MIDD KCNJ11 PNDM KCNJ11 DEND 6q24 TNDM ABCC8 TNDM INS PNDM

WFS1 Wolfram syndrome FOXP3 IPEX syndrome EIF2AK3 Wolcott– Rallison syndrome

Genetic defects in insulin action

INSR Type A insulin resistance INSR Leprechaunism INSR Rabson–Mendenhall syndrome LMNA FPLD PPARG FPLD AGPAT2 CGL BSCL CGL Lipoatrophic diabetes

Diseases of the exocrine pancreas

Fibrocalculouspancreatopathy Pancreatitis

Trauma / pancreatectomy Neoplasia Cystic fibrosis Hemochromatosis Others Endocrinopathies Cushing syndrome Aldosteronoma Acromegaly Pheochromocytoma Glucagonoma Hyperthyroidism Somatostatinoma Others

Drug- or chemical-induced Nicotinic acid Glucocorticoids Thyroid hormone Alpha-adrenergic agonists Beta-adrenergic agonists Thiazides Dilantin Pentamidine Vacor Interferon-alpha therapy Statins L-asparagine

Antipyschotic drugs, e.g. clozapine,

(23)

7 Uncommon forms of

immune-mediated diabetes

Insulin autoimmune syndrome (antibodies to insulin)

Anti–insulin receptor antibodies

―Stiff man‖ syndrome Others

Other genetic syndromes Down syndrome Friedreich’s ataxia Huntington’s chorea Klinefelter syndrome Lawrence–Moon–Biedl syndrome Myotonic dystrophy Porphyria Prader–Willi syndrome Turner syndrome Wolfram syndrome Diagnosis:

Diagnosis is established by demonstration of elevated blood sugar

levels. It includes random blood sugar, fasting and postprandial blood sugar

and OGTT of 75 grams for testing. For children, the oral glucose load is 1.75 g

per kg body weight. HbA1c is also a reliable means of diagnosing diabetes

recommended by the ADA and WHO.

HbA1c (Glycosylated Hemoglobin)

HbA1c is a hemoglobin variant formed by the nonenzymatic attachment

of glucose to hemoglobin. HbA1c has become the cornerstone marker for

monitoring of diabetic patients.HbA1c measurements are done using

standardized assays. Maintaining HbA1c levels within normal range is

important in reducing the risk of micro vascular complications of diabetes.

HbA1c levels predict diabetic retinopathy and macro vascular event mortality.

(24)

8

will be stable for at least one week, patient does not require fasting and its

reflects blood sugar control for 3 to 4 months. The disadvantage in HbA1c is

conditions that alter the red cell turnover and cost of the assay. The cutoff for

HbA1c to diagnose diabetes by WHO is level more than or equal to 6.5% (4).

But diagnosis of diabetes using HbA1c will underestimate the prevalence of

diabetes. Type 2 diabetes mellitus is a threat to human health in the twenty-first

century. Estimates show that by 2025, around 300 million people will have

diabetes with expected 70% increase in developing countries.

The prevalence of diabetes among Asian populations especially in

Indian men and women increases with age up to 60s and then declines. The

prevalence of diabetes were higher in people of India and Singapore than in

most of the Chinese and Japanese people in DECODA study (5). In India there

was 10% prevalence among people in 40–49 years age group, 30% in 50–69

years age group. The ratio of prevalence of blood glucose abnormality does not

show a consistent trend. In the age group of 30 to 69 years, undiagnosed

diabetes and impaired glucose tolerance (IGT) is more common in men. Post

prandial hyperglycemia is more common in elderly men.

American Diabetes Association (ADA) Classification of DM:

Four criteria for diagnosis of diabetes mellitus:

1) Glycated hemoglobin (A1C) value of 6.5% or higher

(25)

9

3) 2 hour plasma glucose more than 200 mg/dl (11.1 mmol/l)

During OGTT done with 75 gram of glucose

4) Classic symptoms of hyperglycemia- polyuria, polydipsia, and

unexplained weight loss or hyperglycemic crisis with a random plasma

glucose of 200 mg/dl (11.1 mmol/l) or higher.

Glucose use and insulin action:

Glucose concentration in plasma is 15% higher than in whole blood and

arterial blood sugar levels are highest when compared to venous and capillary

blood sugar levels. Glucose transport between tissues occurs through plasma

and RBCs. Insulin dependent tissues include brain, liver, kidney, intestine, and

placenta. Uptake of glucose is mediated by tissue-specific glucose transporters

(GLUTs) that occurs in both insulin-sensitive tissues and insulin-insensitive

tissues. Insulin mediated vasodilatation can retain more glucose for use in the

muscles. During fasting, glucose uptake of insulin independent tissues occurs

and two thirds of the glucose is oxidized. Brain uses glucose as a fuel (5).

Insulin dependent tissues use fat as a fuel during fasting and more than fifty

percent of basal energy production is relied on fat oxidation.

The liver (hepatic glucose production) is more sensitive to inhibition by

insulin than the stimulation action by insulin on the peripheral tissues (glucose

(26)

10

DIRECT ACTIONS INDIRECT ACTIONS

Enhancement of glucose transport

glycolytic breakdown & incorporation

into glycogen

Inhibition of lipolysis,

Lipid oxidation &

Protein degradation

Tissues sensitive to insulin have glucose, FFA and amino acids

competing with each other and the effect of counter regulatory hormones is

opposing the effects of insulin.

Physiologic hyperinsulinemia activates the insulin signal transduction

system leading to a coordinated increase in glucose transport/phosphorylation,

glycogen synthesis, and glucose oxidation. Insulin suppresses endogenous

glucose production and promotes glucose uptake into muscle in response to

oral glucose load. GLP-1 by its direct effects and indirect actions of increasing

insulin and inhibition of glucagon causes glucose uptake in liver cells and

inhibits glucose production by liver (6).

Pathogenesis of T2DM:

Type 2 diabetes is characterized by –

 Muscle insulin resistance leading to decreased in glucose uptake

 Hepatic insulin resistance leading to increase in glucose production

 Adipocyte insulin resistance leading to increase in plasma FFA

 Increased insulin resistance stimulate adipocytokine release

(27)

11

 Hyperglucagonemia

 Increase in hepatic sensitivity to glucagon

 Impaired incretin effect (GLP-1 and GIP)

 Increased renal glucose reabsorption

 Brain neurotransmitter dysfunction leading to failure of appetite

suppression resulting in weight gain

Insulin resistance coupled with progressive beta cell failure is responsible

for progression of disease from impaired glucose tolerance to overt diabetes

mellitus. The most dominant feature of insulin resistance is obesity. Evidence

of insulin resistance (IR) in lipid pattern is elevated triglyceride and lower

HDL-cholesterol levels. These along with elevated blood pressure form the

diagnostic criteria for metabolic syndrome (7). Recently elevated levels of ALT

and GGT are indicative of insulin resistance. Insulin resistance is also

associated with alteration in adipokines, vascular dysfunction, and immune

dysregulation.

Insulin resistance:

Insulin resistance is defined as abnormal biologic response to insulin.

Insulin resistance is the key factor in the pathogenesis of T2DM. Action of

insulin is on skeletal muscle, adipose tissue, liver, endothelium, and immune

cells. Insulin resistance leads to hyperglycemia due to reduced muscle uptake

of glucose and increased release of glucose substrates from liver (FFA).

(28)

12

pancreas which is burnt out and unable to produce sufficient insulin to maintain

blood sugar levels within the normal range. This results in diabetes mellitus.

Measurement of insulin resistance:

The method for testing is called euglycemichyperinsulinemic clamp.

This technique measures insulin resistance in the presence of hyperinsulinemic

state the ability to maintain normal blood glucose levels. Glucose is infused at a

rate sufficient to maintain euglycemia and insulin is infused at

supraphysiological rates (9). The role of muscle and adipose tissue is tested

using stable isotopes. After achieving steady state, the rate of glucose infusion

predicts ability of tissue to respond to insulin and tissue take up of glucose for a

standard insulin dosing. This technique is considered gold standard but it is

time consuming and difficult in routine measurements and cannot be followed

in large epidemiologic studies. The risk factors for prediction of T2DM include

—age, gender, measures of adiposity, family history of T2DM, and ethnicity.

Insulin Resistance and Ectopic Fat:

Patients prone to T2DM accumulate visceral or ectopic fat for a given

weight. This leads to impaired subcutaneous fat storage capacity. One entity is

lipodystrophy in which there is accumulation of fat in ectopic tissues and

insulin resistance. The location of fat storage places a role in BMI and

(29)

13 Pancreas Morphology and Diabetes:

Islet β-cell volume is decreased in T2DM and in impaired fasting

glucose. There is a relative increase in the α: β cell ratio. Early in the course of

hyperglycemia there is distortion of islet capillary morphology and as the

disease progresses there is loss of capillary density and associated islet cell

fibrosis (10). The various mechanisms that lead to beta cell loss include

elevated glucose and free fatty acids, amyloid deposition in islet cells and

inflammation of islet cells.

Chronically elevated glucose and/or free fatty acids:

Chronic exposure of β cells to elevated glucose results in impaired β-cell

function due to oxidative stress and activation of Fas receptor-mediated or

mitochondrial apoptosis. Exposure of β cells to increased free fatty acids (FFA)

with associated hyperglycemia can lead to impairment of insulin release. They

also cause beta cell apoptosis. Excess nutrients are thus detrimental to β-cell

secretory function.

Amyloid deposition in islet cells:

Found in patients with T2DM also in cystic fibrosis-related diabetes.

Accumulation of islet amyloid occurs due to aggregation of the normally

solublebeta cell peptide IAPP that gets deposited in the extracellular matrix

which lies between islet capillaries and β cells. Amyloid deposition is

associated with decreased β-cell volume increase in β-cell apoptosis.

(30)

14

surface death receptor Fas or cJun N-terminal kinase (JNK) and that leads to

downstream activation of apoptosis. IAPP aggregation is an important mediator

of β-cell toxicity (11). IAPP deposition leads to stress response of ER

(endoplasmic reticulum). IAPP deposition occurs when its plasma levels are

very high. Also IAPP is proinflammatory that elicits a cytokine and chemokine

production from the macrophages/dendritic cells.

Inflammation of islet cells:

Islet cell inflammation is a hallmark finding in T1DM due to release of

proinflammatory cytokines that lead to beta cell infiltration and lead to beta cell

death. In T2DM there is low-grade, chronic inflammation that is associated

with insulin resistance. Increased production of interleukin 1β in response to

chronic high blood glucose levels by the beta cells can activate signaling

pathways of innate immune response. This leads to β-cell toxicity and death.

Risk factors for type 2 diabetes mellitus:

The risk factors for type 2 diabetes mellitus includes the modifiable and

non-modifiable risk factors. Weight gain, obesity and physical inactivity are

one of the important modifiable risk factors.

Obesity:

Obesity occurs when there is mismatch between energy intake and

energy expenditure. BMI is the weight of a person in kilograms divided by

(31)

15

associated with 12% increased risk of T2DM. Another entity coming up in

recent years is lean diabetes (12). This form of diabetes occurring in young

males deprived of nutrition in childhood coming from a poor socioeconomic

status with onset of disease at early age without ketosis. These patients have

high incidence of beta cell failure. This entity having a multifactorial causation

due to genetic, environmental and behavioral factors with increased risk of

cardiovascular mortality. Talking about the influence of obesity per se- central

obesity which is deposition of adipose tissue in trunk and abdominal area is a

strong risk factor for diabetes mellitus. The surrogate measures of central

obesity are waist circumference (WC), hip ratio (WHR), and

waist-to-thigh ratio (WTR). Subcutaneous and intraabdominal fat can also be measured

using recent techniques like DEXA, MRI and CT. Intraabdominal fat alone can

lead to insulin resistance not taking into account the total body fat (13).

Physical Activity:

Physical activity is defined as bodily movement that increases energy

expenditure that is produced by contraction of skeletal muscle. Exercise on the

other hand is defined as a subset of physical activity (PA) which is done

intending physical fitness. Risk of diabetes is inversely proportional to PA. PA

has an independent effect of reducing the body weight and thereby reduces risk

of obesity. Exercise can also lead to improvement in insulin sensitivity. Studies

have shown that when considering the duration and the amount of exercise the

(32)

16 Sedentary Lifestyle:

Sedentary lifestyle is a risk factor for both diabetes and obesity. Leisure

sedentary behavior and television watching are greater in those who develop

diabetes when compared with those who did not develop diabetes mellitus.

This shows positive association between increased risk of diabetes and

sedentary lifestyle (33). Sedentary behavior is associated with adiposity,

adiposity-associated inflammation and reduced lipoprotein lipase activity,

clearance of triglycerides, clearance of an oral glucose load, and

glucose-stimulated insulin secretion. Lifestyle interventions like Diabetes Prevention

Program (DPP) are beneficialinimprovingglucosemetabolism. Weight loss is

brought by caloric reduction but maintenance of weight loss is brought by

physical activity (PA). Prolonged television (TV) watching is a surrogate of a

sedentary lifestyle and a risk factor for diabetes. Spending 2–10 hours in

television has 66% higher risk of diabetes and risk increases if total duration is

more than 40 hours per week. There is also 23% increase in risk of obesity

(14). For every 2 hour increment in sitting at work there is 5% increase in risk

of diabetes mellitus. Following an active lifestyle in the form of brisk walking

at least 30 to 45 min in a day 5 times in a week and watching television less

than 10 hours per week can reduce the risk of new onset of diabetes by 43%.

Moderate physical activity reduces the progression of IGT (impaired glucose

(33)

17 Dietary factors:

Diet is a phenomenon that varies based on personal preference, cultural

heritage and socioeconomic factors and is made of complex interactions of

numerous foods and nutrients. Measurement of diet is through food diaries and

questionnaires. Diet is assessed based on absolute intake of nutrients, nutrient

intake as a percentage of total energy, dietary patterns, and bioavailability

characteristics of foods like glycemic index.

Dietary fat:

High-fat diet is associated with obesity. Mechanisms involved are

alterations in cell membrane composition due to intake of dietary fat which

alter membrane fluidity, insulin-mediated signal transduction and its action.

There is positive correlation between high-fat, low-carbohydrate diets and

T2DM but the results are not consistent in all the studies (32). Specific types of

fat and carbohydrate that are consumed are important. Increased intake of

polyunsaturated fatty acids and long-chain n-3 fatty acids (fish oil) are beneficial and high intake of saturated fatty acids and trans-fatty acids are harmful (15).

Dietary carbohydrates:

Intake of carbohydrate poses a direct challenge to the beta cells when

(34)

18

with increased risk of diabetes. Composition of the carbohydrate and glycemic

index of the food influence this effect.

Glycemic index:

It measures the post prandial excursion of glucose after ingestion of

food. Foods with high glycemic index cause higher excursions of glucose. The

postprandial excursions depend onthe rate of absorption of glucose. It also

depends on type of carbohydrate(simple or complex) and the amount of fiber

intake. Benefit of consuming foods with low glycemic index in reduction of

risk of diabetes is not clear (16).

Other Food Intake:

High-fiber intakes is associated with reduction in risk of diabetes. But

the mechanism is unknown. It can be attributed to low glycemic index of

high-fiber diet. High intake of vegetables reduces the risk of diabetes. The

antioxidants found in fruits like carotenoids and tocopherols associated with

high fiber and vitamin intake reduce the risk of diabetes. The traditional Pima

diet with high fiber and low fat diet intake has reduced incidence of DM.

Other modifiable risk factors for T2DM:

(35)

19 Inflammation:

Inflammation is found to act as the underlying causative factor that leads

to development of atherosclerosis. The marker of subclinical inflammation

C-reactive protein is associated with metabolic abnormalities like obesity, insulin

resistance, low HDL cholesterol and hypertriglyceridemia. Increased levels of

CRP is associated with increased risk of diabetes. Thus subclinical

inflammation has become an important determinant of T2DM and studies have

shown that use of anti-inflammatory drugs like high-dose aspirin reduces

insulin resistance and improves glucose tolerance.

Smoking:

Smoking is an independent risk factor for the development of diabetes.

Studies have shown that smoking increases risk of DM by 45% (17). Also

current smokers have highest mean HbAlc concentrations and low levels are

seen in non-smokers. HbAlclevels are also correlated in a dose–response

manner with the number of cigarettes smoked per day and smoking measured

in pack-years. Smoking is also associated with insulin resistance. Smokers have

higher

Plasma triglycerides and low HDL-cholesterol levels. Oxidative stress

caused by smoking induces endothelial dysfunction, resulting in insulin

(36)

20 Anthropometry and diabetes:

Waist Circumference (WC) is recorded to the nearest 0.1 cm at level of

umbilicus and hip circumference at the point of maximum diameter of thigh

using an unstretched tape meter, without pressure on the body surface.

Waist-to-hip ratio (WHR) is calculated with WC divided by hip

circumference. Criteria of the National Heart, Lung, and Blood Institute

(NHLBI) is used to define cut-off points for central (or abdominal) obesity.

WC over 88 cm in women and over 102 cm in men is considered as a risk

factor. For Waist hip ratio the cut-off points are ≥ 0.95 for men and ≥ 0.85 for

women (18).

BODY MASS INDEX (BMI) is defined as the weight in kilograms

divided by the square of height in meters. Globally, more than 50% diabetics

have BMI above 21kg/m2.

WEIGHT STATUS BMI IN kg/m2

Underweight <18.5

Normal weight 18.5-24.9

Overweight 25-29.9

Obese ≥30

Class 1 30-34.9

Class 2 35-39.9

(37)

21

The anthropometric measures are used for the screening obesity,

diabetes and CVD. BMI indicates generalized obesity and WC and WHR

indicate central obesity. Central obesity better predicts cardiovascular risk and

mortality than BMI. Also BMI and WHR are better predictors of outcome in

T2DM. WC better predicts intra-abdominal fat than WHR. But which

parameter is best for predicting cardiovascular events and mortality is still

inconclusive (19).

Diabetes with Low Body Weight :( BMI< 18.5 kg/ m2)

There is an entity comprising of occurrence of diabetes in patients with

BMI less than 18.5 which was previously called malnutrition related diabetes

mellitus under subcategory termed protein deficient pancreatic diabetes.

Various other names like Jamaican type diabetes, Tropical diabetes were used

but Ahuja proposed the term ―Ketosis Resistant Diabetes of the Young

(KRDY)‖ which is accepted. These patients are mostly of Asian and African

ethnicity (20).

Criteria for diagnosis of KRDY:

(1) Blood glucose > 200 mg%

(2) Onset < 30 years of age

(3) BMI < 18 kg/m2

(4) Absence of ketosis on insulin withdrawal

(5) Poor socio-economic status or history of childhood malnutrition

(38)

22

The early onset of disease and low BMI mimics TIDM but presence of

islet cell specific antibodies is very less in KRDY. Studies done in India has

shown that around 3.5% patients were lean diabetics and 63% have an ideal

body weight at diagnosis. Micro-vascular complications of diabetes like

retinopathy, nephropathy and neuropathy were more common in lean diabetics

whereas hypertension and coronary artery disease are more common in the

obese patients. Other factors which distinguish it from TIDM are ketosis is

absent in KRDY and also KRDY patients respond to diet modification and oral

antidiabetic drugs. Studies have proven that a period of malnutrition during

postnatal period or early childhood can increase the risk of diabetes (21).

Studies have shown that Asian population has five-fold higher

prevalence in the lean diabetes. Consumption of alcohol, cigarette smoking and

pancreatitis were more among lean diabetics. They achieve poor glycemic

control. The pathophysiology is rapid beta cell failure. They require insulin

earlier and their TG/HDL ratio tends to be low which is considered as an

indirect marker of lower insulin resistance.

The pathophysiology and its distinction from classic type 2 diabetes is

still unclear (30). One difference is that peripheral insulin resistance is the key

factor in T2DM which is in contrast to KRDY that shows insulin deficiency.

The fasting C-peptide levels are intermediate between type1 and type 2 diabetic

patients. Though they have a small beta cell reserve which is denoted by the

C-peptide levels the insulin is not available because of excessive extraction of

(39)

23

activity and the hyperactive futile cycles of carbohydrate metabolism. This also

explains the resistance to ketosis (22). They have lower fasting plasma FFA

and ketone levels and reduced responsiveness to catechol amines that delay the

development of ketoacidosis. They also have exocrine pancreatic deficiency.

A single antibody is neither sensitive nor specific to distinguish between

the phenotypes of type 1 or type 2 diabetes as GAD or ICA positivity is seen in

obese T2DM patients also. So the probable etiology is malnutrition combined

with autoimmune process.

Obesity Paradox:

Obesity paradox is a phenomenon in which diabetes related

complications and mortality were higher among diabetic population with

normal weight when compared to those with obese diabetics (29). It is also

observed in other conditions like heart failure, end stage renal disease and

hypertension. The increased risk of death among lean diabetics who are

smokers. This becomes unreliable in elderly people because of the co-existing

conditions that determine mortality and unreliability of BMI as a measurement

of adipose tissue mass due to age related muscle wasting and reduction in

muscle mass.

Sarcopenic obesity can explain the obesity paradox. Sarcopenic obesity

is defined as presence of high body fat with reduced or normal lean body mass

(23). Sarcopenic obesity reduces physical fitness and cardiopulmonary

(40)

24

diabetics with normal body weight. Patients with good aerobic fitness with high

BMI have lower risk of mortality than those with normal BMI and poor

physical fitness.

Ideal body weight is BMI between 18.5 and 24.9. Central obesity which

is defined as waist circumference > 102 cm in males and> 88 cm in females

defined by NCEP correlates well with the degree of insulin resistance. Chronic

alcohol consumption can induce pancreatic beta cell dysfunction and cell

apoptosis (24). Exposure to both passive and active smoking has positive

association and is a risk factor for diabetes. Genetic defects like polymorphisms

of transcription factor FL2 gene and defective ATP sensitive potassium channel

can lead to defective insulin secretion. Abnormal fat distribution can also occur

in type 2 diabetic patients. Both genetic and environmental factors play a role

in lean diabetes.

Monogenic Diabetes Mellitus:

(41)

25 Maturity Onset Diabetes in Young:

Maturity onset diabetes of the young (MODY) is the commonest form

of monogenic β-cell diabetes in adults. It is divided into two clinical groups:

mutations in Glucokinase (GCK-MODY) and mutations in the transcription

factors—HNF1A and HNF4A (TF-MODY).

Over 80% of people with MODY will initially be misdiagnosed with

(42)

26

MODY patients are not obese, lack insulin resistance and do not have

autoimmune antibodies.

Diagnostic Criteria for MODY:

(i) Age of onset diabetes <25 years

(ii) Non-insulin-dependent diabetes

(iii) Family history of diabetes (due to autosomal dominant inheritance) - can

be absent in as much as 50% of patients.

Types of MODY:

Glucokinase MODY: (GK-MODY)

Have fasting hyperglycemia from birth but do not develop significant

micro vascular complications. Treatment is not required except in pregnancy.

Transcription factor MODY: (TF-MODY)

Diabetes develops in childhood/early adult life and deteriorates. They

respond to sulfonylurea treatment initially and later require insulin. Micro

(43)

27

Maternally Inherited Diabetes And Deafness (MIDD): (25)

It accounts for 0.5% of diabetes. It is due to mitochondrial gene

mutation producing a maternally inherited diabetes. These patients are

generally non-insulin requiring but require insulin after setting of sensineural

deafness.

Neonatal Diabetes:

It is diagnosed in the first six months of life. It can be transient or

permanent. It results due to mutation in KATP mutation and excellent glycemic

control with High-dose sulfonylurea tablets can be achieved instead of insulin

injections.

Lipid and diabetes mellitus:

Diabetes mellitus patients have elevated triglyceride levels, low levels of

high-density lipoprotein cholesterol, and increased small cholesteroldepleted

low-density lipoproteins. The pathophysiology under diabetic dyslipidemia is

insulin resistance which plays a central role in abnormal lipid and lipoprotein

metabolism that occurs in T2DM.There is not much variation in cholesterol

levels when compared between insulin sensitive and insulin resistant

individuals. Hence assessment of CVD risk in a diabetic patient based on lipid

profile should not be limited alone to total cholesterol alone. Dyslipidemia and

IR is also found in prediabetics and worsens as glucose intolerance progresses

(26). There is increased risk of CVD in diabetic women when compared to

(44)

28

associated with increased levels of Apo protein B100 which is considered as

the atherogenesis causing protein in the lipoprotein series and there is reduced

levels of ApoA1 protein. Dyslipidemia occurs in both fasting and postprandial

states. Dyslipidemia during postprandial period can lead to increased CVD risk

in non-diabetic people.

Lipoprotein Metabolism:

Blood triglyceride levels are regulated by the VLDL secreted from the

liver and activity of plasma lipoprotein lipases (LPL) that clear the plasma

triglycerides. DM is characterized by increased release of VLDL from liver and

reduced LPL activity. This leads to increased TGL levels in blood. HDL levels

are low due to increased transfer of cholesterol in exchange to TGL to VLDL

and LDL by CETP (cholesterol ester transfer protein). Hence the LDL particles

become smaller and denser.

Lipoprotein structure:

Lipoproteinsare macromolecular complexes consisting of lipid core

made of TG and cholesterylesters (CEs) anda surface made of phospholipids,

free cholesterol, and one or more Apo lipoproteins. There are five distinct

major classes of lipoproteins which are further divided into subclasses.

Handling of exogenous TGL is through formation of chylomicrons in

the enterocyte and endogenous TGL handling is by the VLDL released from

liver. VLDL, IDL and LDL require Apo B100 as their surface protein and

(45)

29

Microsomal triglyceride transfer protein (MTP) packages Apo B48 with the

core lipids and forms chylomicrons. Increased intestinal expression of MTP in

people with T2DM plays role in increased TGL levels. The chylomicrons enter

the system through the lymphatic system and acquire Apo lipoproteins C1, C2

and C3 HDL surface. Apo C2 activates adipose tissue derived lipoprotein

lipase that mediates chylomicron clearance (27). Apo C3 inhibits

LPL-mediated lipolysis. The TGL from chylomicron releases free fatty acids (FFAs)

which are taken by tissues and they acquire Apo E from HDL and become

chylomicron remnants. These chylomicron remnants are cleared by hepatic

uptake. Hepatic lipase (HL) hydrolyzes chylomicron remnant TGL and

augments hepatic uptake. IR and T2DM negatively affect chylomicron remnant

metabolism. Increased circulating TGL is atherogenic. Insulin targets Apo

B100 for its degradation which in the presence of IR and concomitant chronic

hyperinsulinemia and steatosis is decreased. Apo B 100 degradation increase

ER stress that leads to VLDL secretion from liver and steatosis (28).

TGL availability is essential for VLDL assembly and secretion.

Circulating FAs from the peripheral tissues act as the main source for TGL

synthesis. In case of IR and T2DM there is FAflux into the liver due to insulin

resistance in adipocytes stimulate Apo lipoprotein release and TGL uptake by

liver. Expression of nuclear transcription factor, peroxisome

proliferator-activated receptorγ (PPARγ) is increased in T2DM, IR and hepatic steatosis.

Lipolysis of core TGLleads to formation of smaller, denser VLDL

(46)

30

or IDL undergo further metabolic modifications to generate LDL by the action

of hepatic lipase. LDLparticlesarecomposed of core CEs associated with

surface Apo B100. LDL is cleared through hepatic LDL-receptor-mediated

uptake. IR and uncontrolled DM is associated withreduction in LDL receptors.

LDL participates in CETP-mediated exchange of its CE with

LDLorchylomicron TGL that produces small, dense LDL. The characteristic

hypertriglyceridemia of T2DMis associated with presence of small, dense

LDL.

Weight loss, Exercise and Diet modifications are the key to successful

treatment of all of the lipid abnormalities in patients with T2DM. Statins form

the main stay of treatment which lower LDL cholesterol by up to 50%, lower

triglycerides by about 15–25% and have minimal effects of HDL levels.

Elevated LDL-C is a risk factor for cardiovascular morbidity and mortality.

Treatment for Dyslipidemia:

LDL-C therapy is given for four groups of patients:

1. Those with LDL-C >190mg% and those with prior CVD

2. Those with diabetes and LDL-C ≥70≤190mg% and those without CVD

3. Diabetes with LDL-C ≥70≤190mgdL−1 with risk of 10 year CVD

≥7.5%

Non-HDL-C is a surrogate marker for the Apo B100-containing

lipoproteins. The new AHA/ACC guidelines has concluded that there is no

(47)

31

TGL to less than 150mg% and maintenance of HDL-C by 40mg% in men and

50mg% in women. HDL-C is an independent predictor of CV mortality (28).

Guidelines recommend reduction in LDL-C to 30to 40% in patients more than

40 years age and reduction to less than 100mg%.

Other treatment recommendations include Medical nutrition therapy,

Weight loss in overweight and obese individuals, Diet with reduced intake of

total fat (∼30% of total calories), saturated fat (<7% of total calories), and trans

fatty acids (minimal), cholesterol less than 200mg%, Increased exercise,

Smoking cessation.

Pharmacologic therapy include statin therapy to decrease LDL-C, fibrate

therapy to decrease TG and increase HDL-C and combination therapy with

statin.

Metabolic Syndrome:

Reaven proposed criteria for diagnosis of metabolic syndrome which

includes hypertension, dyslipidemia (specifically hypertriglyceridemia with

low HDL-cholesterol), dysglycemia, and central obesity. Three out of five

(48)

32

Elevated TGL more than 150mg% or taking drugs for hypertriglyceridemia

Reduced HDL less than 40 mg% in male and 50mg% in female or drug therapy

for low HDL levels

Systolic blood pressure ≥130mmHg and/or diastolic ≥85mmHg or drug therapy

with a history of hypertension

Elevated fasting blood glucose more than 100mg% or glucose-lowering

therapy

Abdominal obesity - WC more than 102 cm in male and more than 88 cm in

(49)

33

LIST OF ABBREVATIONS

T2DM Type 2 diabetes mellitus OGTT Oral glucose tolerance test

BMI Body mass index DECODA Diabetes epidemiology;

collaborative analysis of

diagnostic criteria in Asia

WHR Waist to hip ratio FFA Free fatty acids

WC Waist circumference IR Insulin resistance

HDL High density lipoprotein-

cholesterol

PA Physical activity

TGL Triglyceride IAPP Islet amyloid polypeptide

LDL Low density lipoprotein

cholesterol

ADA American Diabetology

Association

VLDL Very low density lipoprotein

cholesterol

HbA1c Glycosylated

haemoglobin

CVD Cardiovascular disease NCEP National cholesterol

education program

HNF Hepatocyte nuclear factor HL Hepatic lipase

MODY Maturity onset diabetes in

young

MRDM Malnutrition related

(50)

34

MATERIALS AND METHODS

SOURCE OF STUDY: Data consists of primary data collected by the

principal investigator directly from the cases of newly detected type 2 diabetes

mellitus admitted in the medical ward in Coimbatore Medical College Hospital

DESIGN OF STUDY: Cross sectional descriptive study

PERIOD OF STUDY: Twelve months (September 2016- September 2017)

METHODOLOGY: This is a cross sectional descriptive study of 200 cases of

newly detected type 2 diabetes mellitus in the medical ward of Coimbatore

Medical College Hospital, Coimbatore, from September 2016 – September

2017

INCLUSION CRITERIA:

Patients fulfilling the ADA criteria for diagnosis of type 2 diabetes

mellitus who are –

Newly detected type 2 diabetes mellitus Age more than 20 years

EXCLUSION CRITERIA:

1. Patients below 20 years of age

2. Acute metabolic complications

3. Diabetic ketoacidosis

(51)

35 5. Acute illness

6. Acute myocardial infarction

7. Cerebrovascular accident

8. Thyroid disorders

9. Liver disorders

10.Secondary dyslipidaemia

11.Pregnancy

12.Drugs (Beta blockers, thiazide, steroids, hypolipidemic drugs, oral

contraceptives, anticoagulants)

The data obtained were analysed using SPSS software 21.0 software.

(52)

36

[image:52.595.119.513.381.647.2]

OBSERVATIONS AND RESULTS

TABLE 1- AGE DISTRIBUTION

AGE IN YEARS NO OF PATIENTS PERCENTAGE

< 30 13 6%

31-40 24 12%

41-50 54 27%

51-60 60 30%

> 60 49 25%

CHART 1- AGE DISTRIBUTION

6% 12%

27%

30% 25%

AGE DISTRIBUTION

< 30

31-40

41-50

51-60

(53)
[image:53.595.136.497.324.541.2]

37

TABLE 2- SEX DISTRIBUTION

SEX NO OF PATIENTS PERCENTAGE

MALE 131 65%

FEMALE 69 35%

CHART 2- SEX DISTRIBUTION

65% 35%

SEX DISTRIBUTION

MALE

(54)
[image:54.595.119.512.307.585.2]

38

TABLE 3- LIPID PROFILE

LIPID PROFILE ABNORMAL NORMAL

TOTAL CHOLESTEROL 64 136

TRIGLYCERIDES 133 67

HDL 91 109

LDL 116 84

CHART 3- LIPID PROFILE

64

133

91

116 136

67

109

84

0 20 40 60 80 100 120 140 160

TOTAL CHOLESTEROL TRIGLYCERIDES HDL LDL

LIPID PROFILE

(55)
[image:55.595.135.501.424.665.2]

39

TABLE 4- MEAN CHOLESTEROL VALUE BASED ON SEX

SEX

TOTAL CHOLESTEROL

MEAN SD

MALE 155.89 46.59

FEMALE 162.3 46.67

P VALUE - 0.356

UNPAIRED T TEST

NON SIGNIFICANT

CHART 4- MEAN CHOLESTEROL VALUE BASED ON SEX

155.

89

162.

3

M A L E F E M A L E

(56)
[image:56.595.104.532.114.322.2]

40

TABLE 5- MEAN TRIGLYCERIDE VALUE BASED ON SEX

SEX

TRIGLYCERIDES

MEAN SD

MALE 173.89 99.79

FEMALE 162.3 91.24

P VALUE - 0.854

UNPAIRED T TEST

NON SIGNIFICANT

CHART 5- MEAN TRIGLYCERIDE VALUE BASED ON SEX

173.89

162.3

156 158 160 162 164 166 168 170 172 174 176

MALE FEMALE

(57)
[image:57.595.125.507.448.686.2]

41

TABLE 6- MEAN HIGH DENSITY LIPOPROTEIN CHOLESTEROL

BASED ON SEX

SEX

HDL

MEAN SD

MALE 44.69 15.66

FEMALE 49.99 14.01

P VALUE - 0.019

UNPAIRED T TEST

SIGNIFICANT

CHART 6- MEAN HIGH DENSITY LIPOPROTEIN CHOLESTEROL

BASED ON SEX

44.69

49.99

42 43 44 45 46 47 48 49 50 51

MALE FEMALE

(58)
[image:58.595.121.511.440.705.2]

42

TABLE 7 - MEAN LOW DENSITY LIPOPROTEIN CHOLESTEROL

BASED ON SEX

SEX

LDL

MEAN SD

MALE 129.54 18.35

FEMALE 132.92 17.06

P VALUE - 0.198

UNPAIRED T TEST

NON SIGNIFICANT

CHART 7 - MEAN LOW DENSITY LIPOPROTEIN CHOLESTEROL

BASED ON SEX

127 128 129 130 131 132 133

MALE FEMALE

129.54

132.92

(59)
[image:59.595.126.518.340.591.2]

43

TABLE 8- DISTRIBUTION BASED ON BODY WEIGHT

BODY MASS INDEX NO OF PATIENTS PERCENTAGE

UNDERWEIGHT 2 1.00%

NORMAL 122 61%

OVERWEIGHT AND OBESE 76 38%

CHART 8- DISTRIBUTION BASED ON BODY WEIGHT

1%

61% 38%

BODY MASS INDEX

UNDERWEIGHT

NORMAL

(60)
[image:60.595.127.503.383.648.2]

44

TABLE 9- COMPARISON BETWEEN BMI AND CHOLESTEROL

BMI

TOTAL CHOLESTEROL

MEAN SD

UNDERWEIGHT 158 3.74

NORMAL 158.97 48.26

OVERWEIGHT 156.71 44.2

P VALUE - 0.947

UNPAIRED T TEST

NON SIGNIFICANT

CHART 9- COMPARISON BETWEEN BMI AND CHOLESTEROL

158

158.97

156.71

155.5 156 156.5 157 157.5 158 158.5 159 159.5

UNDERWEIGHT NORMAL OVERWEIGHT

(61)
[image:61.595.129.503.377.655.2]

45

TABLE 10- COMPRISON BETWEEN BMI AND TRIGLYCERIDE

BMI

TRIGLYCERIDES

MEAN SD

UNDERWEIGHT 80.5 33.23

NORMAL 168.31 88.39

OVERWEIGHT 182.88 18.75

P VALUE - 0.023

UNPAIRED T TEST

SIGNIFICANT

CHART 10- COMPARISON BETWEEN BMI AND TRIGLYCERIDE

80.5

168.

31 182.

88

U N D E R W E I G H T N O R M A L O V E R W E I G H T

(62)
[image:62.595.102.530.102.320.2]

46

TABLE 11- COMPARISON BETWEEN BMI AND HDL-C

BMI

HDL

MEAN SD

UNDERWEIGHT 50 2.82

NORMAL 46.2 13.99

OVERWEIGHT 46.92 12.4

P VALUE

UNPAIRED T TEST

NON SIGNIFICANT

CHART 11- COMPARISON BETWEEN BMI AND HDL-C

50

46.2

46.9

2

U N D E R W E I G H T N O R M A L O V E R W E I G H T

(63)

47

TABLE 12- COMPARISON BETWEEN BMI AND LDL-C

BMI

LDL

MEAN SD

UNDERWEIGHT 148 19.79

NORMAL 131.75 18.5

OVERWEIGHT 128.63 16.73

P VALUE - 0.194

UNPAIRED T TEST

NON SIGNIFICANT

CHART 12- COMPARISON BETWEEN BMI AND LDL-C

148

131.75

128.63

115 120 125 130 135 140 145 150

UNDERWEIGHT NORMAL OVERWEIGHT

(64)

48

TABLE 13- DISTRIBUTION OF WAIST CIRCUMFERENCE

WAIST CIRCUMFERENCE NO OF PATIENTS PERCENTAGE

HIGH 4 2.00%

NORMAL 196 98%

CHART 13- DISTRIBUTION OF WAIST CIRCUMFERENCE

2%

98%

WAIST CIRCUMFERENCE

HIGH

(65)

49

TABLE 14- COMPARISON BETWEEN WC AND CHOLESTEROL

WAIST CIRCUMFERENCE

TOTAL CHOLESTEROL

MEAN SD

HIGH 182.75 44.04

NORMAL 157.6 46.26

P VALUE - 0.028

UNPAIRED T TEST

SIGNIFICANT

CHART 14- COMPARISON BETWEEN WAIST CIRCUMFERENCE

AND CHOLESTEROL

182.

75

157.

6

H I G H N O R M A L

(66)

50

TABLE 15- COMPARISON BETWEEN WC AND TRIGLYCERIDES

WAIST CIRCUMFERENCE

TRIGLYCERIDES

MEAN SD

HIGH 187.8 123.02

NORMAL 172.67 96.45

P VALUE - 0.162

UNPAIRED T TEST

NON SIGNIFICANT

CHART 15- COMPARISON BETWEEN WC AND TRIGLYCERIDES

165 170 175 180 185 190

HIGH NORMAL

187.8

172.67

(67)

51

TABLE 16- COMPARISON BETWEEN WC AND HDL

WAIST CIRCUMFERENCE

HDL

MEAN SD

HIGH 60.75 8.34

NORMAL 46.22 15.26

P VALUE - 0.05 UNPAIRED T TEST

SIGNIFICANT

CHART 16- COMPARISON BETWEEN WC AND HDL

60.7

5

46.2

2

H I G H N O R M A L

(68)

52

TABLE 17- COMPARISON BETWEEN WC AND LDL

WAIST CIRCUMFERENCE

LDL

MEAN SD

HIGH 130.5 22.95

NORMAL 130.7 17.91

P VALUE - 0.979 UNPAIRED T TEST NON SIGNIFICANT

CHART 17- COMPARISON BETWEEN WC AND LDL

130.

5

130.

7

H I G H N O R M A L

(69)

53

TABLE 18- DISTRIBUTION OF WAIST HIP RATIO

WAIST HIP RATIO NO OF PATIENTS PERCENTAGE

HIGH 27 13.00%

NORMAL 173 87%

CHART 18- DISTRIBUTION OF WAIST-HIP-RATIO

13%

87%

WAIST HIP RATIO

HIGH

(70)

54

TABLE 19- COMPARISON OF WHR AND CHOLESTEROL

WHR

TOTAL CHOLESTEROL

MEAN SD

HIGH 174.81 51.95

NORMAL 155.48 45.82

P VALUE - 0.045 UNPAIRED T TEST

SIGNIFICANT

CHART 19- COMPARISON OF WHR AND CHOLESTEROL

174.

81

155.

48

H I G H N O R M A L

(71)
[image:71.595.136.497.399.671.2]

55

TABLE 20- COMPARISON OF WHR AND TRIGLYCERIDE

WHR

TRIGLYCERIDES

MEAN SD

HIGH 186.7 113.59

NORMAL 170.83 93.9

P VALUE - 0.429 UNPAIRED T TEST NON SIGNIFICANT

CHART 20- COMPARISON OF WHR AND TRIGLYCERIDE

186.7

170.83

160 165 170 175 180 185 190

HIGH NORMAL

(72)
[image:72.595.137.497.392.684.2]

56

TABLE 21- COMPARISON OF WHR AND HDL

WHR HDL

MEAN SD

HIGH 49.22 15.69

NORMAL 46.69 15.21

P VALUE - 0.324 UNPAIRED T TEST NON SIGNIFICANT

CHART 21- COMPARISON OF WHR AND HDL

45 45.5 46 46.5 47 47.5 48 48.5 49 49.5

HIGH NORMAL

49.22

46.69

(73)

57

TABLE 22- COMPARISON OF WHR AND LDL

WHR LDL

MEAN SD

HIGH 132.81 15.97

NORMAL 130.4 18.26

P VALUE - 0.518 UNPAIRED T TEST NON SIGNIFICANT

CHART 22- COMPARISON OF WHR AND LDL

132

.81

130.

4

H I G H N O R M A L

(74)
[image:74.595.102.531.132.346.2]

58

TABLE 23- COMPARISON BETWEEN FASTING

BLOOD SUGAR AND SBP

SBP

FBS

MEAN SD

HIGH 171.15 42.36

NORMAL 185.45 42.72

P VALUE - 0.018

UNPAIRED T TEST

SIGNIFICANT

CHART 23- COMPARISON BETWEEN FASTING

BLOOD SUGAR AND SBP

171.15

185.45

160 165 170 175 180 185 190

HIGH NORMAL

(75)
[image:75.595.135.498.495.716.2]

59

TABLE 24- COMPARISON BETWEEN POSTPRANDIAL

BLOOD SUGAR AND SBP

SBP

PPBS

MEAN SD

HIGH 254.23 17.73

NORMAL 275.2 22.74

P VALUE - 0.001

UNPAIRED T TEST

NON SIGNIFICANT

CHART 24- COMPARISON BETWEEN POSTPRANDIAL

BLOOD SUGAR AND SBP

254.

23

275.

2

H I G H N O R M A L

(76)
[image:76.595.135.498.462.680.2]

60

TABLE 25- COMPARISON BETWEEN FASTING

BLOOD SUGAR AND DBP

DBP

FBS

MEAN SD

HIGH 169.77 36.5

NORMAL 182.09 45.43

P VALUE - 0.058

UNPAIRED T TEST

NON SIGNIFICANT

CHART 25- COMPARISON BETWEEN FASTING

BLOOD SUGAR AND DBP

169.77

182.09

162 164 166 168 170 172 174 176 178 180 182 184

HIGH NORMAL

(77)
[image:77.595.134.499.486.732.2]

61

TABLE 26- COMPARISON BETWEEN POSTPRANDIAL

BLOOD SUGAR AND DBP

DBP

PPBS

MEAN SD

HIGH 252.11 39.2

NORMAL 270.32 48.88

P VALUE - 0.009

UNPAIRED T TEST

SIGNIFICANT

CHART 26 - COMPARISON BETWEEN POST PRANDIAL

BLOOD SUGAR AND DBP

252.

11

270.

32

H I G H N O R M A L

(78)
[image:78.595.131.501.464.704.2]

62

TABLE 27- COMPARSION BETWEEN WAIST CIRCUMFERENCE

AND FASTING BLOOD SUGAR

WAIST CIRCUMFERENCE

FBS

MEAN SD

HIGH 168.75 17.87

NORMAL 178.28 43.39

P VALUE - 0.662

UNPAIRED T TEST

NON SIGNIFICANT

CHART 27- COMPARSION BETWEEN WAIST CIRCUMFERENCE

AND FASTING BLOOD SUGAR

168.75

178.28

HIGH NORMAL

(79)
[image:79.595.131.501.463.708.2]

63

TABLE 28- COMPARSION BETWEEN WAIST CIRCUMFERENCE

AND POST PRANDIAL BLOOD SUGAR

WAIST CIRCUMFERENCE

PPBS

MEAN SD

HIGH 253.6 24.33

NORMAL 264.62 47

P VALUE - 0.638

UNPAIRED T TEST

NON SIGNIFICANT

CHART 28- COMPARSION BETWEEN WAIST CIRCUMFERENCE

AND POST PRANDIAL BLOOD SUGAR

253.

6

264.

62

H I G H N O R M A L

Figure

TABLE 1- AGE DISTRIBUTION
TABLE 2- SEX DISTRIBUTION
TABLE 3- LIPID PROFILE
TABLE 4- MEAN CHOLESTEROL VALUE BASED ON SEX
+7

References

Related documents

Study found that serum uric acid, LDL, VLDL, Total Cholesterol, Triacylglycerol were significantly increased in type 2 DM when compared to control group.. Activity

Conclusion: The significant findings of the study concluded the positive correlation of serum magnesium levels with high density lipoproteins and total

Seema Gupta et al JMSCR Volume 06 Issue 10 October 2018 Page 1365 To Study the Association of Free Insulin Levels, Obesity Markers &amp; Lipid Profile Parameters in Newly

Distribution of Serum lipid profile before treatment according to Gender in Atorvastatin 20mg shows no significant difference in mean serum cholesterol level in

The parameters assessed under lipid profile included serum total cholesterol (TC), serum triglycerides (TG), serum low density lipoproteins (LDL), serum high density

Blood samples were collected for estimating serum lipid level (serum cholesterol, triglyceride, LDL-C, HDL-C) and plasma glucose in fasting as well as post prandial condition..

Serum Apo estimated by ELISA and enzymatic methods were used for estimation of serum lipid parameters (Triglycerides, Total Cholesterol and HDL cholesterol were

Secondary outcomes in this study include changes in other glycemic parameters such as fasting glucose, insulin, fructosamine, changes in lipid profile (triglyceride, total