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
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
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
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.
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.
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
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
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
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
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
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
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
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
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
1
AIMS AND OBJECTIVES OF STUDY
1.
To study the occurrence of dyslipidaemia in newly detected type2diabetes mellitus
2.
To study the pattern of dyslipidaemia in this group3.
To assess the relationship between anthropometric measurements and2
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
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
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
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
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,
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.
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
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
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
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).
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
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.
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
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
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
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
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:
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
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
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
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
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
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:
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
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
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
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
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
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
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
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
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
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
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.
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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