Recommendations for Future Work - Enhanced MPPT Controllers for Smart Grid Applications

Chapter 6 Conclusion

6.3 Recommendations for Future Work

Table 4.3 shows the values of the anthropometric parameters used to assess obesity. The three groups were significantly different in the values of their waist circumference, hip circumference, waist to hip circumference ratio, body weight and body mass index but not in the values of their height. The BMI ranges of the Obese Type 2 DM group, Obese non-diabetic females group and the Non-obese Type 2 DM group were 30.0 to 46.0 Kg/m², 30.0 to 52.3 Kg/m² and 19.7 to 29.3 Kg/m² respectively. In accordance to BMI grading by WHO, obesity class I, class II and Class III were present in 41 (68.3%), 15 (25.0%) and 4 (6.7%) of the Obese Type 2 DM subjects.

Among the Obese non-diabetic subjects, 27 (45.0%) had class I obesity, 18 (30.0%) had class II obesity and 15 (25.0%) had class III obesity. The Non-obese Type 2 DM group had 21 (35.0%) subjects with normal weight and 39 (65.0%) subjects who were overweight. The waist

circumference (WC) ranges of the Obese Type 2 DM group, Obese non-diabetic females group and the Non-obese Type 2 DM group were 93.0 to127.0 cm, 85.0 to 129.0 cm and 76.0 to 106.0 cm respectively. Central obesity as defined by WC of at least 88 cm was present in all the Obese Type 2 DM subjects, 59 (98.3 %) of the Obese non-diabetic subjects and in 43 (71.7%) of the Non-obese Type 2 DM subjects.

Table 4.3: Comparison of the anthropometric parameters of the study participants Parameter Obese T2DM

(a)

Obese Non-DM (b)

Non-Obese T2DM (c)

P value (aVbVc)

P value (aVb)

Ht (cm) 157.2 ± 5.1 157.6 ± 10.6 160.3 ± 5.5 0.540 0.963

Wt (Kg) 85.6 ± 10.1 92.1 ± 14.0 66.1 ± 7.6 0.0001* 0.014*

BMI (Kg/m²) 34.5 ± 3.4 36.5 ± 5.1 25.9 ± 2.3 0.0001* 0.044*

WC (cm) 106.3 ± 7.5 105.6 ± 10.4 91.3 ± 6.4 0.0001* 0.969

HC (cm) 113.7 ± 8.9 119.9 ± 10.4 97.9 ± 5.5 0.0001* 0.003*

WHR 0.94 ± 0.06 0.88 ± 0.06 0.93 ± 0.05 0.0001* 0.0001*

WC= Waist Circumference, HC = Hip Circumference, Ht = Height, Wt = Weight, WHR = Waist to Hip Circuference Ratio, BMI = Body Mass Index *P value < 0.05 is statistically significant

4.4: Comparison of the blood pressure measurements of the study participants

Table 4.4 shows the mean and standard deviation of blood pressure measurements of the study population. The three groups had similar mean systolic BP and diastolic BP. The systolic BP ranges of the Obese Type 2 DM group, Obese non-diabetic females group and the Non-obese Type 2 DM group were 100 to 200 mmHg , 100 to 170 mmHg and 94 to 210 mm respectively.

Also the diastolic BP ranges of the Obese Type 2 DM group, Obese non-diabetic females group and the Non-obese Type 2 DM group were 60 to 110 mmHg, 60 to 120 mmHg and 60 to 120 mmHg respectively.

Table 4.4: Comparison of blood pressure measurement and hypertension staging among the study participants

Parameter Obese T2DM (a)

Obese Non-DM (b)

Non-Obese T2DM (c)

P value (aVbVc)

P value (aVb) Systolic BP (mmHg) 133.3 ±19.2 124.8 ± 18.7 130.2 ± 21.2 0.51 0.068 Diastolic BP

(mmHg)

79.2 ± 11.1 78.3 ± 11.8 78.7 ± 10.8 0.908 0.900 Normal BP 11 (18.3%) 19 (31.7%) 13 (21.7%)

Staging

Prehypertension 23 (38.3%) 24 (40.0%) 26 (43.3%) Stage 1

Hypertension

19 (31.7%) 11 (18.3%) 13 (21.7%) Stage 2

Hypertension

7 (11.7%) 6 (10.0%) 8 (13.3%)

BP = Blood Pressure, * P value < 0.05 is statistically significant.

Table 4.5: Comparison of the biochemical parameters of the study participants

Parameter Obese T2DM

(a)

Obese Non-DM (b)

Non-Obese T2DM (c)

P value (aVb)

P value (aVbVc)

Fasting plasma glucose (mmol/l)

8.1 ± 2.9 5.4 ± 0.5 8.3 ± 2.9 0.0001* 0.0001*

HbA1C (%) 8.3 ± 2.9 NA 8.7 ± 3.0 NA 0.457

High density lipoprotein cholesterol (mmol/l)

1.2 ± 0.3 1.2 ± 0.3 1.3 ± 0.3 1.000 0.339

Low density lipoprotein cholesterol (mmol/l)

3.4 ± 0.9 3.1 ± 0.8 3.2 ± 1.0 0.447 0.462

Total cholesterol (mmol/l)

5.4 ± 0.9 5.1 ± 0.8 5.2 ± 1.0 0.363 0.387

Triglyceride (mmol/l) 1.6 ± 0.4 1.6 ± 0.5 1.5 ± 0.4 0.959 0.244 Serum leptin (ng/ml) 20.61 ± 15.13 20.94 ± 17.64 7.59 ± 3.39 0.999 0.0001*

Serum Insulin (µIU/ml) 23.19 ± 19.54 20.67 ± 20.24 7.51 ± 3.84 0.866 0.0001*

HOMA-IR 8.11 ± 7.41 5.07 ± 5.25 2.76 ± 1.77 0.032* 0.0001*

Prevalence of IR (N/%) 60 (100.0%) 59 (98.3%) 40 (66.7%)

HbA1C = Glycosylated haemoglobin, HOMA-IR = Homeostasis model of assessment of insulin resistance. * P value < 0.05 is statistically significant, NA = Not Applicable, IR = Insulin Resistance

4.5 Comparison of biochemical parameters between the obese type 2 diabetic and obese non-diabetic female subjects

Table 4.5 shows the comparison of the mean of biochemical parameters between the Obese type 2 diabetic and Obese non-diabetic female subjects a. The mean serum leptin levels (20.61 ± 15.13 ng/ml) in the Obese Type 2 DM subjects compared to the levels (20.94 ± 17.64 ng/ml) in the Obese non-diabetic females did not differ significantly (p =0.999). Similarly, there was no statistically significant difference in the mean serum levels of insulin (23.19 ± 19.54 µIU/ml) in Obese Type 2 DM compared to the levels (20.67 ± 20.24µIU/ml) in Obese non-diabetic subjects (p = 0.67). The HOMA-IR level (8.11 ± 7.41) in the Obese Type 2 DM subjects was

significantly higher than the level (5.07 ± 5.25) in the Obese non-diabetic females subjects (p = 0.032)

4.6: Comparison of the biochemical parameters of all subjects

Table 4.5 also shows the comparison of the mean of biochemical parameters among the three groups. The levels of their HDL-Cholesterol (p = 0.339), LDL-Cholesterol (p = 0.4620), Total-Cholesterol (P = 0.387) and Triglyceride (P = 0.244) showed no statistically significant

differences between groups. The mean serum levels of leptin (F=18.902, df = 2, p= 0.0001), insulin (F =15.838, df = 2, p = 0.0001 and HOMA-IR (F= 15.143,df = 2, p =0.0001) differed significantly among the groups.

Figure 4.2 Mean serum leptin levels in the groups of study participants

The mean serum leptin levels in Obese Type 2 DM, Obese non-diabetic and Non-obese Type 2 DM subjects were 20.61 ± 15.13(95% CI = 16.70-24.52), 20.94 ± 17.64 (95% CI = 16.38-25.50) and 7.59 ± 3.39 (95% CI = 6.72-8.47) ng/ml respectively as shown in figure 4.2.

Figure 4.3 Mean serum insulin levels in the groups of study participants

The mean serum insulin levels in Obese Type 2 DM, Obese non-diabetic females and Non-obese Type 2 DM subjects were 23.19 ± 19.54 (95% CI =18.14-28.24), 20.67 ± 20.24 (95% CI = 15.44-25.90) and 7.51 ± 3.84 (95% CI = 6.51-8.50) µIU/ml respectively as shown in figure 4.3.

The mean levels of HOMA-IR in Obese Type 2 DM, Obese non-diabetic females and Non-obese Type 2 DM subjects were also 8.11 ± 7.41 (95% CI = 6.20-10.03), 5.07 ± 5.25 (95% CI = 3.71-6.42) and 2.76 ± 1.77 (95% CI = 2.31-3.22) respectively. The prevalence of insulin resistance in each group as defined by HOMA-IR cut off level of ≥ 2 was 100.0% among the obese T2DM subjects, 98.3% among the obese non-diabetic subjects while it was 66.7% among the non-obese T2DM subjects.

Table 4.6: Relationship of Serum Leptin Levels with BMI, WC, Serum Insulin Levels, HOMA-IR, and HbA1C by Group.

Parameter

Obese T2DM Obese Non-DM Non-Obese T2DM r-value

p-value

r-value p-value

r-value

p-value

BMI +0.038 0.776 +0.281* 0.030 +0.039 0.769

WC -0.025 0.849 +0.237 0.068 +0.058 0.660

Serum insulin -0.077 0.558 +0.446* 0.0001 +0.030 0.821

HOMA-IR -0.293* 0.023 +0.385* 0.002 0.000 0.996

HbA1C -0.255* 0.049 NA NA -0.170 0.195

BMI = Body Mass Index, WC= Waist Circumference, r = Spearman’s simple correlation coefficient, *p < 0.05 is statistically significant, NA = Not Applicable.

4.7 Relationship of Serum Leptin Levels with BMI, WC, Serum Insulin Levels, HOMA-IR, and HbA1C by Group.

Table 4.6 shows the correlation coefficients of relationship between serum leptin levels and BMI, WC, serum insulin levels, HOMA-IR, and HbA_1C by group. In the Obese Type 2 DM subjects, serum leptin levels were not significantly correlated with BMI, WC, and serum insulin levels but were significantly and negatively correlated with HOMA-IR and HbA1C. In the Obese non-diabetic subjects, serum leptin levels were significantly and positively correlated with BMI, serum insulin and HOMA-IR but were not significantly correlated with WC. In the Non-obese Type 2 DM subjects, there were no significant correlations between serum leptin levels and BMI, WC, serum insulin levels, HOMA-IR, and HbA1C.

Table 4.7: Relationship of HOMA-IR with BMI, WC, Serum Insulin levels, and HbA1C by Group.

Parameter

Obese T2DM Obese Non-DM Non-Obese T2DM r-value

p-value

r-value p-value

r-value p-value BMI -0.105 0.424 +0.432* 0.001 -0.011 0.932 WC +0.008 0.951 +0.454* 0.0001 -0.007 0.956

Serum insulin +0.483* 0.0001 +0.385* 0.002 +0.279* 0.031

HbA1C +0.196 0.134 NA NA +0.163 0.214

r = Spearman’s simple correlation coefficient, *p < 0.05 is statistically significant, NA = Not Applicable

4.8 Relationship of HOMA-IR with BMI, WC, Serum Insulin Levels, and HbA1C by Group.

Table 4.7 shows the correlation coefficients between HOMA-IR and BMI, WC, serum insulin levels, and HbA1C by Group. In the Obese Type 2 DM subjects, HOMA-IR was not significantly correlated with BMI, WC, and HbA_1C but was significantly and positively correlated with serum insulin levels. In the Obese non-diabetic subjects, HOMA-IR was still significantly and positively correlated with BMI, WC, and serum insulin level. Furthermore, in the Non-obese Type 2 DM subjects, there was no significant correlation between HOMA-IR and BMI, WC, and HbA1C, except for its significant positive correlation with serum insulin levels.

Table 4.8: Classification of diabetes control among diabetic subjects.

Parameters Controlled DM

n (%) = 48 (40%)

Non-Controlled DM n (%) = 72 (60%)

HbA1C (%) 5.9 ± 0.7 10.2 ± 2.4

Obese T2DM 25 (41.7%) 35 (58.3%)

Non-Obese T2DM 23 (38.3%) 37 (61.7%)

T2DM = Type 2 Diabetes Mellitus, n = number of subjects,

4.9 Relationship between serum leptin levels and glycaemic control in subjects with type 2 diabetes mellitus

Table 4.8 and 4.9 show the classification diabetes control and comparison of biochemical parameters between obese subjects with controlled and non-controlled diabetes. The total number of the diabetic subjects in the study was 120. Forty-eight (40%) diabetic subjects were assessed to have controlled diabetes (HbA1c < 7%) with a mean HbA1C of 5.09 ± 0.7% while 72 (60%) diabetic subjects had non-controlled diabetes (HbA_1C ≥ 7%) with a mean HbA_1C of 10.2 ± 2.4%. Among the Obese Type 2 DM subject group, 25 (41.7%) had controlled diabetes with a mean HbA_1C of 5.9 ± 0.8% while 35 (58.3%) were uncontrolled diabetes with a mean HbA_1C of 10.0 ± 2.4%. Among the Non-obese Type 2 DM subject group, 23 (38.3%) werecontrolled diabetes with a mean HbA1C of 5.9 ± 0.7% while 37(61.7%) were uncontrolled diabetes with a mean HbA_1C of 10.4 ± 2.4% as shown in table 4.11. There was no statistically significant difference in the proportion of subjects with diabetic control in both groups (X² =1.39, p = 0.709).

Table 4.9: Comparison of biochemical parameters between obese T2DM subjects with controlled and non-controlled diabetes.

Parameters Controlled DM

n (%) = 25 (41.7%)

Non-Controlled DM n (%) = 35 (58.3%)

P-value

HbA_1C (%) 5.9 ± 0.8 10.0 ± 2.4 0.0001*

Serum leptin (ng/ml) 25.81 ± 21.00 16.90 ± 7.26 0.051 Serum Insulin

(µIU/ml)

24.61 ± 21.20 20.90 ± 18.22 0.284

HOMA-IR 7.80 ± 6.28 8.33 ± 8.20 0.788

DM = Diabetes Mellitus, *P < 0.05 is statistically significant

Table 4.10: Correlation between Serum Leptin Levels and HbAIC in subjects with controlled and non-controlled diabetes.

Subjects

Controlled Diabetes Non-Controlled

Diabetes

r-value p-value r-value p-value

Obese T2DM +0.052 0.806 -0.238 0.168

Non-Obese T2DM -0.096 0.662 -0.202 0.231

T2DM= Type 2 diabetes mellitus, r = Spearman’s simple correlation coefficient, *p < 0.05 is statistically significant

4.10: Relationship between serum leptin levels and glycaemic control in obese type 2 diabetic subjects

Table 4.9 shows the comparison of the mean levels of biochemical parameters between obese T2DM subjects with controlled and those with non-controlled diabetes. The mean serum leptin levels (25.81 ± 21.00 ng/ml) of the obese diabetic subjects with controlled diabetes was higher than the mean level (16.90 ± 7.26 ng/ml) in those with non –controlled diabetes but this was not statistically significant (t = 2.040, df = 28.143, p = 0.051). Similarly, there was no significant correlation between the serum leptin levels and HbA1C in the obese diabetic subjects with controlled diabetes (r = 0.052, p = 0.806) and also in the obese diabetic subjects with non-controlled diabetes (r = -0.238. p = 0.168) as previously shown in Table 4.10.

The mean serum insulin levels (24.61 ± 21.20 µIU/ml) of the obese diabetic subjects with controlled diabetes was also higher than the mean level (20.90 ± 18.22 µIU/ml) in those with non –controlled diabetes but this was not statistically significant (t = 1.081, df = 58, p = 0.284).

The mean HOMA-IR levels (7.80 ± 6.281) of the obese diabetic subjects with controlled diabetes was lower than the mean level ( 8.33 ± 8.20) in those with non-controlled diabetes. This difference was also not statistically significant (t = -.270, df = 58, p = 0.788).

Table 4.11: Comparison of biochemical parameters between non-obese T2DM subjects with controlled and non-controlled diabetes.

Parameters Controlled DM

n (%) = 23 (38.3%)

Non-Controlled DM n (%) = 37 (61.7%)

P-value

HbA_1C (%) 5.9 ± 0.7 10.4 ± 2.4 0.0001*

Serum leptin (ng/ml) 8.18 ± 4.03 7.23 ± 2.92 0.300 Serum Insulin

(µIU/ml)

8.07 ± 5.87 7.15 ± 1.67 0.371

HOMA-IR 2.77 ± 2.60 2.76 ± 1.00 0.982

Prevalence of IR (n/%)

12 (52.2%) 28 (75.7%) 0.06

DM = Diabetes Mellitus, IR = Insulin Resistance, *P < 0.05 is statistically significant

4.11 Relationship between serum leptin levels and glycaemic control in non-obese type 2 diabetic subjects

Table 4.11 shows the comparison of the mean levels of biochemical parameters between non-obese subjects with controlled and non-controlled diabetes. The mean serum leptin level (8.18 ± 4.03 ng/ml) in the non-obese diabetic subjects with controlled diabetes was higher than the mean level ( 7.23 ± 2.92 ng/ml) in those with non -controlled diabetes but this was not

statistically significant (t = 1.047, df = 58, p = 0.300). There was also no significant correlation between the serum leptin levels and HbA1C in the non-obese diabetic subjects with controlled diabetes (r = -0.096, p = 0.662) and in the non-obese diabetic subjects with non-controlled diabetes (r = -0.202. p = 0.231) as shown in table 4.10.

The mean serum insulin levels (8.07 ± 5.87 µIU/ml) in the non-obese diabetic subjects with controlled diabetes was also higher than the mean level (7.15 ± 1.67 µIU/ml) in those with non -controlled diabetes but this was not statistically significant (t = ,902, df = 58, p = 0.371). The mean HOMA-IR level (2.77 ± 2.60) in the non-obese diabetic subjects with controlled diabetes was slightly higher than the mean level ( 2.76 ± 1.0) in those with non –controlled diabetes. This difference was also not statistically significant (t = 0.22, df = 58, p = 0.982).

CHAPTER FIVE

5.0: DISCUSSION

5.1: Preamble

The prevalence of obesity is rising globally and this rising trend has been recognized as a major driver of the increasing prevalence of type 2 diabetes.⁷ Obese subjects, especially females, are also known to have high circulating levels of leptin.^{18, 19} Leptin, in addition to its ability to inhibit energy intake and increase energy expenditure also has ability to regulate glucose metabolism.¹³ Most obese subjects have leptin resistance,² hence this puts them at risk of type 2 diabetes, a condition characterized by chronic hyperglycaemia as a result of impaired glucose metabolism.

5.2: Socio-Demographic Characteristics of Study Population

This was a study of serum leptin, serum insulin and HOMA-IR in 180 female Nigerians in Ile-Ife. The age range of subjects in this study was 34 to 64 years. There were three groups consisting of 60 subjects in each group. The mean ages of subjects in each group were comparable and similar to that observed in Turkish study.⁵⁸ These females were mainly traders (44.4%) and teachers (22.2%) which appear to be the most common occupation for females in our environment. The educational attainments and social habits of subjects were similar in obese and non-obese groups thus suggesting that these attributes may not explain any difference that existed among of the groups of study subjects.

5.3: Clinical Characteristics of Study Population

The mean duration of T2DM was shorter in obese T2DM subjects compared to non-obese T2DM subjects. It could be that non-obese T2DM subjects were also obese initially but had been

subjected to longer period of education on life style modification and treatment that could have resulted in their present body mass index though 71.7% of them still had central obesity.

The prevalence of previously diagnosed hypertension in obese T2DM and non-obese T2DM Subjects were 76.7% and 63.3 % respectively, though about one third of the obese non-diabetic subjects were also hypertensive. This is not surprising as hypertension and T2DM are said to be in tandem. These finding are in keeping with the presence of metabolic syndrome in our subjects wth hypertension, obesity and T2DM being essential components of the metabolic syndrome,⁶⁷ that is associated with increased risk of cardiovascular morbidity and mortality.

Family history of T2DM and obesity was much higher in the obese T2DM subjects compared with non-obese T2DM subjects . Similarly, family history of obesity was more in the obese subjects compared with non-obese subjects. This could affirm the familial tendencies found in certain non-communicable diseases such as T2DM and obesity.

Twin studies have demonstrated that familial aggregation of obesity has a genetic component and is not only due to cultural or environmental factors clustered in families.⁹⁰ In addition, linkage studies have also identified markers and genes related to obesity in virtually all human chromosomes.⁹⁰ This study revealed that 83.3% of the obese T2DM subjects, 75.0% of the obese non-diabetic subjects and 41.7% of the non-obese T2DM subjects had family history of obesity

76 thus supporting the strong familial tendency for obesity.

Majority of the subjects in each of the groups had central obesity as documented by waist circumference irrespective of their BMI. 100% of obese T2DM, 98.3% of obese non-diabetic, and at least 70% of non-obese subjects had central obesity respectively. This high prevalence of central obesity among diabetic subjects was similar to that reported by Fasanmade et al ³⁶ in Lagos among Nigerian females with T2DM. Central obesity is particularly recognized as an independent risk factor for increased cardiovascular morbidity and mortality.

5.4: Comparison of serum leptin levels in the various groups.

Serum leptin levels was significantly higher in both obese subjects with or without type 2 diabetes mellitus than in non-obese type 2 diabetic subjects. The higher levels of leptin in obese than in non-obese subjects is most probably due to the fact that leptin is produced by adipose tissue in proportion to the amount of the adipose tissue in the body. That is the higher the body mass of adipose tissue, the higher the circulating levels of leptin.^{27, 91} Higher serum leptin levels in obese subjects was had been previously reported, ^{16, 18} although when compared to the levels reported in other populations,^{20, 47} the serum leptin levels in our subjects were lower. This is probably due to ethnic variations in serum levels of leptin as a result of variation in the severity of obesity.^{19, 20} Luke et al.,²⁰ demonstrated that serum leptin levels in Nigerians were lower when compared to that of Jamaicans and Americans respectively.

Our study also showed that levels of serum leptin in obese non-diabetic subjects and obese type 2 diabetic subjects were similar. Liuzzi et al.,¹⁸ also found no statistically significance difference in serum leptin levels of their obese diabetic subjects when compared with obese non-diabetics, while Guler et al.,¹⁷ reported that leptin levels were not affected by the presence or absence of type 2 diabetes mellitus among Turkish women like our study.

Moreover, Buyukbese et al.,⁵⁸ in a study among Turkish obese women with and without type 2 diabetes mellitus demonstrated a significantly higher serum level of leptin in the group without type 2 diabetes melltus. This difference in finding could probably be as a result of variation in insulin secretion in T2DM since insulin is also known to increase leptin production.⁵⁷ The non -obese type 2 diabetic subjects group in our study had the lowest serum levels of leptin which is not unexpected considering their body mass index. Their leptin levels were also similar to the levels previously reported for non –obese females with type 2 diabetes mellitus in Nigeria ,⁵⁶ perhaps because they all shared a common ethnic background.

Many investigators demonstrated that leptin had a significant correlation with BMI.20, 52, 58, 92

In our study also leptin had a significant correlation with BMI but only in the obese non-diabetic subjects. This trend was also observed in the relationship between serum leptin and serum insulin. The poor correlation between serum leptin levels, with BMI and serum insulin levels in diabetic subjects may be a reflection of anti-diabetic therapy that modulates insulin secretion and thus influencing leptin secretion.¹⁷ Leptin had a significant inverse correlation with HOMA-IR in obese T2DM subjects and no correlation with HOMA-IR in non-obese subjects while it had had a significant positive correlation with HOMA-IR in obese non diabetic subjects. This suggests that leptin may reduce insulin resistance in obese T2DM subjects and therefore be a potential therapeutic agent.

The levels of fasting lipid profiles (HDL- Cholesterol, LDL-Cholesterol, Total-Cholesterol, and Triglycerde) observed in our study were similar in all subject groups and may be due to the fact that some of our diabetic subjects were already on lipid lowering drugs.

5.5: Relationship between serum leptin levels and glycaemic control in female subjects with type 2 diabetes.

Serum leptin levels were higher in the obese type 2 diabetic subjects with controlled diabetes than the levels in those with non-controlled diabetes though this difference was not statistically significant. Buyukbese et al,⁴⁷ had previously reported significantly elevated levels of leptin in obese female subjects with controlled diabetes. Among the non-obese type 2 diabetic subjects in this study, those with controlled diabetes also had a non-significant elevation in their serum leptin. The elevated serum leptin levels in subjects with controlled diabetes may be attributable to the known regulatory function of leptin on glucose metabolism.^{13, 17} Elevated serum leptin levels therefore appear to be good for glycaemic control.

A previous study demonstrated a weak but significant negative correlation between serum levels of leptin and glycaemic control before and after a period of treatment of DM.¹⁷ Our study also demonstrated a weak positive but non-significant correlation of serum leptin levels and glycaemic control (HbA1C) in both obese T2DM subjects and non-obese T2DM subjects. This variation in findings may all be due to the effect of DM treatments such as insulin secretagogues and insulin sensitizers commonly used by our patients.

5.6: Comparison of severity of insulin resistance in the various groups.

HOMA-IR is a surrogate marker of insulin resistance that has been found to be well correlated with the measure of insulin resistance determined by euglycaemic clamp which is the gold standard.⁸⁵ The higher the HOMA-IR score, the higher the severity of insulin resistance.^{85, 86} In this study, HOMA-IR scores increased significantly across the groups with the lowest scores recorded in non-obese type 2 diabetic subjects and the highest scores recorded in obese type 2 diabetic subjects. The prevalence of insulin resistance was 100% among obese T2DM subjects, 98.3 % among obese non-diabetic subjects, and 66.7% among non-obese T2DM subjects. This finding further illustrates the fact that obesity is a risk factor for insulin resistance which is a known cause of type 2 diabetes mellitus. Oli et al.,⁸⁹ in Enugu, Nigeria had previously shown that insulin resistance estimated by HOMA-IR is a major feature of type 2 diabetes mellitus in Nigerians and that obesity consistently correlated with and predicted insulin resistance. The higher degree of insulin resistance among obese non -diabetic subjects in this present study also suggests that obese subjects can be targeted for the treatment of insulin resistance in order to prevent or delay future occurrence of type 2 diabetes mellitus in them.

There were no significant correlations between BMI and Waist Circumference (WC) with HOMA-IR in both obese T2DM subjects and non-obese T2DM subjects but these correlations were demonstrated to be statistically significant in obese non-diabetic subjects. Liuzzi et al.,¹⁸ have demonstrated a significant positive correlation between HOMA-IR and BMI in a population of obese non-diabetic Italian subjects. The poor correlation between BMI and WC with HOMA-IR in all our diabetic subjects may be due to the modulatory effect of DM therapy on insulin resistance in obese subjects.

CHAPTER SIX

6.0 CONCLUSIONS AND RECOMMENDATIONS

In document Enhanced MPPT Controllers for Smart Grid Applications (Page 91-95)