Life Sci J.2012 9(3):1258-1265

Correlation of the Leptin-to-Adiponectin Ratio (LAR) with Insulin Resistance in Lean and Obese SaudiFemales with Type 2 Diabetes

Adel M. A. Assiri and Hala F. M. Kamel, Life Science Journal 2012;9(3)1258-1265.

Biochemistry Department, Faculty of Medicine, Umm Al-Qura University, Makkha, KSA.

Abstract

    The role of various adipokines as a link between obesity and diabetes mellitus has recently been better elucidated. The aim of this study was to investigate the correlation of the leptin/adiponectin ratio (LAR) with insulin resistance in obese and diabetic Saudi females. Methods: This study included 373 Saudi females divided into two groups: type 2 diabetic (n=196) and normal control (n=177).The groups were further divided according to BMI into normal obese (n=85), normal non-obese (n=92), diabetic obese (n=118) and diabetic non-obese (n=78) subgroups. For all studied groups, levels of leptin, adiponectin, insulin and C-reactive protein were measured using (ELISAs).The glucose, triglyceride, cholesterol, LDL and HDL levels were determined using colorimetric assays, and the homeostasis model assessment ratio (HOMA-IR) was determined using a formula derived from fasting insulin and glucose levels. Results: The leptin levels were significantly higher and the adiponectin levels were significantly lower in the diabetic group compared to the normal control group (P value < 0.05). The LAR showed a significant positive correlation with the HOMA-IR (r=0.129, P=0.01) and a highly significant positive correlation with BMI, glucose, cholesterol, LDL and insulin (r=0.220, P=0.00; r=0.135, P=0.009; r=0.201, P=0.000; r=0.215, P=0.000; and r= 0.212, P=0.000, respectively). There was a statistically significant difference among all subgroups for the LAR (F=20.60, P=0.00) and for the HOMA-IR (F=17.73, P= 0.001). Conclusion: The LAR has the potential to become a new laboratory marker for insulin resistance in patients with obesity and type 2 diabetes mellitus.

Supplementary

Obesity is closely related to insulin resistance, glucose intolerance and type 2 diabetes. The mechanisms linking insulin resistance and obesity are not yet fully understood, but adipose tissue may play a role in this association because it is an active metabolic organ that releases different adipocytokines. Leptin and adiponectin, two of the most abundant adipocyte products, are thought to link obesity, insulin resistance, and related disorders. Obesity is the dominant cause of insulin resistance. in adult humans it is characterized by a combination of adipocytes hypertrophy and, to a lesser extent, adipocytes hyperplasia. As hypertrophic adipocytes secrete more leptin and less adiponectin, the plasma leptin/adiponectin ratio (LAR) has been proposed as a potentially useful measure of insulin resistance and vascular risk, given: the central role of excess adipose tissue in insulin resistance;  the now well-recognized capacity of adipose tissue to produce hormones (adipocytokines) involved in the regulation of energy balance and insulin action; and the fact that the two best characterized adipocytokines (leptin and adiponectin) respond in a reciprocal manner to increasing adiposity. Effects of adiponectin and leptin on energy metabolism differ; leptin improves insulin sensitivity through activation of AMP protein kinase (AMPK), which controls cellular concentrations of malonyl-CoA, thereby inhibiting acetyl-CoA carboxylase .As a result, there is decrease of intracellular malonyl-CoA and a decline of lipogenesis associated with increased fatty-acid beta- oxidation. Adiponectin enhances insulin sensitivity through activation of AMPK . Adiponectin also affects hepatic glucose production by decreasing the mRNA expression of two essential gluconeogenesis enzymes: phosphoenolpyruvate carboxykinase; and glucose-6-phosphatase . LAR has previously been shown to correlate with carotid intimal medial thickness and to predict the presence of the metabolic syndrome .LAR has better ability for correctly classifying subjects with and without metabolic syndrome than adiponectin or leptin alone. However, its correlation with insulin sensitivity has not previously been established. Previous reports have demonstrated that diabetic subjects have lower levels of plasma adiponectin than non-diabetic subjects, independent of body mass index (BMI) , indicating an association between lower adiponectin levels and type 2 diabetes. Although it appears that leptin and adiponectin may contribute to the development of insulin resistance and type 2 diabetes in obese subjects, the association between adiponectin and insulin resistance and type 2 diabetes may be modulated by leptin, or vice versa . Little is known regarding the distribution and the determinants of leptin and adiponectin levels in the general population There is age-related increase in leptin levels that may be  attributable to changes in fat mass in women and probably also in men. Leptin and adiponectin levels are more related to BMI than to body fat mass .

      In our study, we studied correlation of LAR, HOMA-IR among Saudi females: Diabetic obese, non -obese, control non diabetic obese and non-obese. We found that LAR showed significant positive correlation with HOMA-IR and BMI in all studied groups beside LAR showed highly significant difference among whole studied subgroups . Our results showed that LAR had highly significant positive correlation with Glucose, cholesterol, LDL, Insulin and highly significant negative correlation with HDL.LAR showed highly significantly different among whole studied subgroups by ANOVA test while HOMA-IR showed no significant difference for obese and non-obese diabetics type 2 which may indicates that LAR was better than HOMA-IR for discriminating  between diabetics or normal non diabetic females weather obese or non-obese . Our study also  demonstrated that LAR correlated with insulin resistance more closely than leptin and adiponectin alone or HOMA-IR .We concluded that LAR levels were associated with calculated value of insulin resistance HOMA-IR, LAR ratio promises to become a new laboratory marker of insulin resistance in obesity and Type 2 diabetes mellitus. Hala Kamel-1

Corresponding author :

Dr. Hala Fawzy Mohamed Kamel (MBBCH , MSc, MD)

Assistant prof. Medical Biochemistry ,

Biochemistry Department ,

Faculty of Medicine , UQU University ,KSA.

Makkha 7607, Kingdom of Saudi Arabia.

kamelhala@msn.com

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