ABSTRACT
The aim of the present work was to study insulin resistance [IR] in obesity and to detect any possible role of leptin in the mediation of such resistance, as well as its consequences. Subjects and The present study was conducted on twenty obese otherwise healthy women [mean body mass index [BMI], 32.58 +/- 2.09kg/m2] and twenty nonobese healthy control women [mean BMI, 23.13 +/- 1.62kg/m2] of matched age and menopausal status. All subjects were subjected to the following measures: 1] anthropometric measurements including BMI, waist circumference and waist/hip ratio [WHR] [The first parameter was used as a surrogate for overall obesity, while the latter 2 parameters were used as surrogates for abdominal obesity], 2] systolic and diastolic blood pressure [SBP and DBP, respectively] measurements, 3] fasting and 2-hour postoral glucose tolerance test, 4] fasting plasma insulin and fasting plasma glucose/insulin ratio [both are surrogates for IR], 5] fasting serum lipid profile including total cholesterol [TC], high density lipoprotein cholesterol [HDL-C], low density lipoprotein cholesterol [LDL-C], triglycerides [TG], free fatty acids [FFAs], and atherogenicity ratio [TC/HDL-C], and 6] plasma leptin. Compared to the nonobese healthy controls, obese women demonstrated statistically significant increase in the measures of abdominal obesity [waist circumference and WHR], both SBP and DBP, glycemic control measures [fasting and 2 hour postoral glucose tolerance test], fasting plasma insulin and leptin levels. Obese women also demonstrated statistically significant decrease in fasting plasma glucose/insulin ratio. They also showed statistically significant dyslipidemia [hyper-cholesterolemia, low HDL-C, high LDL-C, hypertriglyceridemia, and high FFAs] and high atherogenicity ratio. Conclusions: Obesity is frequently accompanied by both insulin resistance ana by leptin resistance that are parallel to each other. Obese subjects have a tendency for increased high blood pressure, increased blood glucose levels and atherosclerosis. They are also dyslipidemic. Hyperleptinemia of obesity may mediate such cardiovascular and metabolic abnormalities. The strong correlation of plasma leptin to the measures of abdominal [visceral] obesity [especially the waist circumference] and the measures of IR [e.g. fasting plasma insulin and fasting plasma glucose/insulin ratio] supports the possibility of the role of leptin in the link between abdominal visceral obesity and IR