Obesity, a state of hyperleptinemia and leptin resistance, may play a role in the aeitiopathogenesis of type 2 diabetes mellitus. Leptin hormone which was originally recognized for its role as a satiety factor has now been implicated in a wide variety of multisystem biological functions, including the regulation of glucose homeostasis. However, there is paucity of information regarding leptin and its effect on the West African population. This study was therefore aimed at studying the relationship between leptin, obesity and insulin levels in type 2 diabetes mellitus. One hundred and eighty- three diabetics (183) and 96 control non-diabetics were studied. Pulse, blood pressure and anthropometric parameters of all the respondents were measured. Fasting blood sugar (FBS) was analyzed using the glucose oxidase method and lipid profile was determined using enzymatic method. Serum leptin and serum insulin were also analysed using enzyme linked immunoassay (ELISA) method. Homeostasis Model Assessment was used to determine insulin resistance. Type 2 diabetes mellitus patients and non- diabetic controls that were normotensive with no disease complications or associated chronic illness were used for the study. The mean serum leptin levels for the diabetics and non diabetics was observed to be 4.57 ± 0.17 ng/ml and 4.70 ± 0.25ng/ml respectively (p > 0.05) and the mean insulin level for the diabetic and non diabetic groups are 4.70 ± 0.25 μU/mL and 4.49 ± 0.01

μU/mL respectively (p < 0.05). A positive correlation was observed between leptin and body mass index (BMI) in both type 2 diabetic patients (r = 0.36, p < 0.05) and non-diabetics (r = 0.48, p < 0.05). A positive correlation was also found between leptin and waist circumference (WC) in both type 2 diabetic patients (r = 0.32, p < 0.05) and non-diabetics (r = 0.39, p < 0.05). Hip circumference (HC) also correlated positively with leptin in both the diabetics (r = 0.33, p < 0.05) and non-diabetics. The study also found a positive correlation between leptin and FBS in the non-diabetic group (r = 0.21, p < 0.05) but a negative correlation in the diabetic group(r = - 0.18, p < 0.05). A correlation was also found between leptin and HOMA-IR in both the diabetic (r = - 0.018, p < 0.05) and non-diabetics (r = 0.20, p < 0.05). However there was no significant relationship between leptin and insulin in both type 2 diabetic patients (r = 0.11, p > 0.05) and non-diabetics (r = - 0.06, p < 0.05). Age, BMI and WC emerged as the independent predictors of leptin in the diabetic group while BMI, WC and HC emerged as independent predictors of leptin in the non-diabetics.

Leptin is a 167-amino-acid protein transcribed from the obese (ob) gene of mice and human subjects (Zhang et al., 1997; Brennan et al., 2006). The hormone is expressed and secreted from the adipose tissue of mice and humans, and the quantity secreted is highly correlated with body fat mass and adipocyte size (Maffei et al., 1995; Considine et al., 1996). Obese people have been shown to have higher leptin levels than normalweight in people (Maffei, 1995).

Leptin hormone was initially thought to play a vital role only in the regulation of food intake, energy expenditure, and whole-body energy balance in rodents and humans (Janechova et al., 2001). Since the discovery that leptin replacement improves insulin sensitivity and diabetes in mice homozygous for mutations of the obesity gene (obgene), it is now been implicated in the pathophysiology of obesity and is shown to play a significant role in insulin resistance related to obesity (Harris et al., 1996). Leptin is also shown to play a role in blood glucose homeostasis (Heather et al., 2012). It has also been reported to normalize blood glucose and insulin levels in ob/ob mice with type 2 diabetes mellitus (Pellymounter, et al., 1995).