INTRODUCTION
The obese (ob) gene is responsible for the production of the 167-amino-acid protein known as leptin, which is found in both mice and human individuals (Abubakaria & Bhopalb 2021). The quantity of the hormone that is produced is closely associated with the amount of body fat mass and the size of the adipocytes (Maffei et al., 1995; Considine et al., 1996). The hormone is expressed and secreted from the adipose tissue of both mice and humans. It has been demonstrated that persons who are obese have greater leptin levels than those who are of normal weight (Maffei, 1995). At first, researchers believed that the crucial function played by the leptin hormone in the control of food intake, energy expenditure, and whole-body energy balance in rats and humans was limited to those three areas (Adeniyi, Sanya, Fasanmade, Tijani & Uloko 2021). Since it was discovered that leptin replacement improves insulin sensitivity and diabetes in mice homozygous for mutations of the obesity gene (obgene), it has 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). This is due to the fact that Harris et al. discovered that leptin replacement improved insulin sensitivity and diabetes in mice homozygous for mutations of According to Heather et al(2012) .'s research, leptin also plays a part in maintaining normal levels of blood glucose. In addition to this, it has been demonstrated to bring blood glucose and insulin levels back into normal ranges in ob/ob mice who were previously diagnosed with type 2 diabetes (Agarwal1, Gupta, Dev, Kumar, Ahmad & Gupta 2022).
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