Leptin ELISA

INTENDED USE

The Leptin ELISA is a manual enzyme immunoassay for the quantitative measurement of leptin in human serum or Li-heparin plasma. For in vitro diagnostic use. For laboratory professional use. The device is intended to be used as an aid to the diagnosis of adiposity, leptin resistance, and congenital leptin deficiency.

Scientific Validity

Leptin is produced primarily in the adipocytes of white adipose tissue and circulates in blood in free form and bound to proteins (1). In mammals, leptin is pleiotropic, regulating a multitude of physiological processes. Leptin reduces appetite and food intake, and inhibits hepatic glucose production, fatty acid synthesis and the expression of resistin. In contrast, Leptin increases energy expenditure by inducing oxidation of fatty acids in liver and muscle. Moreover, Leptin stimulates insulin secretion and glucose uptake as well as secretion of inflammatory cytokines (2,3). Leptin serves as a lipostatic signal and conveys critical information regarding metabolic state to the brain by stimulating anorexic proopiomelanocortin/cocaine and amphetamine-related transcript neurons and inhibiting orexigenic neuropeptide Y/ agouti-related protein neurons (4,5). The actions of Leptin are opposed by the hormone ghrelin. Both hormones act on receptors in the arcuate nucleus of the hypothalamus to regulate appetite to achieve energy homeostasis (6). Although leptin reduces appetite as a circulating signal, obese individuals generally exhibit a higher circulating concentration of leptin than normal weight individuals due to their higher percentage body fat (7). These people show resistance to leptin, similar to resistance of insulin in type 2 diabetes, with the elevated levels failing to control hunger and modulate their weight. In obesity, a decreased sensitivity to leptin occurs, resulting in an inability to detect satiety despite high energy stores (8). Although regulation of fat stores is deemed to be the primary function of leptin, it also plays a role in other physiological processes, as evidenced by its multiple sites of synthesis other than fat cells, and the multiple cell types beside hypothalamic cells that have leptin receptors. Leptin-deficient pathologies are typically accompanied by hyperphagia and obesity (9,10). Extreme obesity can be observed with mutations in the leptin receptor. The anorexigenic properties of leptin have been well characterized in the context of leptin-deficient humans, resulting in the reduction of food intake and body mass (11,12). In conclusion, Leptin can be measured for the differential diagnosis of obesity with leptin resistance.