Leptin and Obesity: Role and Clinical Implication

The peptide hormone leptin regulates food intake, body mass, and reproductive function and plays a role in fetal growth, proinflammatory immune responses, angiogenesis and lipolysis. Leptin is a product of the obese (ob) gene and, following synthesis and secretion from fat cells in white adipose tissue, binds to and activates its cognate receptor, the leptin receptor (LEP-R). LEP-R distribution facilitates leptin’s pleiotropic effects, playing a crucial role in regulating body mass via a negative feedback mechanism between adipose tissue and the hypothalamus. Leptin resistance is characterized by reduced satiety, over-consumption of nutrients, and increased total body mass. Often this leads to obesity, which reduces the effectiveness of using exogenous leptin as a therapeutic agent. Thus, combining leptin therapies with leptin sensitizers may help overcome such resistance and, consequently, obesity. This review examines recent data obtained from human and animal studies related to leptin, its role in obesity, and its usefulness in obesity treatment.

Citation

Obradovic, M., Sudar-Milovanovic, E., Soskic, S., Essack, M., Arya, S., Stewart, A. J., … Isenovic, E. R. (2021). Leptin and Obesity: Role and Clinical Implication. Frontiers in Endocrinology, 12. doi:10.3389/fendo.2021.585887

Acknowledgements

This work is part of the collaboration between the Department of Radiobiology and Molecular Genetics, “VINČA” Institute of Nuclear Sciences - National Institute of the Republic of Serbia, University of Belgrade, Belgrade, Serbia, and Computational Bioscience Research Center (CBRC) at King Abdullah University of Science and Technology (KAUST). This work was funded by the Ministry of Education, Science and Technological Development of the Republic of Serbia (Contract No#451-03-9/2021-14/200017) and KAUST grant OSR#4129 (awarded to EI and V.B.B.), which also supported MO and ES-M. ME has been supported by the KAUST Office of Sponsored Research (OSR) Award no. FCC/1/1976-17-01, and TG by the King Abdullah University of Science and Technology (KAUST) Base Research Fund (BAS/1/1059-01-01).