Stewart, Alan J.
Isenovic, Esma R.
KAUST DepartmentBiological and Environmental Science and Engineering (BESE) Division
Computational Bioscience Research Center (CBRC)
Computer, Electrical and Mathematical Science and Engineering (CEMSE) Division
Permanent link to this recordhttp://hdl.handle.net/10754/669407
MetadataShow full item record
AbstractThe 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.
CitationObradovic, 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
SponsorsThis 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).
PublisherFrontiers Media SA
JournalFrontiers in Endocrinology
Except where otherwise noted, this item's license is described as This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.