Abstract
Obesity and diabetes mellitus are great public health concerns throughout the world because of their increasing incidence and prevalence. Leptin, the adipocyte hormone, is well known for its role in the regulation of food intake and energy expenditure. In addition to the regulation of appetite and satiety that recently has attracted much attentions, insight has also been gained into the critical role of leptin in the control of the insulin-glucose axis, peripheral glucose and insulin responsiveness. Since the discovery of leptin, leptin has been taken for its therapeutic potential to obesity and diabetes. Recently, the therapeutic effects of central leptin gene therapy have been reported in insulin-deficient diabetes in obesity animal models such as ob/ob mise, diet-induced obese mice, and insulin-deficient type 1 diabetes mice, and also in patients with inactivating mutations in the leptin gene. Herein, we review the role of leptin in regulating feeding behavior and glucose metabolism and also the therapeutic potential of leptin in obesity and diabetes mellitus.
Highlights
Obesity and diabetes mellitus are important public health concerns throughout the world because of their increasing incidence and prevalence
There are many factors to consider in the hypothalamic regulation of food intake, e.g., melanin-concentrating hormone (MCH), neuropeptide Y (NPY), agouti-related protein (AgRP), proopiomelanocortin www.frontiersin.org
The suppressors of cytokine signaling (SOCS) molecules might play an important role in the development of leptin resistance that is observed in the central nervous system (CNS) and in the endocrine pancreatic beta-cells during obesity (Seufert, 2004). These results indicate that SOCS3 represents a transcriptional inhibitor of preproinsulin gene expression, which is induced by leptin via janus kinase (JAK)-STAT3/5b signaling in pancreatic β-cells (Laubner et al, 2005)
Summary
Obesity and diabetes mellitus are important public health concerns throughout the world because of their increasing incidence and prevalence. POMC neurons synthesize and secrete an anorexigenic peptide, α-MSH, which activates melanocortin receptors and leads to decreased food intake. LEPTIN TRANSGENIC ANIMAL MODEL The central or peripheral administration of leptin to rodents reduces food intake and increases energy expenditure (Ahima et al, 2000). In transgenic animal models, such as leptin-deficient (ob/ob) mice and LepRb-deficient (db/db) mice, exhibit the development of marked obesity, insulin resistance, hyperinsulinemia, impaired glucose homeostasis, and diabetes (Schwartz et al, 1996; Cohen et al, 2001; McMinn et al, 2005). Fasting rodents with reduced leptin levels and ob/ob mice exhibit decreased level of hypothalamic POMC mRNA, which is normalized by exogenous leptin administration that subsequently improves obesity and diabetes. In the obesity and hyperleptinemic rat, phenotype impaird hippocampal synaptic plasticity (Grillo et al, 2011a,b)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
