Leptin action via LepR-b Tyr1077 contributes to the control of energy balance and female reproduction
Year: 2012
Type: article
Abstract: Leptin action in the brain signals the repletion of adipose energy stores, suppressing feeding and permitting energy expenditure on a variety of processes, including reproduction. Leptin binding to its receptor (LepR-b) promotes the tyrosine phosphorylation of three sites on LepR-b, each of which mediates distinct downstream signals. While the signals mediated by LepR-b Tyr1138 and Tyr985 control important aspects of energy homeostasis and LepR-b signal attenuation, respectively, the role of the remaining LepR-b phosphorylation site (Tyr1077) in leptin action has not been studied. To examine the function of Tyr1077, we generated a "knock-in" mouse model expressing LepR-b (F1077), which is mutant for LepR-b Tyr1077. Mice expressing LepR-b (F1077) demonstrate modestly increased body weight and adiposity. Furthermore, females display impairments in estrous cycling. Our results suggest that signaling by LepR-b Tyr1077 plays a modest role in the control of metabolism by leptin, and is an important link between body adiposity and the reproductive axis.
Source: Molecular Metabolism
Institutions: University of Michigan, Michigan Medicine
Language: English
Subfield: Endocrine and Autonomic Systems
Field: Neuroscience
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $4,270
Funders: American Diabetes Association, American Heart Association, University of Michigan, National Institutes of Health, University of Michigan Comprehensive Cancer Center, National Heart, Lung, and Blood Institute, National Institute of Diabetes and Digestive and Kidney Diseases, National Institute of Neurological Disorders and Stroke
OpenAlex ID: W2031180487