The impacts of diabetes continue to be of utmost importance for the medical community, with an emphasis on an appetite-suppressant hormone implicated in satiety known as leptin.
In a recent study released in Nature Metabolism, researchers used rodent models to study the role of leptin and the mechanism of satiety.
“Metabolic health depends on the brain’s ability to control food intake and nutrient use versus storage, processes that require peripheral signals such as the adipocyte-derived hormone, leptin, to cross brain barriers and mobilize regulatory circuits,” the study reads.
“We have previously shown that hypothalamic tanycytes shuttle leptin into the brain to reach target neurons. Here, using multiple complementary models, we show that tanycytes express functional leptin receptor (LepR), respond to leptin by triggering Ca2+ waves and target protein phosphorylation, and that their transcytotic transport of leptin requires the activation of a LepR–EGFR complex by leptin and EGF sequentially.”
In the findings, researchers were able to demonstrate how leptin is perceivable vital in the management of energy homeostasis and blood sugar. Inhibiting the transport of leptin to the brain decreases the functioning of the neurons associated with pancreatic insulin secretion.
“Tanycytic LepRb–EGFR-mediated transport of leptin could thus be crucial to the pathophysiology of diabetes in addition to obesity, with therapeutic implications,” the authors concluded in their findings.
