“Leptin resistance is a significant factor, yet the mechanisms that underlie the problem remain unclear,” said Joel Elmquist, DVM, PhD, professor of internal medicine and pharmacology at UT Southwestern and senior author of the study appearing in the March issue of Cell Metabolism. “The fact that this cellular pathway may be involved is a novel observation,” he said in a press release.
Leptin is a hormone released by fat cells that is known to indicate fullness, or satiety, in the brain. If the body is exposed to too much leptin, however, it will become resistant to the hormone. Once that occurs, the body cannot “hear” the hormonal messages telling it to stop eating and burn fat. Instead, a person remains hungry, craves sweets and stores more fat instead of burning it. Leptin resistance causes an increase in visceral, or belly, fat, which has been shown to predispose people to an increased risk of heart disease, diabetes and metabolic syndrome.
For the current study, the researchers induced leptin resistance in brain slices from mice. This research technique, used commonly in neuroscience, enabled the researchers to maintain the cellular and anatomical relationships and some of the network connections that normally exist within the brain.