Jerzy W. Kolaczynski

TL;DR: The data suggest that leptin enters the brain by a saturable transport system, lower in obese individuals, and may provide a mechanism for leptin resistance.

TL;DR: The discovery of a "fat-melting hormone" named leptin by Friedman raised the hopes of one-third of the U.S. population that there is a simple solution to cure their obesity and the concept of leptin resistance has since been extended to other studies in humans and to the animal models of obesity.

TL;DR: In summary, insulin does not stimulate leptin production acutely; however, a long-term effect of insulin on leptin production could be demonstrated both in vivo and in vitro, suggesting that insulin regulates OB gene expression and leptin production indirectly, probably through its trophic effect on adipocytes.

TL;DR: In lean subjects with relatively low adipose tissue, the majority of circulating leptin is in the bound form and thus may not be available to brain receptors for its inhibitory effects on food intake both under normal and food deprivation states.

TL;DR: The study indicates that one of the adaptive physiological responses to fasting is a fall in serum leptin, although the mediator that brings about this effect remains unknown, it appears to be neither insulin nor ketones.