Consuming sucrose solution promotes leptin resistance and site specifically modifies hypothalamic leptin signaling in rats.

This study tested whether leptin resistance in LiqS rats extended beyond a failure to inhibit food intake and examined leptin responsiveness in the hypothalamus and hindbrain of rats offered HS, LiqS or a sucrose free diet (NS). Female LiqS Sprague Dawley rats initially only partially compensated for the calories consumed as sucrose, but energy intake matched that of HS and NS rats when they were transferred to calorimetry cages. There was no effect of diet on energy expenditure, IBAT temperature or fat pad weight. A peripheral injection of 2 mg leptin/kg on Day 23 or 26 inhibited energy intake of HS and NS, but not LiqS rats. Inhibition occurred earlier in HS than NS rats and was associated with a smaller meal size. Leptin had no effect on energy expenditure, but caused a transient rise in IBAT temperature of HS rats. Leptin increased pSTAT3 in the hindbrain and ventromedial hypothalamus of all rats. There was a minimal effect of leptin in the arcuate nucleus and only the dorsomedial hypothalamus showed a correlation between pSTAT3 and leptin responsiveness. These data suggest that the primary response to leptin is inhibition of food intake and that the pattern of sucrose consumption, rather than calories consumed as sucrose causes leptin resistance associated with site specific differences in hypothalamic leptin signaling. PMID: 33206557 [PubMed - as supplied by publisher]
Source: American Journal of Physiology. Regulatory, Integrative and Comparative Physiology - Category: Physiology Authors: Tags: Am J Physiol Regul Integr Comp Physiol Source Type: research