Loss of Gpr17 in ob/ob mice increased insulin sensitivity, lowered baseline serum insulin, and enhanced response to exogenous leptin treatment.
Does general loss of Gpr17 improve insulin and leptin sensitivity in lean and obese mouse models?
Gpr17 acts as an inhibitor of leptin and insulin sensitivity, suggesting its potential as a therapeutic target for obesity treatment.
OBJECTIVE: Obesity, a major driver for diabetes development, is characterized by insulin and leptin resistance. We previously showed that loss of G protein-coupled receptor 17 (Gpr17) in specific hypothalamic neurons and the intestine led to better energy balance and glucose metabolism. Our goal is to test whether general loss of Gpr17 enhances insulin and leptin sensitivity. METHODS: ; ob/ob) backgrounds and characterized their metabolic profile. RESULTS: ob/ob mice had increased insulin sensitivity with lower baseline serum insulin and higher response to exogenous leptin treatment with more reduction in feeding and increased pStat3 activation in hypothalamic nuclei. CONCLUSIONS: These findings highlight the inhibitory effect of Gpr17 in leptin and insulin sensitivity, suggesting its potential as a therapeutic target for obesity treatment.
Sun et al. (Wed,) conducted a other in Obesity. Loss of Gpr17 was evaluated on Insulin and leptin sensitivity. Loss of Gpr17 in ob/ob mice increased insulin sensitivity, lowered baseline serum insulin, and enhanced response to exogenous leptin treatment.