Deletion of neuronal Ghsr in mice almost completely prevents diet-induced obesity
FRIDAY, May 13, 2016 (HealthDay News) — Neuronal growth hormone secretagogue receptor (GHS-R) is involved in regulating energy metabolism, according to an experimental study published online May 10 in Diabetes.
In an effort to understand the roles of neuronal GHS-R, Jong Han Lee, from the Baylor College of Medicine in Houston, and colleagues used Synapsin 1-Cre driver to generate a mouse line where Ghsr gene is deleted in all neurons.
The researchers found that neuronal deletion of Ghsr abolished ghrelin-induced spontaneous food intake, with no impact on total energy intake. Neuronal Ghsr deletion almost totally prevented diet-induced obesity (DIO) and correlated with a significant improvement in insulin sensitivity. Improved metabolic flexibility was seen for mice with neuronal Ghsr deletion. Gene expression analysis indicated that the hypothalamus and/or midbrain may be responsible for mediating the effects of GHS-R on thermogenesis and physical activity, respectively.
“Collectively, our results indicate that neuronal GHS-R is a crucial regulator of energy metabolism and a key mediator of DIO. Neuronal Ghsr deletion protects against DIO by regulating energy expenditure, not by energy intake,” the authors write. “These novel findings suggest that suppressing central ghrelin signaling may serve as a unique anti-obesity strategy.”
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