Bone morphogenetic protein 8B (BMP8B) increases the glucose sensitivity of ventromedial hypothalamus (VMH) glucose-inhibited (GI) neurons in female mice.

Abstract

In female, but not male, mice, bone morphogenetic protein (BMP) 8B affects energy homeostasis by inhibiting AMP activated protein kinase (AMPK) in the ventromedial hypothalamus (VMH). VMH glucose-inhibited (GI) neurons that express neuronal nitric oxide synthase (nNOS) increase blood glucose in an AMPK dependent fashion. We tested the hypothesis that BMP8B increases glucose inhibition on VMH nNOS-GI neurons. We found that more VMH nNOS neurons expressed the BMP8B receptor in females than males. Moreover, BMP8B blunted activation of VMH GI neurons in low glucose. Thus, VMH nNOS-GI neurons may mediate some of the metabolic effects of BMP8B in females.