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Asprosin promotes feeding through SK channel–dependent activation of AgRP neurons
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Asprosin, a recently identified adipokine, activates agouti-related peptide (AgRP) neurons in the arcuate nucleus of the hypothalamus (ARH) via binding to protein tyrosine phosphatase receptor δ (Ptprd) to increase food intake. However, the intracellular mechanisms responsible for asprosin/Ptprd-mediated activation of AgRP
ARH
neurons remain unknown. Here, we demonstrate that the small-conductance calcium-activated potassium (SK) channel is required for the stimulatory effects of asprosin/Ptprd on AgRP
ARH
neurons. Specifically, we found that deficiency or elevation of circulating asprosin increased or decreased the SK current in AgRP
ARH
neurons, respectively. AgRP
ARH
-specific deletion of SK3 (an SK channel subtype highly expressed in AgRP
ARH
neurons) blocked asprosin-induced AgRP
ARH
activation and overeating. Furthermore, pharmacological blockade, genetic knockdown, or knockout of Ptprd abolished asprosin’s effects on the SK current and AgRP
ARH
neuronal activity. Therefore, our results demonstrated an essential asprosin-Ptprd-SK3 mechanism in asprosin-induced AgRP
ARH
activation and hyperphagia, which is a potential therapeutic target for the treatment of obesity.
American Association for the Advancement of Science (AAAS)
Title: Asprosin promotes feeding through SK channel–dependent activation of AgRP neurons
Description:
Asprosin, a recently identified adipokine, activates agouti-related peptide (AgRP) neurons in the arcuate nucleus of the hypothalamus (ARH) via binding to protein tyrosine phosphatase receptor δ (Ptprd) to increase food intake.
However, the intracellular mechanisms responsible for asprosin/Ptprd-mediated activation of AgRP
ARH
neurons remain unknown.
Here, we demonstrate that the small-conductance calcium-activated potassium (SK) channel is required for the stimulatory effects of asprosin/Ptprd on AgRP
ARH
neurons.
Specifically, we found that deficiency or elevation of circulating asprosin increased or decreased the SK current in AgRP
ARH
neurons, respectively.
AgRP
ARH
-specific deletion of SK3 (an SK channel subtype highly expressed in AgRP
ARH
neurons) blocked asprosin-induced AgRP
ARH
activation and overeating.
Furthermore, pharmacological blockade, genetic knockdown, or knockout of Ptprd abolished asprosin’s effects on the SK current and AgRP
ARH
neuronal activity.
Therefore, our results demonstrated an essential asprosin-Ptprd-SK3 mechanism in asprosin-induced AgRP
ARH
activation and hyperphagia, which is a potential therapeutic target for the treatment of obesity.
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