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Pubmed ID :29746171
Publication Date : //

Increased TASK channel mediated currents underlie high fat diet-induced vagal afferent dysfunction.


We have previously demonstrated that satiety sensing vagal afferent neurons are less responsive to meal-related stimuli in obesity, due to reduced electrical excitability. As leak K+ currents are key determinants of membrane excitability, we hypothesized that leak K+ currents are increased in vagal afferents during obesity. Diet-induced obesity (DIO) was induced by feeding C57Bl/6J mice a high fat fed diet (60% energy from fat - HFF) for 8-10 weeks. In vitro extracellular recordings were performed on jejunal afferent nerves. Whole cell patch clamp recordings were performed on mouse nodose ganglion neurons. Leak K+ currents were isolated using ion substitution and pharmacological blockers. mRNA for TASK subunits was measured using quantitative real-time PCR. Intestinal afferent responses to nutrient (oleate) and non-nutrient (ATP) stimuli were significantly decreased in HFF mice. Voltage clamp experiments revealed the presence of a voltage-insensitive resting potassium conductance that was increased by external alkaline pH and halothane, known properties of TASK currents. In HFF neurons, leak K+ current was approximately doubled. The halothane sensitive current was similarly increased. qPCR revealed the presence of mRNA encoding TASK1 (KCNK3) and TASK3 (KCNK9) channels in nodose neurons. TASK3 transcript was significantly increased in HFF mice. The reduction in vagal afferent excitability in obesity is due in part to an increase of resting (leak) K+ conductance. TASK channels may account for the impairment of satiety signaling in diet-induced obesity, and thus a therapeutic target for obesity treatment.

Authors : Park Sung Jin , Yu Yang , Wagner Brittany , Valinsky William C , Lomax Alan E , Beyak Michael J ,

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