Physiology & Behavior 1995-03-01

Hyperpolarization of the cell membrane of mouse hepatocytes by fatty acid oxidation.

R Rossi, M Geronimi, P Gloor, M C Seebacher, E Scharrer

Index: Physiol. Behav. 57(3) , 509-14, (1995)

Full Text: HTML

Abstract

The effect of palmitate and metabolizable and nonmetabolizable monosacharides (D-glucose, D-fructose and 2-deoxy-D-glucose = 2-DG) on the membrane potential (Vm) of mouse hepatocytes was investigated employing a superfused mouse liver slice technique. Palmitate hyperpolarized the liver cell membrane in a concentration dependent manner whereas the monosaccharides tested did not. When mice were fed a fat-rich diet, the hyperpolarisation was greater in comparison to mice fed a low fat diet. The hyperpolarization was reversed by ouabain, an inhibitor of the Na+/K(+)-ATPase, by the K(+)-channel blockers tetra-ethyl-ammonium (TEA) and cetiedil and by three inhibitors of fatty acid oxidation (2-bromopalmitate, 2-bromooctanoate and 4-pentenoate). The results suggest that hyperpolarization of the liver cell membrane is due to fatty acid oxidation and that both activation of Na+/K(+)-ATPase and opening of K(+)-channels are involved. The implications of these findings with regard to control of food intake by fatty acid oxidation are discussed. The results are consistent with a role of the hepatic membrane potential in control of food intake by fatty acid oxidation.