Vol. 281, Issue 5, R1540-R1544, November 2001
Physiological effect of circulating glucagon on the hepatic
membrane potential
Thomas A.
Lutz1,
Alois
Estermann1,
Nori
Geary2, and
Erwin
Scharrer1
1 Institute of Veterinary Physiology, University of Zurich,
8057 Zurich, Switzerland; and 2 E. W. Bourne Behavioral Research Laboratory, New York Presbyterian
Hospital and Weill Medical College of Cornell University, White
Plains, New York 10605
The pancreatic hormone glucagon hyperpolarizes the
liver cell membrane under various conditions. Here we investigated the physiological relevance of this effect by testing the influence of
infusions of glucagon antiserum on the liver cell membrane potential in
vivo. Intracellular microelectrode recordings of liver cells (up to
60/rat over 2 h) were done in anesthetized male rats. Livers were
fixed in place, and recordings were done 10-30 min after
intraperitoneal injections of glucagon or hepatic portal vein infusions
of glucagon or specific polyclonal glucagon antibodies raised in
rabbits. The isotonic lactose vehicle was used as a control for
glucagon, and equal amounts of nonimmunized rabbit IgG were used as a
control for glucagon antibodies. Intraperitoneal glucagon (400 µg/kg)
hyperpolarized the liver cell membrane up to 12 mV, and intraportal
glucagon (10 or 60 µg/kg) dose dependently hyperpolarized the liver
cell membrane by 3-7 mV. Intraportal infusion of glucagon
antiserum (in vitro binding capacity of 4 ng glucagon/rat)
significantly depolarized the liver cell membrane by ~2.5 mV. The
effects of both glucagon and glucagon antiserum reversed after
60-90 min. We conclude that glucagon is a physiologically important modulator of the liver cell membrane potential.
food intake; glucagon antiserum
