Utilization of acetate-1-C¹⁴ by hepatic tissue from cold-exposed and hibernating hamsters

Abstract

When the hamster is exposed to cold (6 ± 1 C), there is a profound block in hepatic lipogenesis from C14-acetate within 48 hr. By 8 weeks of cold exposure this block has been repaired to 74% of the control value. During hibernation, which generally occurs after the 8th week, a block in lipogenesis is again present. By 6 hr of arousal, the degree of lipogenesis has been either slightly repaired or has returned almost to the 8-week level. Accompanying this block in lipogenesis is an increase in the production of C14O2 from C14-acetate in animals exposed to cold. In vitro addition of .02 m glucose did not stimulate lipogenesis in hepatic tissue of cold-exposed hamsters, except for a few of those animals aroused from hibernation for 6 hr. Addition of .02 m succinate in vitro did not increase lipogenesis or C14O2 production from C14-acetate. Fructose repaired the hepatic lipogenesis in all groups of cold-exposed hamsters. It was concluded that the cold-exposed and hibernating hamster has biochemical lesions involving the glucokinase reaction and some other step in the glycolytic pathways of the liver.

The effect of lowered environmental temperature on lipid metabolism in rats fed on normal and high-fat, high-cholesterol diets

“…Mefferd, Nyman & Webster (1958) have found in rats acclimatized to cold an increased incorporation of labelled acetate into total body cholesterol. The tendency towards a lowered hepatic synthesis of cholesterol observed under our experimental conditions may be explained by the fact that in rats exposed to cold an elevated oxidation of acetate occurs through the Krebs cycle (Denyes & Carter, 1961). There is thus less acetate available for cholesterol synthesis.…”

“…Acclimatization to cold is associated with increased food intake and with a general acceleration of metabolism (Smith, 1962), thus enabling the organism exposed to cold to meet the increased requirement for energy. These changes cause increased mobilization of reserve fat from depot tissues into the circulation (Gordon, 1960;Mallov & Witt, 1960;Mallov, 1963) and an increased oxidation of fatty acids and metabolically related substances in the liver (Felts & Masoro, 1959;Denyes & Hasset, 1960;Denyes & Carter, 1961). T h e relationship of these changes in lipid metabolism to the pathogenesis of atherosclerosis remains unexplored; many of the authors believe that exposure to cold enhances the processes which lead to atherosclerosis (Sellers & You, 1956;Wilgram, 1959;Sellers & Baker, 1960;Sodeman & Logue, 1960).…”

OXIDATION OF GLUCOSE-U-C14 AND PALMITATE-1-C14 BY LIVER, KIDNEY, AND DIAPHRAGM FROM HAMSTERS IN COLD EXPOSURE AND HIBERNATION

“…The significant depression in C 0 2 production from glucose and the significant increase in C 0 2 production fro111 palmitate by Iiver after 48 hours in the cold coincides with a dramatic fall in stored glycogen concentrations (7). The glucose formed from liver glycogen is presumably being transported directly to sites such as skeletal inuscle to support the shivering thermogenesis occuring a t this time.…”

“…The fat stores of hibernating mammals are probably utilized during hibernation (6). The glycogen content of the liver also drops during hibernation in hamsters (7).…”

Mammalian Hibernation: An Escape from the Cold

“…Prehibernation cold exposure in Syrian hamsters results in inhibition of lipogenesis in the liver (Denyes and Carter 1961) but a four-to sixfold increase in the in vitro capacity of lipogenesis from acetate in the white adipose tissue (Baumber and Denyes 1963). Further, this increased lipogenic capacity is retained during hibernation unlike the inhibition of lipogenic capacity with the onset of hibernation in ground squirrels and hedgehogs described above.…”