The metabolic effects of single injections of galanin into the paraventricular nucleus of the hypothalamus (PVN) were investigated in an open-circuit calorimeter. Wistar rats were tested, with no food available during the tests. In the dose range of 0.03-0.3 nmol, galanin produced a very short-latency (approximately 2 minutes) and short-lasting (approximately 15 minutes) reduction in energy expenditure. Since the same doses had no effect on respiratory quotient or locomotor activity, the metabolic effect is not secondary to changes in energy substrate utilization or locomotor activity. This antithermogenic effect complements the eating stimulatory action of PVN galanin, and together these phenomena suggest a role for galanin as an anabolic neuropeptide. The similarity of galanin's effects to those of norepinephrine, with which it coexists in PVN nerve endings, further suggests the involvement of this amine and the PVN alpha2-noradrenergic system in galanin's mechanism of action.

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PubMedDate not supplied

Effects of ethanol and tertiary-butanol on energy expenditure and substrate utilization in the rat.

The acute effects of ethanol and tertiary-butanol, an alcohol which is not metabolized via the alcohol dehydrogenase pathway, on whole body metabolism were studied using indirect calorimetry. Ethanol, but not t-butanol, increased energy expenditure in food-deprived rats. Both ethanol and t-butanol reduced respiratory quotient (RQ), an index of overall body energy substrate utilization. The lowered RQ indicates an increased dependence upon lipids as an energy source. Taken together, these data suggest that ethanol, probably within a narrow dose range, can enhance energy expenditure in the rat, either via a metabolite (e.g., acetaldehyde) or through a consequence of its oxidation. The increase in lipid mobilization seen after acute treatment with ethanol, on the other hand, appears to be independent of its oxidation.

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PubMedDate not supplied

Effects of ethanol and tertiary butanol on blood glucose levels and body temperature of rats.

The mechanisms of ethanol's hyperglycemic and hypothermic effects were investigated by comparing the effects of ethanol with those of tertiary butanol. Tertiary butanol is an intoxicant like ethanol, but unlike ethanol it is only minimally metabolized. Consequently, tertiary butanol does not produce appreciable amounts of active metabolites or energy. Tertiary butanol exerts its neural effects primarily by directly altering the physico-chemical properties of nerve cell membranes. It was found that ethanol and tertiary butanol produce hyperglycemic and hypothermic effects whose magnitude and time course are nearly identical. These data suggest that the hyperglycemic and hypothermic effects of ethanol represent a primary physico-chemical effect on nerve cell membranes and are not secondary to its energy content or metabolites.

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PubMedDate not supplied

Influence of different concentrations of ethanol on energy expenditure, substrate utilisation, and activity in the rat.

The acute (one hour) effects of intraperitoneal injections of four concentrations (10%, 30%, 45% and 60%) of a single dose (0.5 g/kg) of ethanol were investigated in unanesthetised rats in an open-circuit calorimeter. Ethanol increased energy expenditure, with the greatest effect being produced by the two lowest concentrations. In contrast, ethanol decreased respiratory quotient, with the greatest effect being produced by the two highest concentrations. The decreased respiratory quotients indicate that ethanol promotes an exclusive reliance on lipids as a source of energy, and further causes lipids to be catabolised for the synthesis of glucose. The peak metabolic effects were produced at a dose that did not significantly affect motor activity, which indicates that the metabolic effects are not secondary to changes in activity. These data support the view that ethanol's effects on energy expenditure and substrate utilisation are mediated by distinct mechanisms. Moreover, since the different metabolic effects were produced by the same ethanol dose, they cannot be due to ethanol's energy content. Thus, ethanol concentration is a major modulator of its effects on energy expenditure and substrate utilisation quite apart from effects due to dose, motor activity or its energy content. This suggests the need to consider the effects of ethanol concentration when analysing ethanol's other pharmacological effects.

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