Recovery from energy deficit in golden hamsters.
Hamsters feeding at greater than 2-h intermeal intervals (IMI) lose weight but recover from weight losses without hyperphagia if they are allowed to feed at 2-h IMIs (Am. J. Physiol. 236 (Endocrinol. Metab. Gastrointest. Physiol. 5): E105-E112, 1979). To determine the relative importance of changes in energy expenditure and fat synthesis in their energy regulation, measurements were made of resting metabolic rate, respiration by brown adipose tissue (BAT), locomotion, fecal energy content, and insulin and hepatic lipogenic enzyme responses to feeding in underweight hamsters allowed to feed at 2- or 5-h IMIs. Energy deficit suppressed the resting metabolic rate and general locomotor activity and increased the activity of fatty acid synthetase (FAS). Heat production by BAT increased in underweight hamsters. Increase in IMIs blocked the postprandial insulin release, reduced plasma insulin concentration and FAS activity, and increased malic enzyme activity. Thus ad libitum feeding hamsters recover from energy deficit by reducing energy expenditure, whereas failure to add additional meals and impaired insulin and changed lipogenic responses to feeding produce energy deficits in infrequently feeding hamsters.
D002001:Adipose Tissue, Brown / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D001833:Body Temperature Regulation; D001835:Body Weight; D006224:Cricetinae / Q000502:physiology*; D004435:Eating; D004734:Energy Metabolism; D064429:Fatty Acid Synthases / Q000378:metabolism; D007328:Insulin / Q000097:blood; D008099:Liver / Q000201:enzymology; D008291:Malate Dehydrogenase / Q000378:metabolism; D008647:Mesocricetus; D009043:Motor Activity
D001786:Blood Glucose; D007328:Insulin; D008291:Malate Dehydrogenase; D064429:Fatty Acid Synthases