An exciting synergistic interaction occurs among researchers working at the interface of reproductive biology and energy homeostasis. Reproductive biologists benefit from the theories, experimental designs, and methodologies used by experts on energy homeostasis while they bring context and meaning to the study of energy homeostasis. There is a growing recognition that identification of candidate genes for obesity is little more than meaningless reductionism unless those genes and their expression are placed in a developmental, environmental, and evolutionary context. Reproductive biology provides this context because metabolic energy is the most important factor that controls reproductive success and gonadal hormones affect energy intake, storage, and expenditure. Reproductive hormone secretion changes during development, and reproductive success is key to evolutionary adaptation, the process that most likely molded the mechanisms that control energy balance. It is likely that by viewing energy intake, storage, and expenditure in the context of reproductive success, we will gain insight into human obesity, eating disorders, diabetes, and other pathologies related to fuel homeostasis. This review emphasizes the metabolic hypothesis: a sensory system monitors the availability of oxidizable metabolic fuels and orchestrates behavioral motivation to optimize reproductive success in environments where energy availability fluctuates or is unpredictable.

To augment the limited work reported in the literature regarding testing of the hormonal temporal synergism hypothesis in Syrian hamsters (Joseph MM, Meier AH. Proc Soc Exp Biol Med. 1974;146:1150-5), a large experiment with female hamsters was conducted. Forty-eight received corticosterone at 18:00 h on January 21, 23, 25, 27, and 29 and ovine prolactin at one of six times of day beginning January 22 for 8 days; 36 received saline (at 18:00) and prolactin at one of the six times of day for 8 days; 35 received only prolactin at one of the six times of day for 8 days; and 16 received no injections. Twelve hamsters receiving corticosterone and prolactin and eight uninjected hamsters were on running wheels. The corticosterone and prolactin group not on wheels had a body weight gain and no circadian rhythm of weight gain, but did have circadian rhythms of response in organ weight, per 100 g of body weight, and in weights of fat pads and uteri. The corticosterone and prolactin group with access to running wheels gained in body weight and had larger ovaries and smaller fat pads. Hamsters receiving saline and prolactin had a body weight gain, but had no circadian rhythms of response in organ weights. The hamsters receiving only prolactin gained in body weight but had no rhythms of response, except for unexpected circadian rhythms in body weight gain and weights of fat pads. The uninjected hamsters had a modest weight gain. Most or all hamsters with access to running wheels free-ran, and the corticosterone injections did not appear to synchronize the locomotor activity rhythms.(ABSTRACT TRUNCATED AT 250 WORDS)

We examined the interaction of the metabolic fuels, glucose and free fatty acids (FFA), in the control of food intake in Syrian hamsters. Hamsters were treated with a 2-deoxy-D-glucose (2DG) which inhibits glucose utilization, and methyl palmoxirate (MP), which inhibits fatty acid oxidation. The 2DG and MP, alone or in combination did not enhance food intake in hamsters fed a standard rodent chow diet. Determination of the circulating glucose, FFAs, and ketones confirmed that the drugs were having the intended metabolic effects. The 2DG caused marked hyperglycemia and decreased ketones consistent with an inhibition of glycolysis, and the MP caused increased FFAs and decreased ketones indicating inhibition of fatty acid oxidation. A third experiment examined the hamsters' willingness to ingest a diet made highly unpalatable with NaCl, another measure of hunger motivation. Although food-deprived hamsters ingested more of a salt-adulterated diet than did control animals, hamsters treated with MP and 2DG did not. These experiments provide further evidence that the control of food intake in Syrian hamsters is appreciably different than that of laboratory rats.

We examined the metabolic control of food intake in Syrian hamsters using methyl palmoxirate (MP), an inhibitor of fatty acid oxidation. If fatty acid oxidation plays a role in the control of food intake in hamsters, as it does in rats, it would be expected that hamsters predisposed toward lipid metabolism would increase food intake in response to inhibition of fatty acid oxidation. To the contrary, female hamsters fed a high-fat diet for several weeks and then treated with MP (0.25-100 mg/kg) did not increase food intake relative to vehicle-treated controls. Furthermore, MP treatment did not enhance food intake in hamsters that had been previously food deprived for 12 hr. Consistent with the inhibition of fatty acid oxidation, plasma levels of total ketone bodies and glucose in the MP-treated hamsters were significantly lower than those of the vehicle-treated controls. Thus, treatment with doses of MP which apparently inhibited fatty acid oxidation did not enhance food intake, even after manipulations which predispose the hamsters toward utilization of fat fuels. The control of food intake in Syrian hamsters is in marked contrast to that of rats and other mammals in which the consequences of glucose and fat metabolism interact to signal changes in food intake.

Physiological and behavioral responses of adult hamsters to starvation were studied by measuring food intake, weight recovery, serum concentrations of glucose, insulin, free fatty acids and beta-hydroxybutyrate, and ketonuria in animals subjected to different weight losses, diets, and durations of fast. Hamsters were debilitated by fasts longer than 12 h or leading to greater than 20% weight loss. Hamsters' feeding patterns were unmodified by fasts ranging between 5 and 12 h and showed no circadian periodicity. Hamsters predominantly recovered from weight losses without increasing their food consumption (unless they were offered a diet of pellets and seeds) and without changing their meal patterns, at a rate of weight gain proportional to the magnitude of preceding weight loss if provided with uninterrupted access to food. By 8 h of fast, blood metabolites were indicative of mobilization of body fat. Hamsters are thus behaviorally unresponsive to duration of fast, but compensate physiologically for weight losses with proportional increases in the rate of weight gain.