Homeostatic competition between food intake and temperature regulation in rats

Rats obliged to leave a thermoneurtral box to feed at air temperatures (T_a) of 25°, 5 or ?15°C reduced the total time spent feeding and the duration of each meal as T_a fell, but increased their food intake by eating faster. Increasing the palatability of the food offered at ?15°C T_a did not prolong feeding but further increased food intake and the speed of eating. The estimated maximum fall in rectal temperature during feeding at ?15°C was small (0.48°±0.15°C, S.E.) but skin temperatures of ears and tail tip fell to near 0°C. These rats were able to maintain near-normal balances of food intake and body temperature by reallocating the times spent feeding and sheltering and by altering the speed of eating; they thus resolved a conflict between hunger and cold discomfort with little evidence of a strain on homeostasis.     

Participation of the olfactory system in the regulation of food intake

Evoked potentials in the olfactory bulb (OB), lateral hypothalamus (HL) and rostral portion of the nucleus of the tractus solitarius (NTS), were recorded after cervical vagus nerve stimulation. The slow component in the OB only was recorded in the periglomerular layer. Electrolytic lesion of the NTS, abolished the evoked potentials in the OB by vagus nerve stimulation. The results of the present experiments indicate that the pathway from the vagus nerve to OB go into the NTS but probably not into the LH.     

Alternative role for prolactin-releasing peptide in the regulation of food intake

Prolactin-releasing peptide (PrRP) is a peptide ligand for the human orphan G-protein-coupled receptor hGR3/GPR10 and causes the secretion of prolactin from anterior pituitary cells. However, the lack of immunoreactive staining for PrRP in the external layer of the median eminence seems to rule out this peptide as a classical hypophysiotropic hormone and, furthermore, PrRP is less effective than another inducer of prolactin secretion, thyrotropin-releasing hormone, both in vitro and in vivo. Here we show a reduction in the expression of PrRP mRNA during lactation and fasting and an acute effect of PrRP on food intake and body weight, supporting the hypothesis of an alternative role for the peptide.     

Consumption of salty food by rats: regulation of sodium intake?

The extent to which sodium levels may be regulated by consumption was examined in two experiments that offered rats foods varying in sodium chloride (NaCl) content. In the first, rats received single purified diets containing from 0% to 3% NaCl. There were no effects of NaCl level on the amount or pattern of daily food intake; water intake, however, increased with salt content. In the second study, rats had choices between a NaCl-free food and a food containing either 1, 2, or 3% NaCl for 1 week each. Total food intake was unaffected. Proportional intake of the salt-free option increased with the salt content of the alternate food, but not sufficiently to maintain a constant NaCl intake. After 8 weeks of exposure to a single food, intake of the salty option increased in the choice tests, but the level of NaCl (from 0.5 to 3.0%) in the exposure-phase food did not affect the subsequent choice. We conclude that when only one food is available, salt intake is governed by caloric requirements and sodium levels are regulated by excretion. When foods differing in NaCl content are available, consumption does contribute to the regulation of sodium balance, but the amount consumed is not tightly controlled. Rats' salt preference appears to increase with age or with experience eating the purified foods offered here, but experience eating salty food does not affect the preferred level of salt.     

Hormonal regulation of renomedullary hyaluronan

Aim: Hyaluronan (HA) is involved in renomedullary water handling through its water‐binding capacity. This study addressed the effect of hormones involved in regulating fluid‐electrolyte homeostasis on renomedullary HA content in vivo and in vitro. Methods: The kidneys from rats treated with l ‐NAME, indomethacin, vasopressin (AVP) or methylprednisolone (MP) during euvolaemia or water loading were analysed for HA by RIA, ELISA and histochemical staining. HA was measured in renomedullary interstitial cells treated with AVP, angiotensin II (Ang II) or a combination of AVP and Ang II. Results: Baseline renal cortical and medullary HA content was unaffected by 2 h of intravenous treatment with l ‐NAME (NOS inhibitor) or indomethacin (cyclo‐oxygenase inhibitor), whereas AVP reduced medullary HA by 33%. During 2 h of acute water loading, diuresis was accompanied by an increase in renomedullary HA (+45%), but cortical HA was unaffected. In both l ‐NAME‐ and indomethacin‐treated animals, the water loading‐induced increase in renomedullary HA was absent, indicating involvement of NO and prostaglandins. After 7 days of MP treatment, medullary HA was reduced by 40%, but the water loading‐induced elevation in HA remained. In cultured renomedullary interstitial cells, AVP reduced the HA content in the supernatant by 63%, and simultaneous treatment with Ang II reduced the HA content even further (95%). Conclusion: AVP reduces HA content, and NO and prostaglandins are needed for the increase in HA during water loading.     

Atypical antipsychotics and the neural regulation of food intake and peripheral metabolism

The atypical antipsychotics (AAPs) are associated with weight gain and an increased incidence of metabolic disease including type 2 diabetes mellitus. Epidemiological, cross-sectional and prospective studies suggest that two of the AAPs, olanzapine and clozapine, cause the most dramatic weight gain and metabolic impairments including increased fasting glucose, insulin and triglycerides. Relative to the other AAPs, both olanzapine and clozapine exhibit a particularly high antagonistic affinity for histamine and muscarinic receptors which have been hypothesized as mediators of the reported increase in weight and glucose abnormalities. In this article, we review the current evidence for the AAP associated weight gain and abnormal glucose metabolism. We postulate that the effects of the AAPs on food intake and peripheral metabolism are initially independently regulated but with increasing body adiposity, the early AAP-induced impairments in peripheral metabolism will be exacerbated, thereby establishing a vicious cycle such that the effects of the AAP are magnified by the known pathophysiological consequences of obesity. Furthermore, we examine how inhibition of the histaminergic pathway may mediate increases in food intake and the potential role of the vagus nerve in the reported peripheral metabolic effects.     

Ovarian influences on food intake and body weight regulation in lactating rats

In the following experiments, an attempt was made to determine the role of the ovary in the control of food intake and body weight regulation during lactation. In the first study, it was found that concentrations of estradiol benzoate effective in suppressing food intake and body weight in nonlactating animals were not effective during lactation. In the second experiment, ovariectomy during lactation was shown not to produce the usual increases in food intake and body weight or change in meal patterns known to occur after ovariectomy in the nonlactating rat. These results suggested that lactating animals behave the as though functionally ovariectomized and that the removal of the ovaries is of no additional consequence. The further observation that animals nursing small litters gained weight considerably more rapidly than animals nursing large litters led to the prediction that these animals would also be more responsive to the suppressive effects of EB. In the third study, EB in concentrations which are not effective in suppressing body weight in animals nursing large litters was found to suppress body weight in mothers with small litters. However, since these animals also showed a decline in milk yield, a number of alternative interpretations of these results were considered. These results, together with data concerning levels of ovarian hormones during gestation and lactation led to the hypothesis that pregnant and lactating animals undergo an elevation in body weight set-point, similar in magnitude and quality to elevations following ovariectomy in the nonlactating animal.     

Relation between gastric emptying and short-term regulation of food intake in the pig

The relation between gastric emptying (GE), measured by gastric evacuation, and food intake (FI) was studied in pigs fed two meals to appetite per day. Duodenal infusion of emulsified fat (Intralipid; KabiVitrum) inhibited both FI and GE of digestible energy by more than the energy infused, but the gastric volume at satiety was more than 20% below the control. Duodenal infusions of glucose inhibited FI calorically, and generally inhibited GE calorically; but gastric volume at satiety was always equal to control volume. Thus GE (via gastric distension) may regulate FI to duodenal infusion of glucose but not to Intralipid. In pigs given no infusions, removal of the gastric contents immediately prior to the p.m. meal increased intake by 10%, However, when the contents were retained the pigs ate two equal-sized meals in the day, even though the gastric volume after the p.m. meal was 24% greater than after the a.m. meal. Therefore, although gastric volume may influence intake it cannot be the only factor determining satiety on this diet.     

Hormonal regulation of longevity in mammals

Multiple biological and environmental factors impact the life span of an organism. The endocrine system is a highly integrated physiological system in mammals that regulates metabolism, growth, reproduction, and response to stress, among other functions. As such, this pervasive entity has a major influence on aging and longevity. The growth hormone, insulin-like growth factor-1 and insulin pathways have been at the forefront of hormonal control of aging research in the last few years. Other hormones, including those from the thyroid and reproductive system have also been studied in terms of life span regulation. The relevance of these hormones to human longevity remains to be established, however the evidence from other species including yeast, nematodes, and flies suggest that evolutionarily well-conserved mechanisms are at play and the endocrine system is a key determinant.     

The animal model in food intake regulation: examples from the opioid literature

Animal models allow us to investigate the basic mechanisms by which food intake is regulated. There are a host of neuroregulators distributed across a complex central network that control eating behavior. The opioid peptides represent one family of such regulators that have been studied extensively in animals. Using anatomical, biochemical and behavioral methods investigators have found that opioids play an important role in reward-related eating. In this brief review we summarize representative animal studies that utilize a variety of experimental techniques to help explain the role of opioids in ingestive behavior.     

Prostaglandins and food intake of rats: A component of energy balance regulation?

Modulation of food intake by signals arising in adipose tissue has been an important component of theories concerning energy balance regulation. Our experiments tested the effects of some prostaglandins (PG) which are produced in adipose tissue, on food and water intakes in rats. Rats were injected intrahypothalamically with 1 μg of either PGE₁ or PGB₁ in 1 μl bilaterally prior to a 2-hr daily meal. PGE₁, but not PGB₁, reduced food intake of the rats in groups with lateral hypothalamic (LH) and anterior commissure (AC) cannulas, but did not reduce food intake in groups with perifornical hypothalamic (PFH) or mammillary body (MB) cannulas. Water intake was reduced in all groups injected with PGE₁ except the LH and MB groups. Anterior and medial hypothalamic groups showed a sustained 2°C rise in rectal temperature following injections of PGE₁. Subcutaneous injections of PGE₁ reduced food intake of three different groups of rats at different levels of adiposity. We hypothesize that some PG's may be components of a signal relating fat depots and energy balance regulation.