Seasonal variations in caloric intake of dogs living in an arctic environment.
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The 5 HT(1A) receptor agonist 8-hydroxy-2-(di-n-propylamino)-tetraline (8-OH-DPAT) increases the food intake of satiated Zucker rats, both lean and obese. Associated with this increased intake are changes in the hypothalamic content of serotonin and its metabolite, 5-HIAA (5-hydroxyindole-3-acetic acid); serotonin is increased while the level of 5-HIAA is decreased. Analysis of individual 5-HIAA/5-hydroxytryptamine (5-HT) ratios, a measure of serotonin turnover indicate that 8-OH DPAT affected serotonin turnover equally and dramatically in both phenotypes. This would be an expected physiological action of an autofeedback mechanism by a 5-HT(1A) receptor agonist. Dehydroepiandrosterone (DHEA) at doses as low as 10 mg/kg blocks the 8-OH-DPAT-induced increase in food intake but does not alter food intake of control satiated Zucker rats. The mechanism of DHEA's action was investigated by monitoring the steroid's effect on hypothalamic neurotransmitters in this satiated model. DHEA by itself induced some change in 5-HIAA in the obese satiated model but not the lean. 8-OH-DPAT, by itself, dramatically decreased serotonin turnover in either lean or obese rats, and DHEA combined with 8-OH-DPAT did not further change serotonin turnover, suggesting DHEA may work through mechanisms other than monoamines to cause its inhibition of 8-OH-DPAT-induced behavioral effects at such low doses.
The development of age-associated proteinuria and renal disease was studied in groups of male Wistar rats fed 12.5, 25, 50 and 75 kcal of food/day, respectively, and in calorie-restricted (40 kcal/day) rats receiving diets rich in fat, protein or carbohydrate. Proteinuria developed faster, kidneys were larger and the incidence of glomerular lesions and proteinaceous casts was greater in rats eating high calorie diets of 50 kcal/day or more. High protein diets, even when calorie-restricted, increased protein excretion and the incidence of glomerular lesions. In old rats acute food restriction (25 kcal/day) decreased protein excretion by 40% in 1 week, with no further reduction in the 2 week. Life duration was greatest in rats fed 50 kcal/day.
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Lung expresses a high concentration of uncoupling protein-2 (UCP-2) mRNA, but neither its pulmonary regulation nor function is known. We measured lung UCP-2 mRNA expression in two animal models: in neonatal rats when both the metabolic rate, as measured by oxygen consumption, and levels of serum free fatty acids (FFAs) increase and in adult mice during decreased food intake, when levels of serum FFAs increase but the metabolic rate decreases. In rat lung, the concentration of UCP-2 mRNA was low and unchanged during late gestation, increased approximately twofold within 6 hrs after birth, and, compared with late gestation, remained approximately threefold higher from day 1 to adulthood. The early postnatal rise in the lung UCP-2 mRNA concentration was partially blocked by an antithyroid drug and was increased by treatment with triiodothyronine. Unlike lung, heart UCP-2 mRNA levels were lower during adulthood than at day 15. In adult mice, lung UCP-2 mRNA concentrations increased approximately fivefold within 12 hrs of 67% calorie restriction (CR), remained elevated during 2 weeks of CR, fell to control levels within 24 hrs of refeeding (CR-RF), and positively correlated with serum FFA concentrations. Heart UCP-2 expression during CR and CR-RF was similar to that of lung; liver UCP-2 mRNA levels were slightly lower during CR and returned to control levels during CR-RF. These data suggest that the regulation of UCP-2 is at least partly tissue-specific and that, in the adult mouse, lung UCP-2 is regulated not by oxygen consumption but by FFAs. Moreover, lung UCP-2 mRNA levels in mice fed ad libitum was increased by the intraperitoneal administration of Intralipid, a 20% fat emulsion. On the basis of these data in adult mice, together with the findings of others that levels of FFAs increase by 2 hrs after birth, we propose lung UCP-2 is regulated by FFA.
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In 112 obese compared with 42 lean children, we found that serum leptin is elevated early in the evolution of childhood-onset obesity (28.4 +/- 1.4 vs. 4.5 +/- 0.4 ng/ml in lean children, P < 0.0001) and correlates with adiposity. Obese children also had higher serum leptin normalized to fat mass. Despite high serum leptin, obese children ingested 2-3 times more calories than did lean control subjects (P < 0.0001) and gained weight rapidly (10.2 +/- 0.3 vs. 2.9 +/- 0.1 kg/year in control subjects, P < 0.0001). Girls had higher leptin levels than did boys, in obese as well as in nonobese children, and showed a closer correlation between adiposity and serum leptin. Elevation of serum leptin was comparable before and after puberty in obese boys, but puberty further increased leptin levels in obese girls (36 +/- 3 ng/ml), resulting in a clear sexual dimorphism with pubertal obese boys (22 +/- 5 ng/ml, P < 0.005). In conclusion, increased serum leptin reflects but does not halt fat deposition in childhood obesity. After normalization to body adiposity, leptin was found to be increased independently by obesity status, female sex, and female sexual maturation.
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Intake of total calories, proteins, lipids and carbohydrates was measured individually in four separate groups each of 26 to 29 children studied during different seasons of the year and an additional group of eight children investigated during all seasons. The subjects came from broken homes, had been abandoned or were orphans; 60% were males, 4 +/- 1.5 years of age (mean and standard error) and were of similar body weight and height. They were residents in one of two separate institutions in Nancy, France, living on similar, rigorously enforced schedules unchanged throughout the year. Socio-ecologic synchronization involved "lights-on" at 0700 "lights-out" at 1830, meals at 0800, 100, 1400 and 1800 with food of similar origin and kind, and similar timing of mental and physical activities. Each child was asked at fixed meal times to select spontaneously the kind and amount of food desired, uninfluenced as far as possible by choices of others, and to consume the food in any order. During seven days of adherence to this request, the amounts of protein, lipid, carbohydrate and total calories consumed at each meal were carefully determined for each individual. Time series thus obtained were analyzed according to the mean cosinor method for detecting and characterizing bioperiodic phenomena. A statistically significant circadian rhythm was detected in each of the 4 variables for each day of the best fitting sine function used to approximate the rhythm occurred around noon in almost all the studied circumstances. In other words the spontaneously larger meals were usually taken at 0800 (breakfast) and 1800 (supper). The trough of both lipid and protein spontaneous intake was clustered around 1800 only on Sunday. Cosinor analysis of individual seven-day time series (of each variable of each season) indicated a statistically significant circaseptan (approximately equal to 7-days) rhythm, with a peak occuring on Saturday, Sunday or Monday, but never on Wednesday. Changes in the weekly mean adjusted levels obtained by this method (as well as changes in mean values resulting from other statistical methods) demonstrate: 1) a circannual variation in spontaneous intake of lipids, carbohydrates and calories (protein changes are not statistically significant): 2) a peak of lipid intake, occuring in spring time, and a peak of carbohydrate and calorie intake, occuring in summer time. The probability of both exogenous and endogenous components of these rhythms is suggested.
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