Food Intake, Weight Changes and Activity of Confined Striped Skunks (Mephitis mephitis) in Winter

Physical activity in the prevention and treatment of obesity and its comorbidities: evidence report of independent panel to assess the role of physical activity in the treatment of obesity and its comorbidities.

Synopsis A series of experiments has been conducted with chicks to study the effects of excess lysine, leucine and incomplete mixtures of amino acids on growth, food intake and plasma amino acid patterns. Excess lysine induced a marked depression in growth within 48 h. Towards the end of the experiment, the chicks lost weight and showed no signs of adaptation to the excess dose of lysine. The plasma concentration of arginine fell within 24 h of feeding excess lysine but the reduction in food intake did not occur until 6 d of the experiment had elapsed. Excess leucine similarly caused a rapid retardation of growth which was followed subsequently by a depression in food intake. Mixtures of amino acids lacking in leucine, isoleucine and valine also induced marked growth inhibitions the severity of which were enhanced by the inclusion of leucine and isoleucine in the mixtures. Growth tended to be adaptive in chicks fed on the incomplete amino acid mixtures but non‐adaptive in those fed on excess leucine. Pair‐feeding studies indicated that appreciable differences in weight gain still occurred when food intake was equated between control groups and groups receiving excess lysine or leucine. The results of the present study indicate that the depression in food intake cannot account completely for the ill‐effects of excess lysine and leucine. They also suggest that the adverse effects of lysine and leucine are distinct from those caused by incomplete mixtures of amino acids.

Effects of ACTH and Corticosteroids in the Regulation of Food and Water Intake

By the 15th day post transplant of the Walker tumor into Sprague-Dawley rats, food intake showed a depression which continued with subsequent tumor growth. A less severe depression of water intake occurred later, indicating dissociation of food and water intake in the tumor bearer. Electrolytic lesions in the lateral area of the hypothalamus of animals at 15 days post transplant produced true aphagia and adipsia; thus the controlling mechanism of the lateral area is functional in the tumor bearer at 15 days. Tumor bearers with sham operations in the lateral area at 15 days showed an initial depression in food and water intakes. Food intake eventually equaled that of nonoperated tumor bearers, but water intake remained depressed, again indicating dissociation of food and water intakes. The Walker tumor was transplanted into rats previously made hyperphagic by lesions in the ventromedial hypothalamus. Food intake began to decline by 15 days, eventually reaching very low levels; thus depression of food intake in the intact tumor-bearing host is not mediated via the ventromedial hypothalamus.

Food and water intakes and Walker tumor growth in rats with hypothalamic lesions

The prevalence of obesity has increased substantially in the past 3 decades and is projected to increase further in the years ahead. It increases the risk of diabetes mellitus, dyslipidemia, hypertension, cardiovascular disease, sleep apnea, nonalcoholic hepatic steatosis, gallbladder disease, osteoarthritis, and cancer. The prevention and treatment of obesity is, therefore, a leading challenge facing public health and medicine in the 21st century. Two stereotypes have dominated thinking in public health, medicine, and the media about obesity. The first stereotype is that the recent surge in prevalence of obesity reflects almost entirely environmental and psychological factors and excludes an important contribution of genetic biological factors. The second stereotype is that obesity should and can be treated primarily by diet and behavioral modification. In this review, I challenge these tenets. I summarize evidence for a strong genetic neurobiological contribution to adiposity and body weight and assert that common human obesity is, like essential hypertension, a complex multifactorial disease where genetic factors promote sensitivity or resistance to obesity in a toxic environment. This concept of a genetic resistance versus sensitivity to obesity helps explain why many people remain thin in a toxic environment whereas others develop profound obesity. I then discuss evidence that dietary therapy for obesity generally fails to achieve weight loss maintenance. There is mounting indication that the high rate of relapse from weight loss during dietary therapy occurs because of compensatory biological adaptations that promote lack of compliance and effectiveness. Relapse from weight loss during dietary therapy is not caused simply by lack of discipline and will power. Finally, I briefly discuss the alternatives to dietary and behavioral therapy, namely bariatric surgery and pharmacotherapy. As a prelude to my critique of dietary therapy, I begin with a discussion of the role of genetic neurobiological factors in obesity. The surge …

Effects of a dietary imbalance of amino acids on the plasma amino acid pattern of the protein-depleted rat are described. The amino acid imbalance was created by adding a mixture of indispensable amino acids lacking histidine to a diet in which the protein was provided by 6% of beef blood fibrin. The addition of this amino acid mixture was previously shown to cause depressions in growth and food intake. In the present study the depression in food intake was preceded by a fall in plasma histidine concentration and at the same time the concentrations of some of the other indispensable amino acids, especially threonine, began to rise. The ratios of several indispensable amino acids to histidine in the plasma were elevated when food intake was most severely depressed.

Preabsorptive factors are not the main determinants of intake depression induced by a high-protein diet in the rat

The effect of atropine upon food and water intake was investigated in the albino rat. Dosages up to approximately 7 mg/kg of atropine sulfate were used in two experiments upon water intake and an experiment upon food intake. Atropine depressed both food and water intake to some limiting value. Eating was reduced to a greater extent than was drinking relative to the control conditions. The experimental arrangements obviated the possibility that the depression of water intake, by atropine, is contingent upon reduced food intake, while the procedure used for studying food intake did not exclude the possibility of the observed reduction of eating being dependent upon reduced drinking. However, the relatively greater reduction of eating as compared with drinking suggests that such a dependency will not account for the total effect.

Arcuate NPY Controls Sympathetic Output and BAT Function via a Relay of Tyrosine Hydroxylase Neurons in the PVN

This study evaluated the dietary pattern of foods and nutrients according to levels of vigorous leisure time physical activity (PA) assessed at recruitment within the Spanish cohort of the European Prospective Investigation on Cancer (EPIC) study (37,287 healthy volunteers with complete information). We used a validated PA questionnaire (PAQ) to measure the weekly frequency and duration of different kinds of sport activities. For dietary assessment, we used a validated diet history questionnaire that included all items consumed with a frequency of at least twice a month. We tested differences in food and nutrient intake according to PA duration by means of both an analysis of variance and an analysis of covariance adjusted for confounding factors. Linear increases or decreases in food and nutrient intake across PA levels were tested by means of a regression analysis. Only 11% of men and 6% of women performed at least 3 hours/week of intense PA, which is similar to current recommendations. Overall, main nutrient and total energy intakes were similar across different PA levels (<2% change in total energy intake between extreme PA categories). However, the intake of some foods and vitamins did significantly (p .05) increase as PA increased. The average gender-weighted percentage change in the intake of food and vitamins increased when moving from the lowest levels of PA to the highest. There was an increase in the intake of the following: 15.9% in vegetables, 6.7% in fruit, 9% in fish, 5.6% in dairy products, 10% in vitamin C, 5.9% in vitamin E, 7.2% in retinol, 19.7% in total carotene, 40.1% in alpha-carotene, 20.4% in beta-carotene, 11.2% in licopene, and 26.1% in lutein. BMI, which was above average for the cohort (mean +/- SD: 28.4 +/- 4.2), decreased steadily when PA increased. To sum up, in this large Spanish cohort, the differences in dietary intake relative to levels of PA were not found either in the amount of total energy consumed nor in the number of main macronutrients but rather in the intake of certain foods which, while having very little or moderate caloric content, are very rich in highly bioactive elements such as vitamins and provitamins.

Oleoylethanolamide (OEA) may be an endogenous regulator of food intake, and intraperitoneal injection of this compound decreases food intake in 24 h-starved rats. It is generally believed that this kind of lipid amide is rapidly catabolized in the gastrointestinal tract, thereby preventing its use as an oral antiobesity compound. We now show that oral OEA inhibits food intake dose dependently at 90 min after food presentation to starved rats. Food intake was reduced by 15.5% (P < 0.01) by administration of 10 mg/kg OEA. [(3)H]OEA was used to assess the degree of catabolism in the gastrointestinal tract. The endogenous level of this acylethanolamide was increased 11 times in the intestinal tissue (to 3.91 +/- 0.98 nmol/g tissue, mean +/- SEM) at 90 min after food presentation, based on the finding of 0.48% of the dose as intact OEA. These findings reveal unexpected properties of orally administered OEA, which may have potential as a cheap and safe antiobesity drug.

The metabolisable energy (ME) of the diet of laying hens at an ambient temperature (Ta) of 20 degrees C was abruptly changed from 10.9 MJ/kg to 12.9 MJ/kg, or vice versa. Food intake during the next 14 d was significantly reduced by the low ME diet and was increased by the high ME diet, that is, the expected compensatory changes in food intake did not occur. Laying hens given the same change of diet as above but kept at 32 degrees C did not show any change in food intake within 14 d. Thus ME intake increased with the high ME diet and decreased with the low ME diet. Daily doses of 10 ml maize oil/kg body weight given directly into the crop of laying hens at a Ta of 20 degrees C, resulted in an immediate, significant, reduction of food intake such that total ME intake remained the same as with normal feeding. Daily doses of 3 ml maize oil/kg, given as before, resulted in an immediate, significant, reduction in food intake at a Ta of 20 degrees C but at a Ta of 32 degrees C food intake remained unchanged; consequently daily ME intake increased. Loading the crop with glucose or sucrose, at Ta 20 degrees C, in quantities which provided a similar ME as 3 ml maize oil/kg, reduced food intake but the adjustment was less precise and daily ME intake increased. Loading with glycerol or protein hydrolysate decreased both food and ME intake. Crop loads of starch were as effective as maize oil in bringing about a significant and compensatory reduction of food intake. Similar volumes of water or liquid paraffin placed in the crop did not affect food or ME intake. A similar weight or cellulose placed in the crop reduced food and ME intake.

The effects of liver denervation on food and water intake in the rat

SummarySheep were infused intraruminally with iso-osmotic solutions of saline, organic acids or lucerne silage extracts with or without additional acids and products of protein degradation found in silage. The post-ingestive effects of silage constituents on food intake were assessed by measuring the voluntary consumption of high dry matter silage over a 20 h period following feeding. In Expt 1, three different silage extracts each depressed food intake up to 4 h following feeding. In Expt 2, one of these extracts, to which 40 g of γ-amino butyric acid (GABA) was added, depressed intake up to 4 h following feeding; with the further addition cf 10 g α-amino butyric acid (AABA) and 28 g amines to this extract, intake was enhanced within 0·5 h but depressed from 4 to 8 h following feeding. In Expt 3, infusion of organic acids alone did not significantly depress food intake relative to saline, nor was there a discernible effect on food intake when graded levels of nitrogenous constituents from silage were added to the infusates. In Expt 4, infusion of an extract, to which only AABA and four other amines were added, depressed cumulative intake up to 8 h following feeding and had a more pronounced effect on food consumption than infusion of the extract with these constituents together with GABA. It was concluded that soluble constituents in silage can inhibit intake but no single constituent is primarily responsible.