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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been demonstrated that opioid peptides are involved in the stimulation of food intake in rats and that the circulating beta-endorphin levels are increased in genetically obese rodents. Therefore, to assess whether the changes in food intake may influence circulating beta-endorphin levels in obese subjects, plasma beta-endorphin, ACTH and cortisol concentrations were determined in obese patients after an oral glucose load and during a 7-day total starvation. Baseline plasma beta-endorphin concentrations were significantly higher in obese patients than in control normal-weight subjects, while ACTH and cortisol levels were similar in both groups. Plasma beta-endorphin, ACTH and cortisol concentrations were not affected by the ingestion of 75 g glucose, neither were plasma beta-endorphin concentrations modified during prolonged starvation. Moreover, the lack of nycthemeral variations in beta-endorphin levels, documented before and during starvation while plasma ACTH and cortisol were significantly reduced in the evening, suggests that some extra anterior pituitary sources or some obesity-related changes in beta-endorphin metabolism may contribute to the pool of circulating beta-endorphin in obese subjects. On the other hand, even the extreme changes in nutritional conditions, such as total food deprivation or glucose ingestion, are devoid of any detectable influence on circulating beta-endorphin levels.
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PMID:The effects of glucose ingestion and fasting on plasma immunoreactive beta-endorphin, adrenocorticotropic hormone and cortisol in obese subjects. 166 98

We have previously reported that blood urea and blood cell amino acids levels are reduced in rats obese by feeding a palatable cafeteria diet. In order to distinguish whether these changes result from the altered diet, or from the obesity per se, we have studied cafeteria fed rats after returning to standard diet. As in previous studies, obesity induced by cafeteria feeding (for 90 days) was maintained when the cafeteria diet was removed and rats were fed standard diet only. After removal of the cafeteria diet, blood urea levels of 24 h starved obese rats were lower (23%) than those of starved control rats. Blood cell amino acid levels of obese were lower than control ones from day 50 onwards, during and after cafeteria feeding (21% lower on day 100 of life), and thus coincided with divergence of body weights; these differences were maintained despite removal of cafeteria diet. The effects of starvation on plasma amino acid levels were more marked in obese than control rats, during and after cafeteria feeding. Thus the effects on blood amino acids and urea levels in cafeteria diet induced obese rats are related to the obese status rather than to the diet composition.
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PMID:Sustained changes in blood alpha amino nitrogen compartmentation during recovery from cafeteria feeding in rats. 172 26

This study was undertaken to examine whether diet-induced obesity alters the amount and/or composition of weight lost during starvation. The amount and composition of weight lost during a 4-day period of starvation was determined before and at 17, 30 and 42 weeks after rats (350 g of body weight) were given a high fat diet (HFD). To control for effects of aging, a second group of rats, fed standard laboratory chow, was also subjected to similar periods of starvation. Although total weight loss during starvation was never greater for HFD rats than for chow-fed rats, the former group showed a clear patter of increasing loss of body fat and total energy and conservation of fat-free tissues with periods of starvation later in life. In addition, chow-fed rats showed substantial energy conservation during each period of starvation (i.e. they lost less energy each day than their pre-starvation energy requirements). In contrast, HFD rats demonstrated substantial energy conservation only at 17 weeks and not at 30 or 42 weeks; during the last period of starvation, their average daily loss of carcass energy exceeded their pre-starvation energy requirements. This suggests the increased fat mass of these rats may have led to increased fuel availability and to an increased metabolic rate during starvation. If these results are applicable to humans, the more obese subjects are likely to show greater total loss of energy than lean subjects, but show a lesser loss of lean body mass, at least initially. If protein requirements are reflected by the ability to mobilize protein during food restriction, protein requirements would be substantially lower in the dietary obese rats than in controls. In summary, diet-induced obesity leads to preferential loss of body fat and conservation of lean mass during starvation.
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PMID:Preferential loss of body fat during starvation in dietary obese rats. 174 7

Effect of hypothalamic lesions on regulation of body weight and fat cell dynamics in obese mice were examined during refeeding after prolonged food deprivation. Obese mice, which were treated with monosodium glutamate for 5 postnatal days and had ventromedial nuclear lesions in the hypothalamus, were used. When adult obese mice were given a glucose electrolyte solution for 20-40 days, the body weight dropped to about 45% of their pre-treatment weight. After reinstituted feeding of normal mouse food ad libitum, their body weight and adipose tissue weight returned to pre-starvation level. Tritiated thymidine autoradiography revealed that cell proliferation occurred in the early stages of refeeding and some fat cells were renewed in the epididymal adipose tissue. Fat cell renewal was found more active in the experimental group than in the control. Thereafter, fat cell size increased gradually via fat storage. These obese mice were found to have the capacity to regulate their body weight and adipose tissue not only through fat storage but also by increasing number of fat cells, in order to replace the cells which were lost during starvation. Therefore, ventromedial nuclear lesion in the hypothalamus does not influence the regulatory mechanism of adipose tissue during starvation and refeeding.
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PMID:Adipocyte dynamics in hypothalamic obese mice during food deprivation and refeeding. 180 74

Starvation and malnutrition are associated with low concentrations of plasma insulin-like growth factor I (IGF-I). To evaluate the utility of IGF-I as a screening test for malnutrition, we compared plasma IGF-I concentrations with anthropometric measurements of nutritional status in 99 cancer patients. Forty-three percent of patients were overweight and 4 percent were underweight. Log IGF-I correlated negatively with body weight (r = -0.31, P = 0.002), midarm muscle area (MAMA) (r = -0.31, P = 0.001), triceps skinfold thickness (TSF) (r = -0.24, P = 0.03) and body mass index (r = -0.31, P = 0.003). In males plasma IGF-I correlated with TSF but not MAMA; in females IGF-I correlated with MAMA but not TSF, suggestive of a sexual dimorphism between plasma IGF-I and indices of adiposity. We conclude that obesity was far more prevalent than undernutrition, and that plasma IGF-I correlated negatively with indices of adiposity in a gender specific fashion. Because IGF-I is significantly reduced in the obese as well as in the malnourished, measurements of plasma IGF-I are unlikely to be of adequate clinical specificity to serve as a useful screening test for subtle alterations in nutritional status.
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PMID:Effect of obesity on plasma insulin-like growth factor-I in cancer patients. 193 95

The objective of this study was to assess the impact of dietary obesity and acute starvation on the activity of placental enzymes involved in amino acid metabolism. Twenty-four hours starvation caused a significant fall (10%) in the foetal weight in rats fed standard diet, and this was associated with only modest changes in amino acid enzyme activities. In contrast, in obese rats, foetal weight was unaffected by acute starvation, and was accompanied by a reduced adenylate deaminase activity (24%) and lower ammonia concentrations (50%) in placentae of obese rats after 24h starvation. Thus obesity may confer a protective effect on the foetus growth during acute starvation of diminishing amino acid utilization.
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PMID:Influence of diet and obesity on placental amino acid enzyme activities in the rat. 198 71

Oxidation in vivo of [14C]triolein to 14CO2 was significantly lower in obese (fa/fa) Zucker rats as compared with their lean (+/?) controls. In response to a 24 h starvation period, both lean and obese rats showed an enhanced rate of [14C]triolein oxidation. There were, however, no changes in the rate of intestinal absorption of [14C]triolein between the lean and obese animals. Conversely, the total tissular [14C]lipid accumulation was significantly higher in white adipose tissue, carcass and plasma in the obese animals, whereas that of brown adipose tissue was lower. This was associated with a marked hyperinsulinaemia and hypertriglyceridaemia in the fa/fa animals. Starvation dramatically decreased [14C]lipid accumulation in white adipose tissue of the lean Zucker rats, but had no effect in the obese rats. The lipogenic rate of the obese rats was significantly higher than that of lean rats in liver, white adipose tissue, skeletal muscle and carcass. Lipoprotein lipase activity (per g of tissue) was significantly lower in both white and brown adipose tissue of obese versus lean rats; however, total activity was higher in both tissues. Starvation significantly lowered perigenital-adipose-tissue lipoprotein lipase activity in the lean groups, and had no effect in the obese ones. These results demonstrate that the tissue capacity of exogenous lipid uptake is involved, but cannot be the only factor influencing the maintenance of obesity in these animals. Thus, in the adult fa/fa rat, the large increase in obesity is not solely dependent on a deviation of energy-producing substrate metabolism towards the storage of lipids in white fat. Other factors, such as a low rate of oxidation, a high lipogenic rate and decreased brown-adipose-tissue activity are involved in the perseverance of the obesity syndrome.
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PMID:Lipid metabolism in the obese Zucker rat. Disposal of an oral [14C]triolein load and lipoprotein lipase activity. 201 94

beta-Lipotropin, a pituitary peptide, is a strong stimulator of lipolysis in rabbit adipose tissue. This polypeptide is shown to be degraded by intact fat pads, homogenized adipose tissue and adipocytes of the rabbit dependent on the amount of adipose tissue, time and the pH of the incubation medium. In subcellular fractions of rabbit adipocytes the proteolytic activity could be localized into the cytosol and the microsomal fraction. To obtain information about the processing of beta-lipotropin in its target cell lipolysis and degradation of this polypeptide were investigated in the presence of inhibitors of distinct cellular mechanisms and in different physiological states such as obesity and starvation. Thus, the stronger lipolytic response in adipocytes from obese rabbits respectively animals fed ad libitum was accompanied by a significantly increased degradation in comparison to lean respectively starved rabbits. The six lysosomotropic agents (chloroquine, NH4Cl, propranolol, quinacrine, acridine orange and tetracaine), the proteinase inhibitors alpha 2-macroglobulin and monodansylcadaverine, cellular ATP depletion by 2-deoxy-D-glucose and 2,4-dinitrophenol and the omission of Ca2+ ions from the incubation medium inhibited dose-dependently the lipolytic activity as well as the degradation of beta-lipotropin in intact and homogenized adipose tissue. Inhibitors of the cytoskeleton such as colchicine, cytochalasin B, vinblastine and concanavalin A also reduced lipolysis but only the degradation in intact adipose tissue. It can be concluded that after receptor-mediated uptake the cytoskeleton and lysosomal proteases are involved in the processing of beta-lipotropin.
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PMID:Processing of the lipid-mobilizing peptide beta-lipotropin in rabbit adipose tissue. 221 32

Rats with diet-induced obesity starved for 8, 15, and 25 d lost liver and muscle glycogen, excess protein, and fat in proportion to duration of starvation. Fat-cell size decreased but fat-cell number did not. Upon refeeding, body fat was only partly restored, with further increase in adipocyte hyperplasia occurring in the starved obese rats. In contrast, fat-cell size was restored to near that of the prefasting value in the starved controls (dry-food-fed, fasted 4 d) after refeeding. With refeeding, food efficiency increased only if starvation had caused a reduction of adipocyte size below normal. Change in food efficiency was not associated with decreases in total carcass protein, specific tissue proteins, or glycogen stores but was correlated with degree of adipocyte filling. It is possible that adipose tissue status somehow modulates energy-dissipating mechanisms.
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PMID:Refeeding after fasting in rats: effects of duration of starvation and refeeding on food efficiency in diet-induced obesity. 234 33

The relative proportion of antilipolytic alpha-2 and lipolytic beta adrenoceptors and the adrenoceptors was studied in adipocytes from lean and obese dogs. The modification of the adrenergic status in the adipose tissue from obese dogs consists of an increase in alpha-2 adrenoceptor number (identified by [3H]yohimbine) and a decrease in beta adrenoceptor number (identified by [3H]dihydroalprenolol). Neither the number of beta adrenoceptors in the leukocytes nor the number of alpha-2 adrenoceptors in the platelets were altered in obesity. This predominance of alpha-2 adrenoceptors in adipocytes from obese dogs induced a reduction of the lipolytic efficacy of epinephrine (i.e., increase in the concentration able to induce half-maximal stimulation of lipolysis). Moreover, the number of beta adrenoceptors in the high-affinity state was increased in adipose tissue from obese dogs. It is concluded first that the striking modifications in the adrenergic status of the adipose tissue in obesity is specific to this tissue and secondly that the rise of the beta adrenoceptor in the high-affinity state could explain the fact that catecholamines remain lipolytic agents and that weight loss is increased by starvation in the obese dog.
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PMID:Obesity modifies the adrenergic status of dog adipose tissue. 255 Jun 13


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