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

Obese mice (C57BL/6J ob/ob) and their lean littermates were studied at various ages from immediately post weaning until 62 weeks of age, at which mortality increased markedly. Several age-related changes were noted. 1) Plasma glucose levels were elevated in obese mice 5-20 weeks and 62 weeks of age, but were similar to those in the lean mice at 20-60 weeks of age. Plasma insulin levels were elevated in obese mice, and there were no age-related differences. 2) Brain serotonin was elevated in obese mice at all ages and increased with age in both obese and lean animals. 3) Pituitary contents of ACTH and beta-endorphin were elevated in young obese mice and increased further as these mice approached their life expectancy. 4) The ratios of ACTH to beta-endorphin immunoreactivities were similar in obese and lean mice, except in obese mice over 50 weeks of age where this ratio was increased. We conclude that: 1) the obese mouse is characterized by hyperinsulinemia and hyperadrenocorticism throughout its life; 2) the insulin resistance of the obese mouse improves at 20 weeks of age, yet deteriorates as its life expectancy is approached; 3) the obese mouse has an elevated brain serotonin content similar to previously described elevations of the putative neurotransmitters dopamine and norepinephrine in these mice; and 4) as the obese mouse approaches its life expectancy, abnormalities may occur in the synthesis, processing, or secretion of ACTH and/or beta-endorphine.
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PMID:A longitudinal hormonal profile of the genetically obese mouse. 624 69

The role of beta-endorphin in the development of several obesity syndromes was examined. Adult female hooded rats received ventromedial hypothalamic lesions, dorsolateral tegmental lesions, parasagittal hypothalamic knife cuts, intraventricular 5,7-dihydroxytryptamine, ovariectomy, control surgery, or were deprived to 75% of normal body weight. Dose-dependent suppression of food intake by the opiate antagonist naloxone (0.5, 1.8, 6.8, or 25.0 mg/kg, ip) was measured during once-daily 4-h food access periods. No difference was found among the groups at any dose. Pituitary beta-endorphinlike immunoreactivity (BELI) was substantially decreased in knife-cut rats, but was unaltered by other treatments. Obesity had no effect on BELI. In another experiment, rats made obese by prolonged maintenance on palatable foods had elevated pituitary BELI levels. Feeding mechanisms involving opioid peptides do not appear to be of etiological significance in the syndromes examined.
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PMID:Pituitary beta-endorphin, naloxone, and feeding in several experimental obesities. 626 42

Pituitary beta-endorphin content was measured in dormice during several distinct phases of the infradian body weight cycle. No significant differences in opiate content among groups were found. It appears unlikely that pituitary concentrations of beta-endorphin have etiological significance in the development of spontaneous obesity in hibernators.
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PMID:Pituitary beta-endorphin content during spontaneous food intake and body weight cycles in the dormouse, Glis glis. 631 9

To investigate whether the impaired growth hormone secretion associated with obesity is a result of a hypothalamic or a pituitary disorder and whether it is a cause or a consequence of obesity, we studied plasma growth hormone responses to growth hormone-releasing factor in morbidly obese patients before gastrointestinal surgical therapy, in formerly obese subjects who had lost considerable weight postoperatively, and in non-obese controls. Growth hormone secretion was also assessed in response to insulin-induced hypoglycemia (in seven patients preoperatively and four postoperatively). In patients studied preoperatively, growth hormone responses to growth hormone-releasing factor were markedly impaired (P less than 0.001 as compared with controls), whereas in patients studied postoperatively they were partially restored to normal (P less than 0.05 as compared with those studied preoperatively). Growth hormone responses to insulin-induced hypoglycemia were similarly diminished in obese patients studied before operation (P less than 0.02). The growth hormone response to growth hormone-releasing factor was inversely correlated with the percentage of ideal body weight (P less than 0.01) and directly correlated with the growth hormone response to insulin (P less than 0.01). The impaired responsiveness to growth hormone-releasing factor suggests that the diminished response to insulin hypoglycemia is mediated by an impaired pituitary response to endogenous growth hormone-releasing factor. The reversibility of the defect after weight reduction suggests that it is a consequence rather than a cause of obesity.
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PMID:Impaired growth hormone responses to growth hormone-releasing factor in obesity. A pituitary defect reversed with weight reduction. 643 6

Thirty-eight obese (13 prepubertal, 25 pubertal) boys, and 17 obese (16 prepubertal, 11 pubertal) girls underwent a thyroid-releasing hormone test with assay of prolactin. Obese pre-pubertal boys had prolactin levels that were significantly below those of the control group both under basal conditions and after stimulus. In the obese pubertal boys the difference was significant only after stimulus. The pituitary prolactin reserve in obese pubertal girls was lower than that of the control group. We conclude that in children and adolescents obesity may induce a hypothalamo-pituitary disorder that affects prolactin secretion.
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PMID:Disordered prolactin secretion in the obese child and adolescent. 678 79

Pituitary and central beta-endorphin have been implicated in the regulation of food intake. It has been suggested that an elevation in hypophyseal beta-endorphin represents the genetic defect in the obese mutant Zucker rat. Both pituitary and central beta-endorphin systems appear to interact with dopamine. We have therefore examined hypophyseal, hypothalamic, and basal forebrain levels of beta-endorphin in the obese Zucker rat, its lean littermate, and lean littermates sustaining neurotoxic lesions of the A10 dopamine cell group in the ventral mesencephalon. The obese mutant exhibits elevated pituitary, but not central, beta-endorphin levels relative to lean littermates. A10 lesions result in a marked increase in both pituitary and hypothalamic beta-endorphin levels, and tend to decrease the amount of the peptide in the basal forebrain. These lesions do not result in either increased food intake or body weight. These data therefore suggest that elevated pituitary beta-endorphin levels do not mediate obesity in the Zucker rat, and also demonstrate that both central and pituitary beta-endorphin are modulated by a dopamine system originating in the ventral mesencephalon.
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PMID:Mesencephalic dopamine modulation of pituitary and central beta-endorphin: relation to food intake regulation. 686 61

This experiment was designed to study in rats the implications of the dietary type of fat at two levels of vitamin E on the life span as well as on several biochemical and anatomopathological age-related changes. For this purpose, six different isoenergetic diets containing 15% coconut oil (SFD), safflower oil (UFD) or a combination of both (CFD) with 2 or 200 mg% of dl-alpha-tocopherol were offered ad libitum to outbred Wistar male rats from weaning to senescence. The results indicated that up to 9--12 months the body weights of rats consuming the CFD or the UFD increased generally faster than those fed the SFD, and that all rats developed moderate degrees of obesity. Age-dependent changes in organ weights (kidneys, testes, spleen, brain, liver and heart) were unaffected by diet. Serum levels of vitamin E generally reflected the corresponding dietary levels, but were also influenced by the type of dietary fat. Serum cholesterol levels were not significantly affected by the type of diet or by age. Only transient hypotriglyceridemic and hypophospholipidemic effects of the UFD were observed and, while the levels of triglycerides decreased with age up to the 18th month followed by an increase at 24 months, the levels of serum phospholipids remained unchanged. Neither diet nor age modified the serum albumin/globulin ratios. While no differences in maximum life span were found between dietary groups, the 50% survival time of rats fed the UFD at high level of vitamin E was significantly longer than in all the other groups. This beneficial effect was related to postponement of the onset and reduction of incidence of malignant neoplasms, but was apparently not related to any particular influence on the incidence or severity of chronic nephropathy which practically developed in all rats. Various neoplastic, degenerative and inflammatory diseases encountered in rats dying during the course of the experiment were tabulated and compared with similar findings reported by others in different strains of rats. Pituitary and adrenocortical adenomas as well as adrenocortical and renal carcinomas were the most frequent tumors found in this study. All the pathological changes provided useful baseline information for the evaluation of data presented in this and subsequent communications of this series of studies.
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PMID:Effects of the type of dietary fat at two levels of vitamin E in Wistar male rats during development and aging. I. Life span, serum biochemical parameters and pathological changes. 741 19

Clinical efficacy of enalapril, a drug belonging to a group of angiotensin-converting enzyme inhibitors, was studied in patients with pubertal juvenile dyspituitarism (juvenile obesity) coursing with arterial hypertension. A reactive increase of plasma renin activity and reduced concentration of plasma aldosterone were revealed. The drug was characterized by a pronounced hypotensive effect. No negative effects on the blood lipid spectrum or carbohydrate metabolism were observed. The study showed that enalapril may be a drug of choice in the treatment of the hypertensive syndrome in patients with juvenile obesity.
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PMID:[An attempt to use enalapril in arterial hypertension in patients with juvenile obesity]. 774 32

Human obesity is characterized by a low basal growth hormone (GH) concentration and a blunted response to GH secretagogues. The aim of this experiment was to determine whether a perturbation in GH synthesis or secretion occurs in rats that develop obesity only in response to a dietary fat challenge. Female Sprague-Dawley rats were fed a purified 32.5% fat diet ad libitum for 21 weeks. Approximately half of the rats fed this diet developed obesity (obesity-susceptible) while the others remained lean (obesity-resistant) compared with chow-fed (control) animals. Pituitary glands obtained from all three groups were enzymatically dissociated, and somatotrope response to GH secretagogues and inhibitors was determined in vitro. Plasma GH concentrations were decreased in obesity-susceptible rats compared with obesity-resistant rats, and in vitro GH secretory response was blunted in cells obtained from the pituitary glands of obese compared with lean rats. In addition, pituitary GH content was reduced in obese versus lean rats even though the proportion of somatotropes in the two groups did not differ. Since the changes in GH concentration in this dietary obese rat model parallel those found in human obesity, this model may be useful in determining the relationship between GH and obesity.
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PMID:Growth hormone secretion and synthesis are depressed in obesity-susceptible compared with obesity-resistant rats. 903 Aug 31

A gender-related impairment of the somatotrophic axis is present in obese Zucker rats, female rats being better preserved than males. We showed that another animal model of obesity, i.e., male rats made obese by feeding a hypercaloric diet had a reduced function of somatotrophic axis which was likely related to impairment of gonadal function. Aim of this work was that of studying the function of somatotrophic axis in female overfed rats and comparing it to that of male rats of the previous study. Sprague-Dawley female rats were fed an energy-rich palatable diet for seven months. At the end of overfeeding, according to the degree of overweight, rats were divided into overtly obese (Obese), overweight (Overweight) and Non-Obese, i.e. rats whose weights were similar to those of controls. Rats fed ad libitum with the standard pellet chow served as controls (Controls). Acute administration of a supramaximal dose of GHRH (2 microg/rat, iv) elicited a plasma GH rise similar to that of Controls in all the groups, except in Obese which had a lower GH response. Growth hormone responses after GHRH administration were inversely related to plasma levels of free fatty acids (FFA). Pituitary GH content and gene expression as well as hypothalamic GHRH and SS mRNA content, were similar in all experimental groups and in Controls and the same was true for plasma concentrations of free IGF-I. These results indicate that, similarly to obese female Zucker rats, also overfed female rats had a better preservation of the somatotrophic axis than their male counterparts. In diet-induced obese rats, also the etiology of the impairment of somatotrophic axis seems to be gender-related i.e. due to a reduction of gonadal function in males and to an elevation of FFA in females.
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PMID:Hypothalamo-pituitary-IGF-1 axis in female rats made obese by overfeeding. 928 81


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