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

The pituitary glands from mice rendered obese by gold thioglucose treatment and by dietary manipulation, and pituitary glands from lean mice after a high food intake or a glucose load, were shown to stimulate insulin secretion from isolated pancreatic islets. The insulin releasing activity of pituitary glands from obese (ob/ob) mice was reduced by fasting for 24 and 48 h. Results obtained with pituitary glands from ob/ob and from lean ob/+ and +/+ mice suggest that the insulin releasing property manifests a gene dosage effect. Pituitary glands from 3-week-old (young) ob/ob mice stimulated insulin secretion to the same extent as pituitary glands from 3-month-old (adult) ob/ob mice. The pancreatic islets of young ob/ob mice were shown to be somewhat more responsive to stimulation by the pituitary factor than were lean ob/+ or +/+ islets from this age group. The concept that high insulin level, partly under pituitary control, and high caloric intake may be interlinked and may, in combination, be a major factor in producing obesity is discussed. Furthermore, it is suggested that the pituitary insulin releasing factor may play a role in the early development of obesity in the animal models studied.
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PMID:Acute regulation of insulin release by the pituitary gland in relation to hyperinsulinaemia and obesity. 38 64

In order to investigate whether the impaired GH secretion associated with obesity is due to a pituitary disorder we studied GH mRNA levels by in situ hybridization in genetically obese and lean Zucker rats. The levels of GH mRNA were at least two fold lower in obese rats in comparison to that in lean controls as quantified by both the scanning of autoradiographs of tissue sections and Northern blot analysis. Quantification of somatotrophs revealed no significant difference in their number between lean and obese rat pituitaries. It is therefore likely that the attenuated GH mRNA levels in genetically obese Zucker rats are due to a decrease in GH transcripts per somatotroph rather than a result of a pituitary defect involving a preferential decrease in somatotroph population.
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PMID:In situ hybridization study of obesity-associated alteration in growth hormone mRNA levels. 132 69

The concentrations of glycosylated (G-PRL) and nonglycosylated (non-G-PRL) forms of PRL and GH were measured during pregnancy in pigs of lean and obese (high backfat thickness) lines. Pregnant sows of the two genetic lines were killed, in groups of five to eight, at 60, 75, 90, and 105 days of gestation, and their pituitary glands and plasma were analyzed for the two hormones by immunoblotting, lectin-binding, and RIA techniques. In both lean and obese pigs, pituitary concentrations of G-PRL and non-G-PRL increased with advance in pregnancy, but there were no significant changes in either form of pituitary GH. Plasma concentrations of radioimmunoassayable PRL also increased with advance in pregnancy, with no consistent changes in serum GH concentrations. The dominant PRL constituent in plasma during the second half of pregnancy was G-PRL, and its concentration either increased or remained constant with advance in pregnancy. In contrast, plasma non-G-PRL concentrations decreased with advance in pregnancy in both lines of pigs, resulting in a steady rise in the plasma G-PRL/PRL ratio toward term. Compared to lean pigs, obese pigs had less radioimmunoassayable PRL and GH in their plasma and less GH (glycosylated as well as nonglycosylated) in their pituitary glands, but obese pigs had more G-PRL in their pituitary glands than lean pigs, and their plasma G-PRL levels tended to be higher and non-G-PRL levels lower than those of lean pigs. Pituitary concentrations of non-G-PRL in the two lines of pigs were similar. Overall, the results show a preponderance of G-PRL over non-G-PRL in the plasma of pregnant sows, with a preferential secretion of the glycosylated form during the latter half of pregnancy. Furthermore, they indicate a prevalence of higher G-PRL/PRL ratios in the pituitary glands of obese than lean pigs. These findings raise the possibility of a functional role for the glycosylated variant of PRL in the initiation and/or maintenance of events associated with pregnancy and obesity in the pig.
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PMID:Changes in the glycosylated and nonglycosylated forms of prolactin and growth hormone in lean and obese pigs during pregnancy. 236 78

We have previously reported an impaired arginine vasopressin (AVP) response to insulin-induced hypoglycemia in obese men, suggesting a hypothalamic-posterior pituitary disorder in obesity. In the present study, we examined the AVP response to other releasing stimuli with a central site of action. The AVP response of 10 obese men to metoclopramide (MCP) or nicotine inhaled with cigarette smoking was compared with that obtained in eight sex- and age-matched controls. The AVP increase during nicotine and MCP tests were significantly lower in the obese patients than in the normal controls. Obese men were restudied after substantial weight loss. The AVP response to nicotine and MCP administration was significantly higher than before slimming and did not differ from that observed in the normal weight subjects. These results demonstrate obesity-related alterations in the AVP responsiveness to nicotine inhaled with cigarette smoking and MCP, supporting the hypothesis for a hypothalamic-posterior pituitary disorder in obesity.
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PMID:Effect of obesity and weight loss on arginine vasopressin response to metoclopramide and nicotine from cigarette smoking. 237 76

An increase in the number of diagnostic parameters (in addition to the determination of the urine level of 17-OCS, a study was also made of the level of 17-KS, blood concentrations of ACTH, prolactin, cortisol, and glucose before and after dexamethasone administration at a dose of 0.5 mg every 6 h for 2 days) and strict rules to be observed by examinees prepared for test performance made in possible to raise the differential-diagnostic role of Liddle's minor dexamethasone test. This conclusion was based on the examination of 34 persons without obesity, 25 patients with exogenous constitutional obesity, 75 patients with juvenile pubertal dyspituitarism, 107 patients with hypothalamic obesity, 8 patients with Cushing's syndrome determined by adrenal corticosteroma, one patient with ACTH-ectopic syndrome, and patients with Itsenko-Cushing disease (128 untreated patients, 99 patients with recurrence, 98 patients in remission). The comparison of clinico-instrumental results with the results of the test has shown its informative value for objective assessment of the gravity of disease. Stages of body responses to small doses of dexamethasone (the stage of lost responses, the stage of incomplete loss and the stage of recovered responses) were identified contributing to objective assessment of the gravity, course, presence, recurrence and remission of Itsenko-Cushing disease.
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PMID:[Use of the "extended" minor dexamethasone test in Itsenko-Cushing disease]. 285 54

Nine patients (4F, 5M) aged 12-17 years with "fear of obesity" were studied with a sequential stimulation test utilizing insulin, LRH, TRH, and L-dopa. The comparative groups were nine female with classic anorexia nervosa, five males with undifferentiated nutritional dwarfing, and nine children (1F, 8M) with constitutional growth delay. The serum TSH, glucose, cortisol, somatotropin, prolactin, LH, and FSH were sampled periodically over 2 hours. Basal T3, T4, transferrin, and Somatomedin-C levels were also obtained. The "fear of obesity" patients did not have any pituitary function changes that were unique. These patients, as well as the comparison groups, revealed a delayed TSH response in proportion to the weight deficit which, when expressed as an integrated response, correlated well to the weight deficit for height (P less than 0.001) and to the ability to recover from hypoglycemia (p less than 0.001). The Somatomedin-C level was low and correlated to the T3 level (p less than 0.05) and not correlated to the elevated Somatotropin levels. The pituitary response to combined stimulation in patients with fear of obesity was determined to be a component of the spectrum starting at normal and proceeding to the extreme undernutrition of anorexia nervosa. Pituitary responsiveness, therefore, changes not as a function of the etiology of the malnutrition, but simply as a function of its severity.
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PMID:Pituitary-hypothalamic response in adolescents with growth failure due to fear of obesity. 310 48

The response of plasma oxytocin to an iv bolus injection of crystalline insulin (0.15 U/kg) was evaluated in 14 normal weight [mean body mass index (BMI) = 23] and in 9 obese (mean BMI = 42) men. Similar blood glucose decrements after insulin injection were observed in the two groups. Obese and normal weight subjects presented similar basal oxytocin levels. In both groups, oxytocin rose significantly during the insulin tolerance test (ITT); however, the peak oxytocin response in the obese men was significantly lower than in the normal weight subjects. Obese men were restudied after substantial weight loss. Basal oxytocin levels and glucose response to insulin did not change after weight reduction. The oxytocin response to the ITT was significantly higher than before slimming and did not differ from that observed in the normal weight subjects. A significant negative correlation between BMI values and oxytocin peak levels during ITT was observed in the lean controls and obese subjects (r = 0.516, p less than 0.02). These results demonstrate that in obese subjects the oxytocin secretory response during an insulin tolerance test is reduced, suggesting the existence of a hypothalamic-pituitary disorder in obesity.
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PMID:Oxytocin response to insulin-induced hypoglycemia in obese subjects before and after weight loss. 328 8

Arginine vasopressin (AVP) response to insulin-induced hypoglycaemia was evaluated in 16 men with normal weight and in 9 obese men. Obese subjects were restudied following substantial weight loss. The decrease in blood glucose concentrations after insulin injection (0.15 U/kg i.v. bolus) had a similar pattern and magnitude in the normal controls and in the obese subjects both before and after weight loss. Basal plasma insulin concentrations in the obese patients were significantly higher than in the normal weight subjects, but were back to normal after weight reduction. During all tests, blood osmolality, haematocrit and blood pressure remained constant. The AVP rise during the insulin tolerance test (ITT) was significantly lower in the obese patients than in the normal controls. The mean peak plasma AVP level was 2.3 times higher than the basal value in the normal controls, but only 1.6 times in the obese patients. After weight loss, the obese men regained normal AVP responses during the ITT. These data indicate that a hypothalamic pituitary disorder affects the AVP response to insulin-induced hypoglycaemia in obese men.
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PMID:Effect of obesity and weight loss on the arginine vasopressin response to insulin-induced hypoglycaemia. 331 83

Healthy persons, patients with noncomplicated alimentary and hypothalamic obesity and those with pubertal dyspituitarism or Icenko-Cushing's disease were studied for serum and erythrocytic levels of alpha-tocopherol. In normal subjects the levels of alpha-tocopherol in the blood serum are increasing with age. In patients with alimentary obesity and pubertal dyspituitarism the percentage of alpha-tocopherol elevation correlates with that of serum lipids and alpha-tocopherol erythrocytic levels are not higher than in normal subjects. In patients with hypothalamic obesity and in particular with Icenko-Cushing's disease relative incompetence of alpha-tocopherol in the blood serum was accompanied by decreased levels of alpha-tocopherol in red blood cells (absolute deficit of alpha-tocopherol in tissues).
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PMID:[Alpha-tocopherol concentration of the blood plasma and erythrocytes in patients with symptomatic obesity due to hypothalamo-hypophyseal-adrenal diseases]. 376 69

Pubertal juvenile dyspituitarism (PJD) is one of the common types of obesity in adolescents. Literature data on the involvement of the renin-angiotensin-aldosterone, hypophysis-adrenal cortex system in the formation of this syndrome are of controversial nature, and the pathogenesis of the development of arterial hypertension in PJD is obscure in many respects. The purpose of the study was to investigate the activity of plasma renin, potassium and sodium in the blood serum as well as the excretion of potassium and sodium with daily urine in PJD patients. A total of 148 PJD patients aged 14 to 21 were examined, of them 22 had exogenous constitutional obesity. The control group was composed of 54 healthy persons of the same sex and age. Electrolyte metabolic derangement, an increase in the ACTH level and hyperaldosteronemia were shown to play a certain role in the development of arterial hypertension in PJD. The above changes developed in the presence of disordered interrelationships in the hypophysis-adrenal cortex, renin-angiotensin-aldosterone system.
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PMID:[Pathogenesis of arterial hypertension in puberal juvenile dyspituitarism]. 390 40


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