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

Plasma growth hormone, glucose, insulin and cortisol response to oral administration of L-dopa and in insulin-tolerance test were investigated in 18 obese subjects. The results were compared with the results obtained in 10 normal subjects. The obese subjects displayed a lack of growth hormone responsiveness to L-dopa and a diminished GH responsiveness to hypoglycemia. There was no significant difference in glucose response to hypoglycemia in normal and obese subjects. Obese subjects showed normal increments of plasma cortisol following induction of hypoglycemia although there was no consistent cortisol response after L-dopa administration. A blood glucose response following L-dopa administration was seen in most of normal subjects while no increment of blood glucose was noticed in obese subjects.
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PMID:Effect of l-dopa on growth hormone, glucose, insulin, and cortisol response in obese subjects. 634 98

The entero-insular axis comprises direct substrate stimulation of the islet cells by the absorbed nutrients and signal transmission by endocrine factors and nerves. The extent of neural influences has not yet been evaluated. GIP is the main incretin candidate. GIP release is dependent on nutrient absorption. Therefore, GIP abnormalities occur in a large number of gastrointestinal and metabolic diseases. These secondary changes are rarely of clinical significance. GIP hypersecretion may, however, contribute to the increased lipogenesis in obesity and the hypoglycemia in the late dumping syndrome. In type II diabetes hyper- and hyposecretion of GIP has been found but no correlation between GIP and insulin response. GIP abnormalities are not identical with disturbances of the entero-insular axis. These can only be evaluated by estimating the incretin effect (comparing the insulin response to oral glucose with the insulin response to an isoglycaemic iv glucose infusion). A decreased incretin effect has been observed in patients with jejuno-ileal bypass and in type II diabetes. In neither condition was a correlation found between incretin effect and GIP response. It is concluded that disturbances of the entero-insular axis are rarely explained by GIP abnormalities. Therefore, other humoral gut factors must exist. Also the neural part of the entero-insular axis requires exploration in health and disease.
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PMID:Disturbances of the entero-insular axis. 635 14

Animal experiments and clinical observations have demonstrated significant effects of vagotomy on body weight. Weight loss or inability to regain are partly due to impaired motility and secretomotor activity of the vagus nerve causing disturbances in digestion which, however, are not sufficient to explain most of the weight deficit after vagotomy in animals or morbidly obese patients. The body weight deficit is also due to reduced caloric intake with changes in the quantity and quality of food and liquid intake, the latter accounting for more than one-third of the total reduction in caloric intake. Obese patients have consistent decreases in hunger ratings after vagotomy and also reveal changed hedonic ratings and estimations of taste intensity. Validation of vagotomy studies requires tests of vagal integrity to confirm the completeness of the surgery and rule out regeneration of nerve tissue or recruitment of function. Tests of completeness of vagotomy are difficult to perform and evaluate in morbidly obese patients due to insulin resistance. The finding of an inadequate gastric acid response to insulin hypoglycemia implies a defect hypothalamic response to hypoglycemic stress in these patients. A new postoperative test of completeness of vagotomy based on disrupted drinking after intravenous hypertonic saline challenge is introduced as an attractive alternative to the potentially hazardous insulin test.
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PMID:Behavioral effects of vagotomy in humans. 636 99

Proinsulin is the single chain precursor of insulin. It consists of insulin, plus a peptide which connects the A and B chains of insulin. This peptide is termed C-peptide. C-peptide an insulin are secreted in equimolar amounts from pancreatic beta-cells, Hence, circulating C-peptide levels provide a measure of beta-cell secretory activity. C-peptide measurements are preferable to insulin measurements because of lack of hepatic extraction, slower metabolic clearance rate, and lack of cross reactivity with antibodies to insulin. This article reviews the methods for determination of C-peptide levels in body fluids, and discusses the applications of C-peptide measurement. These include the investigation of hypoglycemia and the assessment of insulin secretory function in insulin-treated and non-insulin-dependent diabetics. The contribution of C-peptide measurement to the understanding of the interrelationships between insulin secretory function and age, sex, obesity, blood lipids, and blood glucose concentrations will also be evaluated.
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PMID:C-peptide measurement: methods and clinical utility. 637 42

Alcohol may provoke reactive hypoglycaemia when drunk with a sucrose mixer (gin and tonic) but not in the form of a starch-based beverage. In the present study alcohol-potentiated reactive hypoglycaemia was shown to depend on the nature of the carbohydrate ingested together with the alcohol. When 14 men (9 normal weight and 5 obese) aged between 20 and 50 years consumed a 50 g glucose load together with 50 g ethanol over an hour, their early plasma insulin response was significantly higher and their later fall in plasma glucose significantly lower than after drinking the same amount of a starch solution (maize meal) and alcohol. In four subjects (3 of them non-obese) plasma glucose concentrations dropped below 2.8 mmol/l after drinking the glucose-alcohol solution. Obesity seemed to be associated with features of peripheral insulin resistance. We conclude that the common social custom of drinking alcohol together with a simple sugar mixer should probably be modified.
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PMID:Alcohol-potentiated reactive hypoglycaemia depends on the nature of the carbohydrate ingested at the same time. 638 88

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

Twenty nine (1.8%) of a national cohort of 1600 patients with growth hormone deficiency presented before the age of 2 years. Sixteen of the 29 presented before 6 months of age--11 with symptomatic hypoglycaemia, four with failure to thrive, and one with obesity. Hypoglycaemia was persistent and difficult to control until growth hormone treatment was started. Ten of the 11 hypoglycaemic patients had multiple pituitary hormone deficiencies compared with two of the remaining five. Thirteen children presented between 6 months and 2 years of age; 12 had failure to thrive and one had spontaneous hypoglycaemia. Twelve of the 29 were boys and all but one of these had microgenitalia . Growth hormone deficiency should be considered in the differential diagnosis of infants presenting with refractory hypoglycaemia and in boys with failure to thrive and microgenitalia .
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PMID:Growth hormone deficiency presenting under age 2 years. 674 76

To investigate a possible hypothalamic alteration in obesity, we have studied the pattern of PRL secretion in response to insulin hypoglycemia, arginine infusion and TRH injection in 12 grossly obese patients and in 12 normal-weight controls. In the obese patients, PRL secretion was significantly lower than in normal subjects in response to insulin hypoglycemia and arginine infusion, while it was not significantly different from that in controls in response to TRH. The mean +/- SE values of the areas subtended by the PRL curves in the 3 above tests were 54.7 +/- 155.81 vs 3677.3 +/- 520.30 ng/2h, p less than 0,01, 210.3 +/- 148.93 vs 1034.8 +/- 203.15 ng/2h, p less than 0.05 and 1476.8 +/- 275.13 vs 2148.6 +/- 682.06 ng/2h, NS, respectively, in the obese and in controls. These results are compatible with the concept of impaired hypothalamic control of PRL secretion in obesity, although it is still unclear what role this may play in the pathogenesis of this disorder.
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PMID:Impaired prolactin secretion in obese patients. 679 62

The sensitivity to insulin hypoglycemic convulsions has been shown to decrease at early times (16 and 24 hr) and increase at later times (1 week) after gold thioglucose (GTG) treatment. Systemically administered GTG is well known to produce hyperphagia, resulting in obesity, and cytological damage focused relatively selectively in the ventromedial hypothalamic area (VMH). Both of these effects on insulin hypoglycemic convulsions occur before the weight gain, but at a time when histological damage visible with cresyl violet stain has already appeared. Both of these changes reflect a difference in the convulsive response to hypoglycemia, rather than a differences in the degree of hypoglycemia in response to insulin. No functional change in the convulsive sensitivity was found at still earlier times during the latency in establishing the histological damage visible with cresyl violet. These results suggest that GTG lesions a relatively discrete brain region involved in adjusting the functional response of the brain to hypoglycemia, including a composite of two opposite regulatory components. The significance of such a control center in relation to energy metabolism in brain is discussed. Moreover, it has been postulated that the glucose moiety of GTG binds to glucoreceptors in the VMH to focus the cytoxicity of the gold thioportion at that site. These results are also discussed in relation to this proposed mechanism for concentration and hence localization of GTG toxicity in the VMH.
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PMID:Change in sensitivity to insulin hypoglycemic convulsions after gold thioglucose treatment: time course of development. 679 12

Systemic gold thioglucose (GTG) is well known to produce hyperphagia, resulting in obesity, and histological damage focused relatively selectively in the ventromedial hypothalamus (VMH). Although structurally very different, bipiperidyl mustard (BPM) produces apparently similar effects. However, a proposed mechanism for concentration and hence localization of GTG toxicity depends on its structural similarity to glucose, binding it to glucoreceptors and focusing the cytotoxicity of the gold thio-portion. We recently showed that GTG treatment also produces an early decrease and a later increase in sensitivity to insulin hypoglycemic convulsions. We report here that BPM also produces a similar biphasic change in sensitivity to insulin hypoglucemic convulsions. For both, the differences are in the brain's convulsive response to hypoglycemia, rather than in the degree of hypoglycemia in response to insulin. Thus, GTG and BPM cytotoxic lesions appear similar in this regard as well. BPM is another way of producing a relatively discrete brain lesion which alters the brain's functional adjustment to hypoglycemia. The significance of this control center and its relationship to the control(s) of feeding and systemic metabolism are discussed.
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PMID:Effects of bipiperidyl mustard (BPM) lesions on insulin hypoglycemic convulsions. 681 53


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