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

Hyperglycemic obese and hyperinsulinemic mice of DBM strain develop a diabetic syndrome which can be compared to human maturity onset diabetes. In this study 6 to 49 weeks old female mice were used. Hyperglycemia and concomitant obesity were observed at 9 weeks. Plasma immunoreactive insulin (IRI) was maximum at 15--20 weeks, then decreased progressively with broad individual variations. Metformin, administered at 200 mg/kg per os, ineffective dosage in normal mice, showed a strong hypoglycemic effect in younger mice (11--18 weeks) with a plasma IRI decrease and no blood lactate and liver glycogen alteration. Plasma metformin concentration curve showed an exponential elimination fitted to a one compartment model with a plasma half-life of 2.7 hours. Metformin-induced hypoglycemia was lower in older mice (23--29 weeks) and corroborated their lower initial plasma IRI. All these results are in accordance with those reported in man and show that DBM mice provide a suitable model for a better understanding of antidiabetic drugs effects.
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PMID:DBM mice as a pharmacological model of maturity onset diabetes. Studies with metformin. 52 68

We studied secretion of growth hormone (GH), insulin, and prolactin in eight women with anorexia nervosa and nine women with refractory obesity before and during treatment with bromocriptine, 10 mg/day. In the anorexic patients the raised plasma GH concentrations occurring during an oral glucose tolerance test fell significantly while on bromocriptine treatment, but there was no change in plasma insulin or blood glucose concentrations. In the obese patients, however, plasma GH concentrations remained low during the oral glucose tolerance test, and were not modified by bromocriptine. Blood glucose and plasma insulin concentrations were also unchanged. Plasma GH and plasma 11-hydroxycorticosteroid responses to insulin-induced hypoglycaemia were unaffected. Serum prolactin concentrations which were raised in five anorexic patients and marginally raised in two obese subjects, fell significantly in both groups during treatment. We observed no consistent weight changes in either groups.
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PMID:Growth hormone, insulin, and prolactin secretion in anorexia nervosa and obesity during bromocriptine treatment. 57 73

Dynamic quality of HGH secretion in women with hypothalamic, maternal and simple obesity has been examined by means of the following tests: 1. glucose loading 2. hypoglycaemia following the insulin administration. Comparisons have been made with regard to normal, non-obese women. In all the obese women HGH mobilization was noted to be handicapped under the influence of the after-insulin hypoglycaemia. In some patients of all the obesity groups a paradoxical response of HGH secretion after the glucose administration was noted. In some cases of the hypothalamic and simple obesity groups there occurred a paradoxical response of HGH secretion relating to the insulin hypotlycaemia test. Differences discovered in the dynamics of HGH secretion with appropriateness to the etiopathogenetic forms of obesity are slight: their significance is rather quantitative than qualitative.
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PMID:Growth hormone secretion in women with hypothalamic, maternal and simple obesity. Part II. 59 Feb 6

The effect of intravenous injection of 0.1 I.U./kg insulin on blood glucose response and on lipolysis, induced by intravenous infusion of 0.2 microgram/kg - min norepinephrine, were studied in 12 normal subjects and 17 obese patients with normal 50 g oral glucose tolerance test and normal thyroid function. In the obese group the insulin-induced hypoglycemia during norepinephrine-infusion was significantly less than in normal subjects. Moreover, the inhibition of norepinephrine-stimulated FFA and glycerol-release by insulin was significantly less in obesity as compared with the non-obese group. It is concluded that in obesity the action of insulin is decreased both in carbohydrate metabolism and in lipolysis. These results provide arguments for the role of an impaired antilipolytic insulin effect in the pathogenesis of hyperinsulinism in obesity.
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PMID:[Effect of insulin on stimulated lipolysis in obesity with normal carbohydrate tolerance and unimpaired thyroid function]. 59 Feb 7

1. The syndrome of obesity induced by neonatal injection of monosodium glutamate (MSG) has been further studied in mice. In confirmation of previous studies stunting and decreased pituitary and gonadal weights were observed. 2. After weaning food intake was consistently less in MSG-treated than control mice. Body lipid stores were significantly elevated in MSG-treated mice by 2 weeks of age and increased progressively up to 4 months. 3. Plasma glucose was comparable between MSG-treated and control mice in the fed state whereas after an overnight fast MSG-treated mice exhibited relative hypoglycaemia. 4. Obese MSG-treated mice did not exhibit resistance to exogenous insulin and disposed of an intravenous glucose load more rapidly than control mice. 5. Hyperinsulinaemia was present inconsistently in both fed and fasted mice and in response to administered glucose. 6. Neonatal administration of MSG provides a useful additional model for studying the role of the hypothalamus in obesity.
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PMID:Effects of monosodium glutamate-induced obesity in mice on carbohydrate metabolism in insulin secretion. 63 58

In 17 normal subjects and 126 patients with various endocrine disorders, including 13 patients with Cushing's syndrome, plasma levels of fluorogenic corticosteroid were measured at 9 AM and midnight, and again at 9 AM the following morning, after the patient had received 1 mg of dexamethasone by mouth immediately after the midnight sampling. Basal morning levels of plasma corticosteroids were of little diagnostic value in differentiating between Cushing's syndrome and non-Cushing's states because of the wide overlap of values observed. At midnight the overlap almost completely disappeared. After overnight suppression, only one patient with a mild form of Cushing's disease had normal (false-negative) results in two of four instances. There were virtually no false-positive results, except for two patients with anorexia nervosa showing minor abnormalities of the test. The results were in general agreement with those of the classic Liddle test. However, one patient with Cushing's disease had repeatedly abnormal responses to overnight suppression and normal responses to the Liddle test. When the inhibitory tests gave equivocal results in the differential diagnosis between exogenous obesity and Cushing's disease due to adrenal hyperplasia, the response of plasma corticosteroids to hypoglycemia, normal in obesity and absent in Cushing's disease, proved to be an excellent ancillary test in differentiating between the two conditions.
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PMID:Clinical experience with a simple screening test for Cushing's syndrome combining the determination of plasma cortisol circadian rhythm with the overnight dexamethasone suppression test. 66 10

Growth hormone (HGH) response to glucose-induced hyperglycemia and insulin-induced hypoglycemia in 13 obese adults without carbohydrate intolerance and with normal thyroid function were compared with 16 normal weight subjects. HGH levels measured 30 min after placing an indwelling needle in an antecubital vein were significantly lower in obese than in the non-obese controls. HGH concentrations were inversely related to the body weight in all subjects. In the obese group a suppression of serum HGH level was lacking during glucose-induced hyperglycemia and furthermore it was recorded that HGH response to insulin was significantly less as compared with controls. These data indicate that abnormal HGH response is a characteristic in obesity with normal carbohydrate tolerance and normal thyroid function. HGH is a potent physiological stimulatory of lipolysis and it is thus tempting to speculate that an impaired HGH secretion leads to a diminished lipolysis and further deposition of excessive fat in obesity.
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PMID:Abnormal growth hormone response in obesity with normal carbohydrate tolerance and normal thyroid function. 73 10

The authors present 21 cases of severe hypoglycaemic side effects in diabetics treated with oral sulphonylurea drugs, including two deaths. The medications involved the most frequently were glibenclamide followed by glybutamide and glicalzide. Such side effects often occur early and are unrelated to dose. The classical predisposing factors were noted : old age, renal insufficiency, hepato-cellular insufficiency, drug associations -- in particular oral anticoagulants and salicylates. The indications for such drugs in the treatment of diabetes are discussed. Their use seems doubly illogical in the case of late onset obesity diabetes since the latter is accompanied by cardiovascular complications. It is dangerous in the elderly, particularly sensitive to the risks of hypoglycaemia and in who the diagnosis of "diabetes" is too often made on inadequate grounds.
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PMID:[Hypoglycemic complications of oral drug therapy of diabetes mellitus. 21 cases]. 81 20

The development of obesity, hyperglycemia, and hyperinsulinemia, was examined in obese-hyperglycemic (ob/ob) mice, their lean littermates, and homozygous lean mice (+/+) between 17 days and 8 wk of age. By 4 wk of age ob/ob mice displayed many of the metabolic characteristics that are typical of the syndrome in adult animals, including elevated systemic insulin and glucose levels, increased body weight, obesity, reduced skeletal growth, and in vivo evidence of insulin resistance. In addition, 4-wk-old lean littermates of obese mice had greater body weights, increased per cent carcass lipid, and higher insulin levels than did +/+ mice of the same age that were raised under identical conditions. At 17 or 21 days of age ob/ob mice, defined by either (1) elevated carcass fat content when compared to littermates at time of killing or (2) by phenotypic expression of obesity at 6 wk of age, exhibited moderate hyperinsulinemia, hypoglycemia, reduced skeletal growth, and "obesity", as expressed by the Lee index. The present results indicate that altered pancreatic beta-cell function, obesity, and abnormalities of somatic growth all precede the onset of hyperglycemia and insulin "resistance" in ob/ob mice. Furthermore, the occurrence of these characteristics before 17 days of age suggests that the transition to laboratory diet is not essential for the expression of the ob mutation. The present data also support recent studies that have described a small but reliable effect of the ob gene on the metabolism of heterozygous lean mice.
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PMID:The development of obesity, hyperinsulinemia, and hyperglycemia in ob/ob mice. 99 38

The metabolic effect of ventromedial hypothalamic (VMH) lesions, which are known to cause hyperphagia and obesity, has been studied in rats kept on a controlled light and food regimen. The animals were sacrificed at 4 different times during the second postoperative day. A feeding-induced hypersecretion of insulin was found to the VMH-lesioned animals. It was accompanied by a marked hypoglycemia as compared to the control groups during the feeding period. The glycogen content of liver and diaphragm in the lesioned groups is increased as compared to the controls during the same period. The VMH-lesioned animals showed hypertriglyceridemia both in the fed and fasted state, whereas the postabsorptive plasma levels of free fatty acids and glycerol were decreased. An increased level of urea was observed in all lesioned groups. This is in accordance with the demonstrated protein catabolism which follows VMH lesions.
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PMID:The effect of ventromedial hypothalamic lesions on metabolism and insulin secretion in rats on a controlled feeding regimen. 102 15


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