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

Subnormal plasma 11-deoxycortisol (compound S) responses to metyrapone were found in patients with adrenal insufficiency or with Cushing syndrome caused by adrenal tumors and in those receiving long-term glucocorticoid or diphenylhydantoin sodium therapy. High normal or exaggerated responses were seen in women receiving oral contraceptives, patients with Cushing syndrome caused by adrenal hyperplasia, and those with untreated hypothyroidism. Diabetes mellitus, hypoglycemia, congestive failure, and obesity also were associated with exaggerated responses. Subnormal plasma S responses were observed in 15 patients who responded normally to a repeat test or to the standard metyrapone test. The abnormal response resulted from insufficient metyrapone, administration at the wrong time, or delay in obtaining the blood sample. The single-dose metyrapone test may be the procedure of choice in screening for adrenal insufficiency.
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PMID:Single-dose metyrapone test: review of a four-year experience. 105 66

The dynamics of insulin secretion from pancreatic islets of the Zucker-obese rat were studied by in vitro perfusion of individual islets. Glucose and L-leucine were used as insulinogenic stimuli. Control pancreatic islets were obtained from both normal weight Zucker-thin littermates and equivalent weight Sprague-Dawley rats. Our results demonstrate that pancreatic islets from 13-wk-old Zucker-obese rats hypersecrete insulin in the basal state and in response to both glucose and amino acid (L-leucine) stimuli. Neither pancreatic islets from control Zucker-thin littermate animals (matched with the Zucker-obese animals for age or for total body weight), nor islets from Sprague-Dawley rats of comparable age and weight demonstrate comparable hypersecretion of insulin. These findings; i.e., hypersecretion of insulin from obese pancreatic islets, suggest that the plasma hyperinsulinism characteristic of the obese state is maintained, at least in part, by an inherent abnormality of beta cell secretion. Whether this abnormality in beta cell secretion results from a genetic trait in the Zucker-obese strain or is induced by the insulin resistance of the obese animal is not resolved by this study. In any case, the observed in vitro hyperinsulin secretion from these islets supports the postulation that in vivo peripheral insulin resistance characteristic of obesity may be a physiological response that protects the animal from insulin-induced hypoglycemia.
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PMID:Insulin secretion by perfused islets from the obese Zucker rat. 109 49

This long-term study of the natural history of glucose tolerance in the aged is now in its eleventh year. Of 411 nondiabetic persons screened on admission to the Jewish Home for the Aged (J.H.A.) since 1968, 15 per cent had abnormally elevated levels of postglucose blood sugar (PGBS) as compared with 25 per cent in the period 1964-1968. Fewer positive reactors were discovered with annual screenings and with the glucose tolerance test (GTT). Although the proportion of positive reactors and of diabetic-type GTT curves was higher in subjects over age 80 than under age 80, there were 83 residents screened annually for five to nine years who retained normal glucose tolerance despite advancing age. The relatively lower rate of deterioration of glucose tolerance in the second period was attributable to: 1) the younger age of residents admitted since 1968, and 2) the diabetes-oriented diet plus emphasis on exercise and prevention of obesity. The reactive hypoglycemia found in 6 per cent of the residents was asymptomatic, whereas iatrogenic hypoglycemia was usually symptomatic and often severe. This led to a deliberate policy of undertreatment. Dietotherapy induced a lasting remission in about 60 per cent of newly diagnosed cases of diabetes, often to the point of normal glucose tolerance. Early diagnosis of chemical diabetes, by postponing or obviating the need for antidiabetic therapy, reduced the incidence of iatrogenic hypoglycemia. Diabetes-oriented measures are recommended for the aged in general, and for residents of homes for the aged in particular.
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PMID:Progressive deterioration of glucose tolerance in the aged. 110 84

Ninety-five pregnant women, not previously known to have diabetes but suspected of being at risk for the disease because of obesity, glycosuria, family history, or obstetric history, underwent oral and intravenous glucose tolerance tests in the last trimester of pregnancy. Several methods were used to categorize the degree of abnormality, but none was of value in predicting pregnancy outcome. Perinatal mortality and malformation rates in the offspring of these women were no greater than those of the over-all infant population at this Center and were much lower than those in infants born to women with overt diabetes. Causes of infant morbidity were not increased, with the exception of overweight babies, hypoglycemia, and hypocalcemia. Umbilical vein glucose level correlated significantly with the mothers' blood glucose at the time of delivery. Cord insulin level correlated with infant birth weight and with University Group Diabetes Program number. Birth weight correlated with the degree of the mothers' obesity. It was concluded the documentation of the degree of glucose intolerance in the mother is of little value in predicting fetal outcome but may indicate infants at risk for hypoglycemia and hypocalcemia.
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PMID:Effect of abnormal glucose tolerance in pregnancy on infant mortality rate and morbidity. A prospective study. 114 21

Two patients are described in whom hypercortisolism occurred prepubertally as a consequence of bilateral adrenocortical hyperplasia. In contrast with the manifestations of Cushing's syndrome in adults, these children presented with obesity and reduced stature and no other symptoms. Both patients excreted amounts of urinary 17-OHCS before and during a conventional suppression test with dexamethasone (0.5 mg every six hours) which were within the usual normal range. However, when urinary 17-OHCS excretion was expressed per gram of urinary creatinine or per square meter of surface area, and when the dose of dexamethasone was tailored to body mass (20mug/kg/day) the results were clearly abnormal, as were plasma corticoids and (in one patient) cortisol secretion rate. Resumption of linear growth occurred after bilateral adrenalectomy in both patients and was associated, in the one patient so studied, by a return of hypoglycemia-stimulated increases in plasma growth hormone levels from previously suppressed values to the normal range, and by a slight increase in the fasting plasma somatomedin concentration. The observations suggest that pediatric patients with hypercortisolism are likely to be overlooked when conventional criteria for laboratory diagnosis are used, but can be recognized by the simple diagnostic modifications used in these studies.
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PMID:Hypercortisolism in childhood: shortcomings of conventional diagnostic criteria. 119 38

Parasagittal knife cuts through the perifornical hypothalamus either medial or lateral to the fornix produced hyperphagia and obesity and altered the rat's ingestive responses to dilute glucose solutions. The lateral knife cut rats drank less dilute glucose solution under both nondeprived and food deprived conditions and displayed less of a feeding suppressive response to glucose ingestion compared to controls. The lateral cut rats were also deficient in their feeding response to insulin-induced hypoglycemia, although their altered sensitivity to glucose and insulin did not appear to be causally related. The medial knife cuts decreased the responsivity to glucose, but less so than the lateral cuts, and did not alter the ingestive response to insulin. Both the medial and lateral knife cuts did not appear to change the rat's responsivity to concentrated blucose solutions. The neuroanatomical and functional nature of the disorder responsible for these effects and its relationship to the hyper-phagia-obesity syndrome are discussed.
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PMID:Effects of hypothalamic knife cuts on the ingestive responses to glucose and insulin. 119

By provoking insulin hypoglycemia (activating the hypothalamus action) and by following-up of the subsequent cortisole response in plasma, the authors study the functional state of the hypothalamic-hypophyseal-suprarenal system in 18 patients with obesity, fourteen of them with regulative type, three -- with metabolic and one -- with hypogonadial type. The cortisole response proved to be within the normal limits in the patients with metabolic and hypogonadial obesity type. the insulin test shows pathological deviations in six, out of all 14 patients with regulative type of obesity. In those cases the cortisole response is low, its curve is with a plateau-like progress and represents a reliable index for a lesion in the hypothalamic-hypophyseal region. The normal test does not speak against the existence of similar lesions. In the presentce of other clinical and paraclinical data for hypothalamic-hypophyseal damage, the normal hypoglycemic test shows that the functional link between hypothalamus-hypophysis-suprarenals is still preserved and in that sence it also aids the determination of the lesion degree and is of diagnostic value. Based on their experience, the authors recommend a wider application in the clinical practice of insulin-hypoglycemic test.
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PMID:[Insulin hypoglycemia, a functional test of the state of the hypothalamo-hypophyseo-adrenal system in obesity]. 122 11

Fifty-eight patients with biochemical reactive hypoglycemia (blood glucose 45 mg% or less after a 100 g OGTT) were tested, of whom 11 subjects were obese with normal glucose tolerance, 9 were obese with chemical diabetes, 9 had chemical diabetes without obesity, 6 had undergone gastrectomy, 7 had renal glycosuria and 16 were apparently isolated. An exaggerated insulin response to oral glucose was associated with reactive hypoglycemia in the post-gastrectomy syndrome, in normal-weight patients with chemical diabetes and 44% of the patients with the isolated syndrome. In contrast, plasma-insulin values cannot account for the reactive hypoglycemia observed in obese patients (with or without chemical diabetes), in subjects with renal glycosuira and in 56% of the patients with the isolated syndrome. A study of pancreatic-glucagon secretion in a group of twelve subjects with "isolated normoinsulinemic reactive hypoglycemia" failed to demonstrate any significant abnormality in the secretion of this hormone during oral glucose tolerance test or intravenous insulin tolerance test. As suggested by Permutt et al. (1973) biguanide therapy may be useful in the treatment of patients presenting severe and symptomatic reactive hypoglycemia which does not respond to classical dietary management.
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PMID:Studies on the pathogenesis of reactive hypoglycemia: role of insulin and glucagon. 127 43

Insulin resistance and hyperinsulinemia is now recognized in non-insulin-dependent diabetes, essential hypertension, obesity, atherosclerotic heart disease, dyslipidemia, heart failure, and in heavy smokers. Several mechanisms have been proposed to explain hyperinsulinemia, insulin resistance and its relationship to hypertension; reduced sodium excretion, activation of the sympathetic nervous system, increased activity of the sodium/hydrogen pump, and stimulation of cellular growth. Some of the nonpharmacological methods to control hyperinsulinemia are of benefit in the management of hypertension, most notably weight loss, exercise program, and reduced salt intake. High-fiber and reduced-protein diets also reduce hyperinsulinemia. Thiazide diuretics can result in insulin resistance, and insulin secretion may be inhibited, possibly associated with concomitant hypokalemia. beta-Blockers result in some reduction of glucose tolerance and mask some of the features of hypoglycemia. Angiotensin-converting enzyme (ACE) inhibitors and alpha-receptor blockers do not effect insulin resistance; probably the same is true for calcium antagonists. Although the effect on risk factors should not be discounted, it is the effect of treatment on hard end points, cerebrovascular accidents, myocardial infarction, or death that is most important. Evidence in hypertension is at present restricted to diuretics and beta-blocking drugs.
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PMID:Hypertension and insulin resistance. 128 47

The impact of hyperinsulinemia on the establishment of insulin resistance was investigated. This was done by treating normal rats with insulin for 3-4 days via osmotic minipumps, and by comparing them with saline-treated controls. Hyperinsulinemia produced by prior insulin treatment (i.e. prior insulinization of the normal rats) resulted in a well tolerated hypoglycemia, increased food intake and body weight gain. Euglycemic-hyperinsulinemic clamps were carried out at the end of the insulinization to assess the acute effects of insulin in control and insulinized rats. It was found that prior insulinization of normal rats resulted in increases in total insulin-stimulated glucose utilization and hepatic lipogenesis, while hepatic glucose production (HGP) was normally suppressed by the hormone. Glucose utilization index by individual tissues was then measured (labelled 2-deoxy-D-glucose method). Prior insulinization of normal rats resulted in increased insulin-stimulated glucose utilization index of white adipose tissue, accompanied by increased insulin-stimulated de novo lipogenesis and glycogen synthesis. In contrast, prior insulinization of normal rats resulted in a decreased insulin-stimulated glucose utilization index of most muscles studied. The decreased insulin-stimulated muscle glucose utilization index brought about by prior insulinization persisted in adrenomedullectomized or propranolol-treated rats, ruling out a role of catecholamines in the effects observed. It is concluded that hyperinsulinemia is a pathological driving force in producing both incipient obesity by overstimulating white adipose tissue and liver metabolic activity, and concomitantly producing incipient muscle insulin resistance.
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PMID:Hyperinsulinemia and its impact on obesity and insulin resistance. 133 81


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