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

The authors report the results of a 12-year screening for type II diabetes in their Health District (Emilia-Romagna, Northern Italy). The method consisted of two steps, following Pavel and Sdrobici, for early diagnosis of clinical diabetes and IGT. The authors found 1.03% of clinical diabetes and 2.65% of IGT cases in the population examined (200,000 subjects). Statistically significant correlations existed with regard to the various risk factors (familiarity, obesity, fetal macrosomia, occupation). Follow-up after 6 years for IGT subjects showed a 25.5% return to normal of OGTT values, 21.7% improvement, 19% unchanged, 33.8% deterioration. There was a correlation between these results and life-style (diet, reduction in calorie intake, weight loss). Twelve years after these screenings, a 2.7% drop in incidence was observed for type II diabetes in this Health District.
Acta Diabetol Lat
PMID:Long-term results in preventive medicine for type II diabetes. 407 68

We have studied the effects of starvation and of obesity on somatostatin, insulin, and glucagon release from an isolated perfused organ system in fed and 3- and 5-day fasted Holtzman rats and in obese (fa/fa) and lean (Fa/?) Zucker rats. Fasting for 3 days significantly decreased basal (-71%) and amino acid-stimulated (-62%) somatostatin output. After 5 days of starvation, there was a significant increase over the 3-day level in somatostatin output stimulated by amino acid plus glucose (+540%) and by amino acids plus tolbutamide (+238%). Three and five days of starvation severely depressed insulin output while having no statistically significant effects on glucagon secretion. Somatostatin output from obese Zucker rats was significantly greater than that from lean controls in response to amino acids (41.2 +/- 13.2 vs. 16.3 +/- 10.3 ng/25 min, P less than 0.05). Insulin output was greatly increased from obese compared to lean Zucker rats, whereas there were no statistically significant differences in glucagon output. These data show that fasting decreases and obesity increases both somatostatin and insulin release. They suggest that altered stimulation by nutrients was primarily responsible for changes in somatostatin and insulin release observed in starving and obese rats.
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PMID:Effects of starvation and obesity on somatostatin, insulin, and glucagon release from an isolated perfused organ system. 611 33

Twenty-six female in-patients, aged 14-34 years, suffering from polycystic ovarian syndrome (PCOS) were investigated. Sixteen normal women, matched with patients for age and weight, were used as controls. Both glucose and insulin curves and areas, insulin/glucose area ratio [insulin resistance index (IA/GA)] were studied by oral glucose tolerance test (OGTT), i.v. glucose tolerance test (IVGTT) and tolbutamide test (TT). Plasma insulin and insulin area values of the patients were significantly higher than those of controls. Insulin/glucose area ratios were significantly higher in patients when compared to controls. A correlation was found in some patients (subgroup A) between insulin/glucose area ratio and urinary dehydroepiandrosterone output after the TT. The presence of hyperinsulinism and insulin resistance in our patients suffering from PCOS was confirmed even in the absence of obesity. A relationship between androgens and hyperinsulinism and insulin resistance may thus be confirmed in patients with PCOS.
Acta Diabetol Lat
PMID:Hyperinsulinism and insulin resistance in polycystic ovarian syndrome: a verification using oral glucose, I.V. Glucose and tolbutamide. 622 86

The gastric inhibitory polypeptide (GIP) is the main hormone of the incretin type acting on the entero-insular axis. It is released after fat, glucose or meal ingestion. The variations of this secretion are described in obesity and in some pancreatic and gastrointestinal diseases: it is increased in maturity onset diabetes mellitus, obesity or duodenal ulcer, variable according to the food taken and the severity of the pancreatic lesion in chronic pancreatitis and cystic fibrosis, normal in insulinoma and decreased in celiac disease. The impaired absorption of the food-stuffs and the defective feed-back regulation of GIP secretion by insulin are the major causes of these variations. To a lesser degree, gastric acid secretion, gastric emptying and vagal control may also influence GIP secretion.
Acta Diabetol Lat
PMID:Clinical aspects of GIP secretion. 628 Apr 23

Serum insulin, blood glucose and plasma free fatty acids (FFA) were determined in 14 subjects with a simple obesity under basal conditions and during the tests with tolbutamide, propranolol and epinephrine before and after fasting of 14 days duration, on restricted diet of 1300 kcal. After refeeding some changes in pancreatic B cells reactivity and an altered metabolic responsiveness to epinephrine and propranolol were found as compared to prefasting values. It may be concluded that after refeeding a further increment of beta-adrenergic function seems to contribute to accelerated lipid mobilisation and partly to increased insulin secretion.
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PMID:Effect of refeeding after starvation on basal and tolbutamide-stimulated insulin secretion and beta-adrenergic receptor function in the regulation of insulin release and lipolysis in obese patients. 629 50

An 18-year-old man had cystic fibrosis (CF) and insulin-resistant carbohydrate intolerance characterized by (1) obesity, basal hyperinsulinemia, and hyperglucagonemia; (2) impaired oral glucose tolerance; (3) hyperinsulinemia in response to oral and intravenous (IV) administration of glucose and to IV administration of tolbutamide; (4) exaggerated gastric inhibitory polypeptide secretion following orally administered glucose; and (5) diminished sensitivity to insulin administered IV compared with other patients with CF. Both parents also demonstrate basal and stimulated hyperinsulinemia in response to orally administered glucose. The long-term outlook for patients with CF is improving, and more patients are surviving childhood. Thus, it should be recognized that an insulin-resistant form of carbohydrate intolerance may develop in patients with CF with obesity and/or genetic risk factors.
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PMID:Insulin resistance in a young man with cystic fibrosis. 637 49

In summary, the present review provides evidence in support of the proposition that pancreatic islet cell hyperplasia precedes the development of insulin insensitivity in the obese mouse and, it is likely, that similar events occur in obese humans. Moreover, the hyperplastic pancreatic islet appears to be responsible for the development of insulin insensitivity, since suppression of the hyperplastic islet, by either alloxan or streptozotocin administration to the obese mouse, results in amelioration of insulin insensitivity in vivo. Since no change occurred in the degree of obesity or in adipocyte cell size or number, it is evident that insulin sensitivity is independent of obesity per se. Hence, although obesity and insulin insensitivity frequently co-exist, insulin insensitivity is independent of obesity and is due rather to the presence of pancreatic islet cell hyperplasia. Light and electron microscopy of the hyperplastic pancreatic islets of the obese mouse reveal increased numbers of A- B- and D-cells. Islet suppression with alloxan or streptozotocin results in the selective reduction of B-cells with preservation of A- and D-cells. Therefore, restoration of insulin sensitivity in the obese mouse following pancreatic islet cell suppression appears to be directly related to suppression of B-cell hypersecretion. Biochemical studies of muscle and adipose tissues from the obese mouse reveal profound insulin unresponsiveness without clear cut improvement in vitro following pancreatic islet cell suppression and restoration of insulin sensitivity in vivo. These data are consistent with a relatively modest reduction in the number of available insulin receptors upon these tissues in relation to the marked insulin resistance and imply an impairment of insulin action beyond the insulin receptor interaction [either transport or intracellular action(s)] as the major site(s) of insulin resistance in the muscle and adipose tissues of obese mice. Conversely a reduction of insulin receptors upon hepatocytes of obese mice and their improvement following a reduction of B-cell hypersecretion support the proposition that the number of available insulin receptors may be the major site for the regulation of insulin action upon that tissue. Finally, evidence is presented which suggests that an inability of insulin to limit hepatic gluconeogenesis may be the predominant cause of insulin insensitivity in the obese mouse.
Acta Diabetol Lat 1981
PMID:The relationship between the hyperplastic pancreatic islet and insulin insensitivity in obesity. 645 13

The aim of this research was to study both insulin secretion and insulin resistance index (IRI) in seventeen females, aged 16-30, affected by polycystic ovarian syndrome. The diagnosis was made using clinical, hormonal, radiological and echographic criteria. Eight healthy women, carefully matched with our patients for age and for statistical obesity incidence, were studied as controls. Both glycemic and insulinemic curves, areas, insulinemic/glycemic area ratio (IRI) were studied by tolbutamide test (1 g i.v.). Areas were assessed by planimeter, blood glucose by Trinder method, blood insulin by a RIA method, statistical study by t Student test and correlation coefficients. These latter were determined by comparing individual plasma testosterone, FSH, LH and LH/FSH ratio values together with urinary total 17-ketosteroid and delta HEA output values on the one hand and insulin areas and IRI values on the other. Increased glycemic areas, insulinemic peaks and areas, associated with markedly increased IRI values, were observed in the patients. A correlation exists between hyperinsulinism, insulin resistance on the one hand and increased urinary androgens output on the other. delta HEA resulted particularly increased over other androgenic fractions.
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PMID:[Hyperinsulinism and insulin resistance in the polycystic ovary syndrome as tested with tolbutamide]. 676 18

Two cases of insulin resistance are described, and recent developments in the pathogenesis and treatment of insulin resistance are reviewed. Both immune and nonimmune types of insulin resistance have been described. Immune resistance is related to the presence of circulating antibodies directed against exogenous insulin or the insulin receptor sites. Nonimmune resistance is associated with obesity, ketoacidosis, infection, or endocrinopathies. Treatment of insulin-resistant diabetics can include proper diet and weight control; use of insulin in large quantities; selection of less antigenic forms of insulin, such as pork, fish, or sulfated insulin; oral hypoglycemics such as tolbutamide; and immunosuppressive therapy with corticosteroids. The production of human insulin by recombinant DNA technology promises benefits to patients with high levels of antibodies directed against insulin from animal sources. True insulin resistance is a rare phenomenon, which must be documented adequately before vigorous treatment is considered.
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PMID:Insulin resistance: definition and treatment. 677 14

It is generally accepted that high density lipoprotein cholesterol (HDL-C) is protective against cardiovascular disease, and that diabetics are at a significant excess risk of cardiovascular disease. Previous studies of HDL-C levels in noninsulin-dependent diabetics have reported divergent results, possibly due to case selection or failure to adjust for covariables known to effect HDL-C, such as obesity, cigarette smoking, alcohol intake, exercise, or exogenous estrogen use. The authors compared 97 adult noninsulin-dependent diabetics identified by history or fasting hyperglycemia from a population survey in southern California with 194 age- and sex-matched euglycemic controls from the same community. HDL-C levels were significantly lower in noninsulin-dependent diabetics of both sexes, and these differences persisted after adjustment for obesity, cigarette smoking, alcohol, exercise, and estrogen use in women. These data support the concept that reduced levels of HDL-C may be one mechanism whereby diabetics experience an excess risk of cardiovascular disease. In contrast to the published literature, HDL-C levels were not significantly different in diabetics treated with tolbutamide vs. diet therapy. This finding does not support the suggestion that the excess risk of cardiovascular disease mortality in diabetics assigned to tolbutamide reported from the University Group Diabetes Program was a consequence of tolbutamide-induced reductions in HDL-C.
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PMID:A community study of high density lipoproteins in adult noninsulin-dependent diabetics. 682 48


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