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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

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

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

Fat mass per se has little effect on the progression of obesity towards diabetes. Predominance of fat in the upper part of the body resulting in android obesity is at least the clinical reflection of factors which lead obesity to progress towards diabetes and atherosclerosis. Therefore this type of obesity may be termed diabetogenic and atherogenic obesity. Insulin and cortisol secretion in obesity are not correlated with body fat but with the predominance of fat in the upper part of the body. Diabetogenic obesity may evolve through 5 stages from initial obesity without diabetes to insulin-dependent diabetes in previously obese subjects. Aside from the characteristics of body fat distribution, the mechanisms which induce or interrupt this progression remain unknown.
Acta Diabetol Lat
PMID:Obesity and diabetes. 700 45

Obese-hyperglycemic mice (genotype ob/ob) have hyperglycemia, hyperinsulinemia, increased resistance to insulin action and decreased insulin receptors on their liver, fat cell and muscle plasma membranes. Hypoglycemic sulfonylureas are reported to improve diabetic control by decreasing the insulin resistance of subjects with Type II diabetes mellitus: however, it is not clear if their mechanism is to increase plasma membrane insulin receptors or to decrease post-receptor insulin resistance. In this study we treated obese-hyperglycemic mice and their normal weight litter mates with the oral hypoglycemic sulfonylurea tolbutamide for 28 to 34 weeks. Tolbutamide administration to normal mice resulted in the following changes that were indicative of increased insulin action: (1) increased body weight; (2) increased epididymal fat-pad weight; (3) increased 2-deoxyglucose transport into the intact diaphragm muscle preparation. There was no alteration in plasma glucose, plasma insulin or pancreatic insulin content suggesting that the tolbutamide effect was an extrapancreatic effect that was probably not mediated by increased insulin secretion. There was no change in the insulin receptor number or affinity of liver cell membranes prepared from tolbutamide treated mice supporting the notion that the extrapancreatic effect of tolbutamide may occur at a post-insulin receptor location. In contrast to the normal mice, tolbutamide did not increase the body weight, epididymal fat pad weight, the already increased 2-deoxyglucose transport into diaphragm muscle or the decreased number of insulin receptors on hepatic plasma membranes. The tolbutamide caused a striking decrease in pancreatic insulin concentration and degranulation of the islets in obese but not normal mice. This is compatible with previous information that the obese mice have abnormal islets that are not under the normal feed-back control of ambient insulin concentration as are the islets of normal mice. We conclude that tolbutamide potentiates insulin action in normal, but not obese, mice and that this potentiation may be due to a post-insulin receptor action.
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PMID:Effect of chronic tolbutamide administration on normal and obese-hyperglycemic mice: evidence for post-receptor potentiation of insulin action. 704 79

Hyperlipoproteinemia occurs commonly in diabetics and may contribute to early atherosclerosis in these patients. The effect of dietary carbohydrate restriction on lipid abnormalities has been examined in 42 newly diagnosed maturity-onset diabetics, in whom plasma lipoproteins were measured before treatment was started and at regular intervals during ten months of dietary therapy. Twenty-four patients (57%) had abnormal lipids when diabetes was first diagnosed. Nine were classed as Type II and 15 as Type IV hyperlipoproteinemia. Plasma lipids reverted to normal in half these patients after dietary treatment for one month. Only 8 diabetics (19%) showed persistent lipid abnormality after ten months' treatment: all had been unable to diet satisfactorily as judged by persisting obesity and hyperglycemia. The common lipoprotein abnormalities of maturity-onset diabetes can usually be returned to normal by the simplest possible carbohydrate-restricted diet, if patients adhere to this. Specialized and complex diets or lipid-lowering drugs are unncessary in the majority of patients.
Acta Diabetol Lat
PMID:Effect of carbohydrate restriction on lipoprotein abnormalities in maturity-onset diabetes mellitus. 741 53

Resting energy expenditure (REE) was investigated by indirect calorimetry in relation to body composition and to different degrees of obesity in order to assess if a defective energy expenditure contributes to extra body fat accumulation. Differences were found between control subjects (group C; BMI 23 +/- 0.5 kg/m2, REE 5890 +/- 218 kJ/day; mean +/- SEM) and obese subjects (group O; BMI 34.2 +/- 0.9 kg/m2, REE 7447 +/- 360 kJ/day; P < 0.0001) and between group C and morbidly obese subjects (group MO; BMI 49.9 +/- 1.6 kg/m2, REE 8330 +/- 360 kJ/day; P < 0.0001); REE was not significantly different between groups O and MO. Body composition data were obtained by means of body impedance analysis. Even though group MO had a fat mass higher than group O, body cell mass, the metabolically active body compartment, was similar in groups O and MO, and this fact may have contributed to the similar REE in the two groups. Multiple regression analysis gave the following equation as the best predictor of REE: REE (kJ/day) = 1591 +/- 49BW + 74BCM - 737G (R2 = 0.88), where BW is body weight, BCM is body cell mass and G is a dummy variable coding group membership (group C = 1; group O = 2; group MO = 3). Thus the analysis showed a negative impact of obesity on REE beyond body composition variables.
Acta Diabetol 1994 Apr
PMID:Resting energy expenditure and body composition in morbidly obese, obese and control subjects. 804 98

We investigated the feedback inhibition of insulin and glucagon secretion during euglycemic-hyperinsulinemic clamp at about 350 pmol/l in 16 patients with abdominal obesity [8 with normal glucose tolerance (oNGT), 8 with impaired glucose tolerance (oIGT)] and 8 normal-weight subjects matched for age, sex and blood pressure. In oNGT and oIGT, fasting plasma C-peptide levels were twice those in the controls (962 +/- 51 and 915 +/- 85 vs 439 +/- 28 pmol/l, P < 0.001) and their suppression was lower than in the controls, both in absolute terms (155 +/- 19 and 185 +/- 17 vs 274 +/- 18 pmol/l, P < 0.001) and as a percentage decline from basal levels (16 +/- 2% and 21 +/- 2% vs 63 +/- 2%, P < 0.001). Fasting plasma glucagon levels were similar in the patients and in the controls, but were less suppressed during clamp in oNGT and oIGT, both in absolute terms (7.0 +/- 0.9 and 5.6 +/- 0.6 vs 13.2 +/- 1.2 pmol/l, P < 0.001) and as a percentage change from basal levels (23 +/- 3% and 19 +/- 2% vs 44 +/- 4%, P < 0.001). These results suggest that the insulin feedback on B and A cells is impaired in abdominal obesity, and that this defect is of similar degree in oNGT and oIGT. These alterations could be implicated in the pathogenesis of hyperinsulinemia in obesity.
Acta Diabetol 1993
PMID:Feedback inhibition of insulin and glucagon secretion by insulin is altered in abdominal obesity with normal or impaired glucose tolerance. 811 Oct 76

To test the hypothesis that the high circulating FFA levels in the diabetes of obesity could contribute to the altered dynamics of insulin secretion seen in that condition, insulin release was measured in isolated perifused rat islet cells, without or with added palmitate. Acutely, as in other systems, palmitate (1 mM) stimulated insulin release. Palmitate (1 mM) suppressed both first and second phase insulin release after 2, 3, or 4 h of perifusion, but not after 1 h. No significant effect was noted with 0.3 mM palmitate, and the effect was maximal at 1 mM. The stimulatory effects of arginine were essentially unaffected. Tolbutamide (1 mM) reversed or counteracted the effect. Glucose oxidation was suppressed in islets incubated with 1 mM palmitate for 4 h. Inhibitors of fat oxidation, alpha-bromostearate (1 mM) and methyl-3-tetradecylglycidate (100 microM) reversed the effects of palmitate on glucose-stimulated insulin release and glucose oxidation. Thus, prolonged incubation of rat islet cells with 1 mM palmitate could suppress the glucose-stimulated release of insulin from perifused rat islets. This suppression could be reversed by inhibitors of fat oxidation. This supports the hypothesis that elevated FFA levels and/or increased fat oxidation could contribute to the altered dynamics of insulin secretion in obese diabetics by fuel antagonism as well as the previously documented suppression of peripheral glucose uptake and stimulation of hepatic gluconeogenesis and may be a key link between obesity and the development of diabetes.
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PMID:Chronic perifusion of rat islets with palmitate suppresses glucose-stimulated insulin release. 831 69


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