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

To determine quantitative and qualitative differences in insulin secretion equimolar amounts of glucose and arginine were infused in 9 healthy subjects, in 8 individuals each with obesity without and with impaired glucose tolerance, and in non-obese and obese non-insulin-dependent diabetic patients (NIDDM). Insulin secretion was calculated after individual determination of metabolic clearance rate of C-peptide (MCRcp) both as the area under the C-peptide concentration curve times MCRcp, and by a mono-compartment mathematical model, both yielding identical results. MCRcp fell consistently with increasing C-peptide infusion rate (e.g.: healthy subjects: C-peptide, 10 nmol/h, 4.2 +/- 0.4; 20 nmol/h, 3.3 +/- 0.3; 30 nmol/h, 3.1 +/- 0.2 ml/kg.min; p less than 0.05 to p less than 0.01). Basal insulin secretion was 2.1-fold greater in the obese with impaired glucose tolerance than in healthy subjects, but was unchanged in non-obese NIDDM. Glucose and arginine triggered insulin release was greater than in healthy subjects at almost identical area under the respective substrate concentration curve (AUC/kg body weight) in obese subjects without (2-fold) and with impaired glucose tolerance (4-fold), and in NIDDMs following i.v. arginine (2-fold). The mean ratio of incremental insulin release to i.v. glucose and arginine was smaller in NIDDM (normal weight, 1.3 +/- 0.4; obese, 1.0 +/- 0.2) than in healthy (2.0 +/- 0.3), or obese subjects with impaired glucose tolerance (2.8 +/- 0.7). Stimulated C-peptide/insulin ratio was reduced in all patients vs that in healthy subjects (p less than 0.05). We conclude that (a) MCR of C-peptide is in part a saturable process; (b) insulin clearance may be impaired in obesity and NIDDM; and (c) insulin secretion differs in obese states and NIDDM both quantitatively and qualitatively, and thereby separates the two disorders as different entities. In addition, quantitation of insulin release in obese states may also help (d) to better define primary algorithms for insulin replacement in normal- and overweight insulin-dependent diabetic patients.
Acta Diabetol Lat
PMID:Quantitative and qualitative differences in basal and glucose- and arginine-stimulated insulin secretion in healthy subjects and different stages of NIDDM. 207 83

The total and ganglioside-bound sialic acid content of unfractionated blood lymphocytes obtained from normal-weight healthy subjects (n = 17) and non-insulin-dependent diabetic patients on oral hypoglycemic drugs arbitrarily divided into normal-weight (n = 11), moderately overweight (n = 14) and severely overweight (n = 17) subgroups were examined. In normal-weight diabetics the level of lipid-bound sialic acid (gangliosides) of lymphocytes was found to be reduced (p less than 0.01). A more pronounced decrease (p less than 0.001) was observed for the lymphocyte total sialic acid of normal-weight and moderately overweight diabetics as compared to healthy subjects. In severely overweight non-insulin-dependent diabetics the decrease of total sialic acid was less pronounced compared to that found in healthy subjects. Whether this finding was due to obesity in these patients remains to be clarified.
Acta Diabetol Lat
PMID:Total and ganglioside-bound sialic acid content of lymphocytes from non-insulin-dependent diabetic patients. 208 37

Substrate cycles (SC) are formed by a 'forward pathway' (FP) and a 'backward pathway' (BP), the difference between FP and BP forming the 'metabolic flux' (MF) through the route of which the cycle is part. SC modulate regulatory effects, i.e. amplify or reduce the % change in MF compared to the % change in FP and BP, thus affecting the sensitivity to regulatory factors, including hormones. A formula is given to calculate (with an approximation of +/- 0.5) the 'flux response index' (FRI), i.e. the factor by which the % change in FP plus the % change in BP must be multiplied to obtain the % change in metabolic flux, when FP and BP undergo opposite, non-unidirectional changes (as is often the case in metabolic regulation). The formula is: FRI = [( FP + BP)/(FP-BP)]/2. By this formula we evaluated the hepatic activities of glucose-6-phosphatase and glucokinase (which roughly reflect hepatic glucose production and uptake, respectively), i.e. the two enzymes that catalyze the cycle between glucose-6-phosphate (glucose-6-P) and glucose. Based on data obtained in normal, nonobese diabetic and obese diabetic subjects as well as in normal, streptozotocin-diabetic, and obese diabetic (ob/ob) mice, we found that FRI was reduced in non-obese diabetic humans and animals whereas it was increased in obese-diabetic humans and mice, compared to normal controls. Thus, diabetes without obesity decreases, and obesity with diabetes increases, the sensitivity of the glucose-6-P/glucose cycle to regulatory agents.
Acta Diabetol Lat
PMID:A formula for quantifying the effects of substrate cycles (futile cycles) on metabolic regulation. Its application to glucose futile cycle in liver as studied by glucose-6-phosphatase/glucokinase determinations. 215 82

The factors which are involved in the development of diabetes and obesity have been reviewed. These include the age of the individual, the duration and magnitude of the obesity, whether there is a family history of diabetes mellitus, the regional distribution of body fat, and the function of the pancreatic islet. These factors help in understanding the reasons why obesity poses such a high risk for developing diabetes mellitus.
Acta Diabetol Lat
PMID:Obesity and diabetes. 218 89

In high degree obesity there a significantly smaller area under the curve of C-peptide after stimulation with Tolbutamide and significantly lower insulin sensitivity measured in vivo by euglycemic hyperinsulinemic clamp-technique (Biostator) than in moderate obesity. This allows the conclusion that high degree obesity is a risk factor for the development of diabetes mellitus.
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PMID:[High-degree obesity--a risk factor for the development of diabetes mellitus]. 228 4

The authors evaluated whole blood filterability (VB) in 29 post-menopausal obese women with (n = 14) or without (n = 15) hypertension, and in 22 age matched women with normal body weight. After 3 months of a low-calorie (18 kcal/kg IBW) and moderately low-salt (max 6 g NaCl/day) diet, the obese subjects were restudied. In all women plasma fibrinogen values and various indices of metabolic status were evaluated before and after the diet and correlated to VB values. VB values and plasma fibrinogen concentrations were similar in normal controls and in women with simple obesity, whereas they were, respectively, significantly lower and higher in obese subjects with hypertension. Three months of diet significantly improved whole blood filterability and decreased fibrinogen levels in these patients. Before the diet a significant negative correlation was found between VB and plasma fibrinogen values in hypertensive obese patients. Metabolic parameters did not change in the different groups before and after the diet and did not correlate with VB values. The present study indicates that low-calorie, low-salt diet decreases plasma fibrinogen levels and improves whole blood filterability in elderly obese women with hypertension.
Acta Diabetol Lat
PMID:Effect of diet and weight loss on whole blood filterability and plasma fibrinogen values in hypertensive obese postmenopausal women. 262 50

The response of immunoreactive gastric inhibitory polypeptide (IR-GIP), immunoreactive insulin (IRI) and immunoreactive C-peptide (IR-C-peptide) to the ingestion of mixed liquid test meals containing 1031 kcal (550 ml) and 422 kcal was studied in 17 obese and 17 normal weight control subjects. When the 422 kcal load was ingested in a volume of 550 ml, the plasma IR-GIP response was significantly greater than in a volume of 225 ml at 15 and 30 min in lean and obese subjects, but the total integrated IR-GIP response was not significantly different between the obese and lean group. Also intraduodenal infusion of 150 ml (280 kcal) of the test meal elicited identical plasma IR-GIP concentrations in lean and obese subjects. An exaggerated IR-GIP response in obese subjects was seen only following the 1031 kcal load (integrated IR-GIP response: 23.6 +/- 1.9 in lean subjects vs 50.3 +/- 3.8 nmol/l/180 min in obese subjects; p less than 0.01). The IRI response was always significantly greater in obese than in lean subjects and not related to the GIP response. Fasting plasma IR-C-peptide levels were significantly elevated in obese subjects (lean: 0.52 +/- 0.04; obese: 1.42 +/- 0.12 nmol/l; p less than 0.005), but the postprandial integrated IR-C-peptide responses in the obese and lean group were identical, indicating decreased hepatic insulin extraction in obesity. It is concluded that an exaggerated IR-GIP response in obesity occurs only after ingestion of a high calorie meal probably as consequence of an increased gastric emptying rate and that the hyperinsulinemic response of obese subjects is not attributable to GIP hypersecretion.
Acta Diabetol Lat
PMID:Gastric inhibitory polypeptide (GIP) hypersecretion in obesity depends on meal size and is not related to hyperinsulinemia. 266 6

The possibility that dietary-induced thermogenesis may be decreased in obesity has been proposed in recent years. However, the results of human studies so far obtained are conflicting. The present research was undertaken in order to clarify this question. We studied postprandial thermogenesis induced by ingestion of a mixed meal and of a carbohydrate mixture in 15 normal and 12 obese subjects. Blood glucose and plasma insulin levels were measured at the same time. The data obtained have shown that the mean resting metabolic rate (RMR) expressed as a function of body weight3/4, is almost the same in obese as in normal-weight subjects (0.115 +/- 0.018 vs 0.133 +/- 0.021 kj/min/kg3/4, respectively). Moreover, the increment of mixed-meal induced thermogenesis (MM-IT) was 48 +/- 22% in normal and -0.8 +/- 12% in obese subjects, respectively (p less than 0.01). Carbohydrate induced thermogenesis (CHO-IT) appeared slightly higher in normal-weight than in obese subjects (159 +/- 66 vs 98 +/- 46). After carbohydrate ingestion we observed a higher glycemic and insulinemic response in obesity. These results indicate that thermogenesis induced by ingestion of food is reduced in obese subjects; they are also compatible with the idea that insulin resistance could play a role in this phenomenon.
Acta Diabetol Lat
PMID:Dietary-induced thermogenesis in obesity. Response to mixed and carbohydrate meals. 267 20

In order to establish whether obesity alters whole blood filterability, the corrected whole blood filtration (VRBC) was measured in 54 elderly obese women (mean age +/- SE = 67 +/- 2 years) without (n = 15) or with associated cardiovascular risk factors such as impaired glucose tolerance (IGT) (n = 11), non-insulin dependent diabetes mellitus (NIDDM) (n = 14) or hypertension (n = 14). Twenty-two age matched women with normal body weight participated as controls. VRBC values were similar in normal controls and obese women with normal glucose tolerance (NGT), whereas they were significantly lower in obese subjects with hypertension, NIDDM or IGT. When subjects with normal and impaired glucose tolerance were combined, a significant negative correlation was found between glucose incretory areas during OGTT and VRBC values. These data demonstrate that obesity per se does not alter whole blood filterability; furthermore, our results indicate that this modification is a precocious and sensitive index of altered glucose metabolism.
Acta Diabetol Lat
PMID:Whole blood filterability in elderly obese women. 368 12

Obesity is considered an insulin resistant state. Dietary guar gum supplementation is able to reduce blood glucose and plasma insulin response to a carbohydrate meal. In order to evaluate whether guar is able to reduce hyperinsulinemia and insulin resistance in gross obesity, we studied 9 obese patients, greater than 50% overweight with impaired glucose tolerance before and after 4 + 4 g/day guar for 6 weeks. Six patients repeated the treatment with 8 + 8 g/day guar after a 3-month interval. Guar was added to the usual diet in order to maintain the body weight constant. Pre-treatment and post treatment study included: total specific insulin binding on circulating monocytes; 3H-glucose infusion and euglycemic hyperinsulinemic clamp at approximately 100 microU/ml. The differences between post-treatment and pre-treatment values were not significant for any of the parameters studied. Fasting glucose production was: 2.17 +/- 0.33 SEM (pretreatment) vs 2.18 +/- 0.18 (4 + 4 g/day) vs 2.28 +/- 0.14 (8 + 8 g/day) mg/kg/min; glucose utilization was: 3.52 +/- 0.43 vs 3.22 +/- 0.44 vs 3.49 +/- 0.63 mg/kg/min; total specific insulin binding was: 2.80 +/- 0.20 vs 2.75 +/- 0.25 vs 2.78 +/- 0.31%; body weight was: 101.4 +/- 5.4 vs 100.2 +/- 6.2 vs 100.5 +/- 7.0 kg. These results indicate that dietary guar gum supplementation per se is unable to reduce insulin resistance in gross obesity if overweight is maintained constant.
Acta Diabetol Lat
PMID:Dietary guar gum supplementation does not modify insulin resistance in gross obesity. 390 31


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