Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is known that obese subjects have a blunted GH secretory response to stimulation, but little is known about the inhibition of GH secretion in obesity. The present study was designed to evaluate the effects of obesity on the suppression of GH by hyperglycemia and/or somatostatin. Plasma GH concentrations were measured in eight nondiabetic obese subjects and eight nonobese healthy controls during a 4-h hyperglycemic clamp. During the third hour synthetic cyclic somatostatin-14 was infused at the rate of 2.5 nmol/min. Baseline plasma GH levels were similar in obese and nonobese subjects (0.9 +/- 0.1 vs. 0.8 +/- 0.2 micrograms/L; mean +/- SEM). In the last 20 min of the glucose infusion period preceding somatostatin administration (100-120 min of the study) plasma GH averaged 0.8 +/- 0.1 micrograms/L in obese patients and 0.4 +/- 0.1 micrograms/L in control subjects (P less than 0.01), with a reduction of 6 +/- 5% in the former and 35 +/- 10% in the latter (P less than 0.01). In both groups somatostatin infusion did not result in a further decrease in plasma GH. Discontinuation of the somatostatin infusion resulted in a rise in both groups; the increase was higher in nonobese subjects (8.1 +/- 3.8 vs. 2.3 +/- 0.9 micrograms/L in the period 220-240 min; P = NS). These results suggest that in human obesity, hyperglycemia has a diminished inhibitory effect on GH secretion, and somatostatin administration has no additional effect in either obese or nonobese nondiabetic subjects.
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PMID:Plasma concentrations of growth hormone during hyperglycemic clamp with or without somatostatin infusion in obese subjects. 197 27

The aim of the present study was to evaluate whether the inhibitory effect on pancreatic A-cell exerted by hyperglycemic hyperinsulinemia and/or by somatostatin administration is impaired in human obesity. For this purpose plasma glucagon concentrations were measured in 8 obese and 8 nonobese nondiabetic subjects during a 4-h hyperglycemic clamp. Synthetic cyclic somatostatin-14 was infused at the rate of 2.5 nmol/min during the third hour of the study. Fasting plasma glucagon was higher in obese than in nonobese subjects (242 +/- 32 vs 163 +/- 15 pg/ml, p less than 0.05) (mean +/- SEM). In the last 20 min of the glucose infusion period preceding somatostatin administration (100-120 min of the study) plasma glucagon averaged 195 +/- 26 pg/ml in obese and 122 +/- 13 pg/ml in nonobese subjects (p less than 0.05), with a reduction of 19 +/- 3% in the former and 28 +/- 4% in the latter (p = n.s.). In both groups somatostatin infusion did not result in a further decrease in plasma glucagon, which averaged 192 +/- 27 pg/ml in obese and 123 +/- 16 pg/ml in nonobese subjects (p less than 0.05) in the 160-180 min period of the study. Also after discontinuing somatostatin infusion plasma glucagon levels did not change. These results suggest that in human obesity hyperglycemic hyperinsulinemia has a normal inhibitory effect on pancreatic A-cell and that somatostatin administration has no additive effect on hyperglycemia and hyperinsulinemia in either obese or nonobese nondiabetic subjects.
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PMID:Plasma concentrations of glucagon during hyperglycemic clamp with or without somatostatin infusion in obese subjects. 198 86

To examine whether moderate obesity and differences in body fat distribution are associated with abnormalities of protein metabolism, leucine turnover was measured in three groups of age-matched premenopausal women. Ten upper-body-obese (UB Ob), 10 lower-body-obese (LB Ob), and 10 nonobese (Non Ob) women were studied in an overnight postabsorptive condition (basal) and again during an infusion of low physiologic amounts of insulin (insulin clamp). Results showed that basal leucine carbon flux was greater (P less than 0.05) in UB Ob and LB Ob women than in Non Ob women (2.96 +/- 0.08 vs 3.14 +/- 0.16 vs 2.68 +/- 0.08 mumol.kg lean body mass-1.min-1, respectively; mean +/- SEM). Leucine carbon flux was not suppressed during the insulin-clamp study in UB Ob women but was in the LB Ob and Non Ob women. We conclude that moderate obesity is associated with increased proteolysis and that insulin's antiproteolytic actions are impaired in upper-body obesity. These findings could have implications for future studies of and treatment of obesity.
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PMID:Protein metabolism in obesity: effects of body fat distribution and hyperinsulinemia on leucine turnover. 198 43

Atherosclerosis is more common and severe in DM. The purpose of this study was to compare the blood lipids profile and the prevalence of different coronary risk factors (CRF) in a mexican population with CHD (coronary heart disease) and DM compared with non DM patients. All had a history of myocardial infarction. Patients with nephropathy or other secondary causes of dyslipidema were excluded. There were two groups of 45 patients, 32 males, 13 females; age was 60 +/- 1 (SEM), body mass index (BMI) 26 +/- 6. Diabetes duration was 10 +/- 1 years. Diabetic individuals referred smoking in 58%, high blood pressure 55%, obesity (IQ greater than 27) 42%. There were no statistical differences with the non DM group. The mean values of total cholesterol, LDL cholesterol and triglycerides were similar in diabetics and non diabetics. HDL cholesterol was significantly lower in diabetic females (p less than 0.01). Hypoalphalipoproteinemia (HDL-C less than or equal to 30 mg/dL) was the most common abnormality in both groups (52% DM vs 38% nonDM) (p less than 0.01) Type IV phenotype was present in 40 vs 29% (NS). Lipid values were not related to BMI, metabolic control or diabetes type of treatment. To conclude, non insulin dependent diabetic patients with CHD have a high prevalence of CRF. Lipid abnormalities, particularly hypoalphalipoproteinemia and hypertriglyceridemia, could be a cause for the increased atherogenic risk, particularly in females.
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PMID:[Diabetes mellitus and ischemic cardiopathy: their relation to changes in plasma lipids and other coronary risk factors]. 209 Nov 76

Obese patients are characterised by several neuroendocrine abnormalities, including characteristically a decrease in growth hormone responsiveness to GH-releasing hormone. In normal subjects, the GH response to GHRH is enhanced by the acetylcholinesterase inhibitor, pyridostigmine. We have studied the effect of this drug on GH secretion in gross obesity. Twelve obese patients were studied (mean weight 156% of ideal) and compared with a group of 8 normal volunteers. Each subject was initially studied on two occasions, in random order, with GHRH (1-29) NH2 100 micrograms iv alone and following pretreatment with pyridostigmine 120 mg orally one hour prior to GHRH. In obese patients, the GH response to GHRH was significantly blunted when compared to controls (GH peak: 20 +/- 4 vs 44 +/- 16 micrograms/l; mean +/- SEM). After pyridostigmine, the response to GHRH was enhanced in the obese subjects, but remained significantly reduced compared to non-obese subjects treated with GHRH and pyridostigmine (GH peak: 30 +/- 5 vs 77 +/- 20 micrograms/l, respectively). In 6 subjects, higher doses of GHRH or pyridostigmine did not further increase GH responsiveness in obese patients. Our results suggest that obese patients have a disturbed cholinergic control of GH release, probably resulting from increased somatostatinergic tone. This disturbed regulation may be responsible, at least in part, for the blunted GH responses to provocative stimuli.
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PMID:Pyridostigmine enhances, but does not normalise, the GH response to GH-releasing hormone in obese subjects. 210 45

Diet-induced thermogenesis (DIT) denotes the increase in energy expenditure that occurs in response to food ingestion. The purpose of the present study was to examine the possible influence of age, training state and sympatho-adrenal activity on the early phase of DIT in healthy individuals and further to study whether the magnitude of DIT is reduced in human obesity and, if so, to what extent DIT is influenced by weight reduction induced by surgical treatment, i.e. gastric banding or vertical banded gastroplasty. In addition, the effect of an artificial abdominal insulation on the DIT reaction was examined in healthy subjects in order to find out if the spontaneously enhanced thermal insulation of the body in obese individuals may be accompanied by a reduced DIT. The subjects were studied in the basal state and during 2-3 hours after a mixed meal. The energy expenditure was determined by indirect calorimetry. Blood temperature and blood flow in the hepatic vein were measured and splanchnic oxygen uptake and blood-drained heat from the splanchnic region were calculated. The meal was in liquid form, consisting of 17% kJ protein, 28% kJ lipids and 55% kJ carbohydrates, corresponding to either 60% of the individually measured 24-h resting energy expenditure or to 40% of the individually predicted basal metabolic rate. DIT was expressed as the average increase in energy expenditure above the basal level (means +/- SEM). After a 60% meal it was less (21 +/- 3%, P less than 0.01) in 8 elderly (70 +/- 1 years) and 7 middle-aged (51 +/- 3 yrs) individuals (24 +/- 2%, P less than 0.05) than in 10 young (27 +/- 1 yrs) men (29 +/- 2%). Its magnitude was similar (n.s.) in 7 well-trained men with a higher (58 +/- 2 ml/min/kg BW) maximal oxygen uptake (25 +/- 2%) and 7 sedentary individuals with a lower (39 +/- 2 ml/min/kg BW) aerobic capacity (29 +/- 2%). An intravenous pharmacological inhibition of the beta-adrenergic receptor function failed to influence the DIT in 10 men, irrespective of whether the beta-blockade was instituted by a selective-beta-1 antagonist (atenolol) or a non-selective blocker (propranolol). The DIT was 29 +/- 1% with and 29 +/- 2% (n.s.) without a beta-blockade and it was 29% in 2 subjects after 1 week of oral propranolol medication.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Diet-induced thermogenesis. An experimental study in healthy and obese individuals. 217 97

We studied fat distribution and metabolic risk factors in 434 38-year old women selected from population registrars in 5 cities in different parts of Europe. In the present study we focussed on the geographical variation in serum concentrations of free testosterone and its relation to measures of obesity, fat distribution and indicators of cardiovascular risk (serum lipids, insulin, and blood pressure). There were significant differences in free testosterone levels (F = 5.4, p less than 0.001) with lowest levels in Polish women (mean +/- SEM: 1.56 +/- 0.08 pg/ml) and highest in women from Italy (2.07 +/- 0.12 pg/ml). In the pooled data, free testosterone levels were correlated with several anthropometric variables (strongest with subscapular/triceps ratio r = 0.27, with subscapular skinfold and waist/thigh circumference ratio r = 0.25 p-values less than 0.001). In addition, free testosterone was positively correlated with serum total cholesterol (r = 0.11), HDL/total cholesterol fraction (r = 0.12), serum insulin (r = 0.20) and diastolic blood pressure (r = 0.15). These associations remained significant after adjustment for body mass index and waist/thigh ratio (not for diastolic blood pressure) but were no longer significant after further adjustment for insulin levels. There were considerable differences in strength of the associations mentioned between the 5 centers. We conclude that degree of obesity, fat distribution and serum levels of free testosterone all, to a limited degree, contribute to the metabolic profile of randomly selected 38-year old women but that adjustment for such variables increases the differences in metabolic profiles between women from different centers of Europe.
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PMID:Androgenicity in relation to body fat distribution and metabolism in 38-year-old women--the European Fat Distribution Study. 218 Oct 77

Obesity is characterized by decreased rates of skeletal muscle insulin-mediated glucose uptake (IMGU). Since IMGU equals the product of the arteriovenous glucose difference (AVGd) across muscle and blood flow into muscle, reduced blood flow and/or tissue activity (AVGd) can lead to decreased IMGU. To examine this issue, we studied six lean (weight 68 +/- 3 kg, mean +/- SEM) and six obese (94 +/- 3 kg) men. The insulin dose-response curves for whole body and leg IMGU were constructed using the euglycemic clamp and leg balance techniques over a large range of serum insulin concentrations. In lean and obese subjects, whole body IMGU, AVGd, blood flow, and leg IMGU increased in a dose dependent fashion and maximal rates of all parameters were reduced in obese subjects compared to lean subjects. The dose-response curves for whole body IMGU, leg IMGU, and AVGd were right-shifted in obese subjects with an ED50 two- to threefold higher than that of lean subjects for each parameter. Leg blood flow increased approximately twofold from basal 2.7 +/- 0.2 to 4.4 +/- 0.2 dl/min in lean, P less than 0.01, and from 2.5 +/- 0.3 to 4.4 +/- 0.4 dl/min in obese subjects, P less than 0.01. The ED50 for insulin's effect to increase leg blood flow was about fourfold higher for obese (957 pmol/liter) than lean subjects (266 pmol/liter), P less than 0.01. Therefore, decreased insulin sensitivity in human obesity is not only due to lower glucose extraction in insulin-sensitive tissues but also to lower blood flow to these tissues. Thus, in vivo insulin resistance can be due to a defect in insulin action at the tissue level and/or a defect in insulin's hemodynamic action to increase blood flow to insulin sensitive tissues.
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PMID:Decreased effect of insulin to stimulate skeletal muscle blood flow in obese man. A novel mechanism for insulin resistance. 218 93

Controversy regarding defective postprandial thermogenesis in obesity may partly be due to methodological factors such as duration of measurement. To clarify further the role of blunted thermogenesis in obesity, the thermic effect of food was compared in seven lean (mean +/- SEM, 15.7% +/- 1.5% body fat, by densitometry) and seven obese men (37.3% +/- 3% fat) over 3 and 6 hours. The groups were matched for age (35 +/- 2 and 33 +/- 2 years for the lean and obese groups; range, 25 to 39 years), fat-free mass (FFM), and aerobic fitness. Resting metabolic rate (RMR) was measured by indirect calorimetry for 6 hours on two mornings, in randomized order: (1) after a 720-kcal liquid mixed meal, which was 24% protein, 21% fat, and 55% carbohydrate; and (2) in the postabsorptive state. The thermic effect of food, calculated as postprandial minus postabsorptive RMR, was significantly greater for the lean than obese men for the first 3 hours of measurement (67 +/- 6 v 49 +/- 3 kcal/3 hours; P less than .01). During the second 3 hours, the thermic effect of food was marginally, but not significantly, greater for the lean than obese men (34 +/- 8 v 20 +/- 4 kcal/3 hours; P = .10, NS). Over the entire 6 hours, the thermic effect of food was significantly greater for the lean than obese men (100 +/- 12 v 69 +/- 5 kcal/6 hours; P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Thermic effect of a meal over 3 and 6 hours in lean and obese men. 220 89

Glucose tolerance and insulin response were evaluated in 9 normal-weight and 6 obese cats after IV administration of 0.5 g of glucose/kg of body weight. Blood samples for glucose and insulin determinations were collected immediately prior to and 2.5, 5, 7.5, 10, 15, 30, 45, 60, 90, and 120 minutes after glucose infusion. Baseline glucose concentrations were not significantly different between normal-weight and obese cats; however, mean +/- SEM glucose tolerance was significantly impaired in obese vs normal-weight cats after glucose infusion (half time for glucose disappearance in serum--77 +/- 7 vs 51 +/- 4 minutes, P less than 0.01; glucose disappearance coefficient--0.95 +/- 0.10 vs 1.44 +/- 0.10%/min, P less than 0.01; insulinogenic index--0.20 +/- 0.02 vs 0.12 +/- 0.01, P less than 0.005, respectively). Baseline serum insulin concentrations were not significantly different between obese and normal-weight cats. Insulin peak response after glucose infusion was significantly (P less than 0.005) greater in obese than in normal-weight cats. Insulin secretion during the first 60 minutes (P less than 0.02), second 60 minutes (P less than 0.001), and total 120 minutes (P less than 0.0003) after glucose infusion was also significantly greater in obese than in normal-weight cats. Most insulin was secreted during the first hour after glucose infusion in normal-weight cats and during the second hour in obese cats. The impaired glucose tolerance and altered insulin response to glucose infusion in the obese cats was believed to be attributable to deleterious effects of obesity on insulin action and beta-cell responsiveness to stimuli (ie, glucose).
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PMID:Glucose tolerance and insulin response in normal-weight and obese cats. 220 97


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