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

A total of 41 patients with hypertension were identified in a survey of 732 healthy factory workers. Twenty-three of these individuals were receiving antihypertensive medication, whereas 18 cases were newly discovered. Plasma glucose and insulin responses to oral glucose and fasting plasma triglyceride (TG), cholesterol, and high-density-lipoprotein (HDL) cholesterol concentrations of these 41 individuals were compared with those of 41 other factor workers, with normal blood pressure, matched with the hypertensive group in terms of gender, age, degree of obesity, job in the factory, and leisure-time activity. Patients with hypertension had significantly higher plasma glucose (P less than 0.05) and insulin (P less than 0.05) concentrations in response to oral glucose, as well as a higher plasma TG concentration (P less than 0.05). Similar findings were obtained when the treated and untreated hypertensive groups were analysed separately and compared with their respective control groups. However, there were no differences between the treated and untreated hypertensive groups. Ninety per cent of the normotensive group had a plasma insulin concentration of less than 500 pmol l-1 2 h after the glucose load. Using this value as the criterion for definition of hyperinsulinaemia, 41% of the patients with high blood pressure were hyperinsulinaemic. In addition to meeting this cut-off point, the patients with hypertension and hyperinsulinaemia were also glucose intolerant and dyslipidaemic. In conclusion, approximately 50% of an unselected group of patients with hypertension were hyperinsulinaemic. Insulin levels were comparable in treated and untreated patients with high blood pressure, and hyperinsulinaemic patients also tended to be glucose intolerant and dyslipidaemic.
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PMID:Prevalence of hyperinsulinaemia in patients with high blood pressure. 155 20

Hypertension appears to predispose to both atheroma and thrombus formation and is a risk factor for stroke and coronary artery disease. Insulin resistance and hyperinsulinaemia are also associated with hypertension, whether treated or untreated and irrespective of obesity. In an attempt to treat the possible insulin resistance in hypertension, an antidiabetic agent, metformin, which enhances glucose uptake, was given to non-obese, non-diabetic, untreated hypertensives in a pilot study. Metformin improved insulin sensitivity, decreased plasma insulin, serum cholesterol and triglycerides, increased fibrinolytic activity and markedly decreased blood pressure. These findings support the concept that insulin resistance may be important in cases of primary hypertension, i.e. those with concomitant metabolic and possibly also fibrinolytic abnormalities. Furthermore, the results indicate that insulin resistance may precede hypertension in these cases.
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PMID:Metformin and blood pressure. 158 82

Despite there being a number of mathematical models of glucose and insulin dynamics, there have been no evaluations of their operation in large groups of subjects. We have carried out intravenous glucose tolerance tests on a group of 182 healthy males, with determination of plasma glucose, insulin, and C-peptide concentrations. Parameters of glucose and insulin dynamics were determined using the minimal model of glucose disappearance, a minimal model of peripheral insulin delivery, and two different models of pancreatic insulin secretion (models I and II). Successful identifications were obtained in 96, 95, 76, and 100% of cases, respectively. The models were evaluated in terms of their ability to recover effects of obesity and aging on carbohydrate metabolism. The glucose disappearance model successfully detected the insulin resistance of both obesity and aging, whereas the peripheral insulin delivery model indicated an increased responsiveness of insulin delivery to glucose in obesity but detected no significant change associated with age. No parameter of pancreatic secretion model I exhibited a significant association with either age or obesity. Insulin secretion model II indicated that the hyperinsulinemia accompanying obesity resulted from both increased pancreatic secretion and decreased hepatic insulin uptake.
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PMID:Evaluation of four mathematical models of glucose and insulin dynamics with analysis of effects of age and obesity. 159 Mar 86

Obesity is a well-known risk factor for the development of non-insulin-dependent diabetes mellitus (NIDDM). Both insulin resistance and concomitant B-cell dysfunction are necessary for the development of NIDDM. Insulin resistance, probably genetically determined but worsened by obesity, appears to be the primary defect that leads to impaired glucose tolerance. However, B-cell dysfunction plays a critical role during progressive deterioration from mild impaired glucose tolerance to severe NIDDM.
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PMID:From obesity to type 2 diabetes. 160 59

Hepatobiliary characteristics of untreated obese patients and those of patients reducing weight through very-low-calorie diets (VLCDs) are reviewed. In untreated obesity, hepatobiliary abnormalities are prevalent. Fatty change is common and may be related to insulin resistance. Moreover, portal inflammation and fibrosis are prevalent findings, also in the absence of alcohol abuse. The liver plays a key role in the hyperinsulinism and hyperlipidemia, and hepatic drug metabolism is influenced by enhanced glucuronidation and sulphatation. Predisposition to gallstone formation can be ascribed to increased biliary cholesterol secretion in concert with changed nucleating factors and altered gallbladder motility. Weight loss by VLCD reduces fatty change but may induce slight portal inflammation and fibrosis. Insulin resistance and pharmacokinetic abnormalities regress. During VLCD the risk of gallstone formation is markedly increased. The deleterious effects described of a rapid weight loss should draw some attention to the liver and biliary tract during VLCD treatment.
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PMID:Liver and gallbladder disease before and after very-low-calorie diets. 161 89

Insulin resistance is a major pathologic feature of human obesity and diabetes. Understanding the fundamental mechanisms underlying this insulin resistance has been advanced by the recent cloning of the genes encoding a family of facilitated diffusion glucose transporters which are expressed in characteristic patterns in mammalian tissues. Two of these transporters, GLUT1 and GLUT4, are present in muscle and adipose cells, tissues in which glucose transport is markedly stimulated by insulin. To understand the mechanisms underlying in vivo insulin resistance, regulation of these transporters is being investigated. Studies reveal divergent changes in the expression of GLUT1 and GLUT4 in a single cell type as well as tissue specific regulation. Importantly, alterations in glucose transport in rodent models of diabetes and in human obesity and diabetes cannot be entirely explained by changes in glucose transporter expression. This suggests that defects in glucose transporter function such as impaired translocation, fusion with the plasma membrane, or activation probably contribute importantly to in vivo insulin resistance.
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PMID:Alterations in glucose transporter expression and function in diabetes: mechanisms for insulin resistance. 161 26

Insulin binding to the plasma membrane is known to be altered by modifying the membrane composition through dietary treatment. As insulin binding receptors are also present on nuclear membrane, this study was undertaken to investigate if specific binding of insulin to the liver nuclei is altered by diet. 8-wk-old female C57 B 6J lean and ob/ob mice were fed semipurified diets containing 20% (w/w) fat of either high or low polyunsaturated-to-saturated (P/S) fatty acid ratio for 4 wk. Liver nuclei were prepared, insulin binding was measured and nuclear phospholipids were isolated for lipid analysis. Insulin binding was highest in nuclei prepared from lean mice fed a high P/S diet. Specific binding of insulin to nuclei prepared from obese mice was also increased by the high P/S diet, but to a lesser extent compared to lean mice. Feeding a high P/S diet increased polyunsaturated fatty acid content of membrane phospholipids from both lean and ob/ob mice. Obese mice were characterized by higher levels of arachidonic acid and lower levels of linoleic acid in phosphatidylcholine. The present study establishes that insulin binding to liver nuclei is increased by feeding a high P/S diet, and that insulin binding to liver nuclei from obese mice is lower than from lean mice.
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PMID:Insulin binding to liver nuclei from lean and obese mice is altered by dietary fat. 162 90

Hypertension is only one component of a multifaceted metabolic-hemodynamic complex that also includes obesity, subtle and overt glucose intolerance, dyslipidemia, enhanced vascular resistance and accelerated atherosclerosis. Results of a number of studies in the past 5 years have shown that even nonobese, nondiabetic individuals with hypertension display insulin resistance, which is located in peripheral tissues (primarily skeletal muscle), is limited to nonoxidative pathways of glucose disposal, and appears to be directly correlated with the severity of hypertension. Insulin resistance and associated hyperinsulinemia in hypertensive individuals are also associated with increased plasma triglyceride levels and decreased high-density lipoprotein concentrations, which likely contributes to enhanced atherosclerosis. Hyperinsulinemia may directly promote atherosclerosis by enhancing LDL-cholesterol accumulation in vessel walls, vascular smooth muscle migration, and proliferation, augmenting connective tissue synthesis in the vascular wall, and decreasing the regression of lipid plaques. The enhanced peripheral vascular resistance that characterizes insulin resistance/hyperinsulinemic states may be related to decreased vascular smooth muscle responses to insulin, which normally modulates (attenuates) vascular contractile responses to vasoactive agents.
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PMID:Insulin resistance, hyperinsulinemia, dyslipidemia, hypertension, and accelerated atherosclerosis. 163 39

Obesity is associated with impaired insulin action in glucose disposal, but not necessarily in other aspects of intermediary metabolism or insulin clearance. Sixteen morbidly obese and 14 normal-weight subjects (body mass index, 51.2 +/- 11.5 v 22.1 +/- 2.2 kg.m-2; mean +/- SD) were studied with sequential, low-dose, incremental insulin infusion with estimation of glucose turnover. In obese patients, basal plasma insulin was higher (10.5 +/- 3.8 v 2.4 +/- 3.0 mU.L-1, P less than .001) and remained elevated throughout infusion (F = 492, P less than .001), as did C-peptide (F = 22.7, P less than .001). Metabolic clearance rate for insulin (MCRI) at the highest infusion rate was similar (1,048 +/- 425 v 1,018 +/- 357 mL.m-2.min-1, NS). Basal hepatic glucose production in obese subjects was less than in normal-weight subjects (270 +/- 108 v 444 +/- 68 mumol.m-2.min-1, P less than .01), as was the basal metabolic clearance rate for glucose (MCRG, 77 +/- 26 v 108 +/- 31 mL.m-2.min-1, P less than .05). Insulin infusion caused blood glucose to decrease less in the obese patients (1.4 +/- 0.5 v 1.9 +/- 0.5 mmol.L-1, P less than .05); hepatic glucose production was appropriately suppressed in them by hyperinsulinemia, but their insulin-mediated glucose disposal was reduced (1.67 [0.79] v 4.45 [2.13] mL.m-2.min-1/mU.L-1, P less than .01). Concentrations of nonesterified fatty acids (NEFA), glycerol, and ketones were elevated throughout the insulin infusions in obese patients, despite the higher insulin concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of morbid obesity on insulin clearance and insulin sensitivity in several aspects of metabolism as assessed by low-dose insulin infusion. 164 Aug 47

When Australian Aborigines make the transition from their traditional hunter-gatherer life-style to a westernized life-style, they develop high prevalence rates of obesity (with an android pattern of fat distribution), non-insulin-dependent diabetes, impaired glucose tolerance, hypertriglyceridemia, hypertension, and hyperinsulinemia. Insulin resistance may be the common pathogenetic characteristic of this cluster of conditions associated with increased risk of cardiovascular disease. The traditional hunter-gatherer life-style, characterized by high physical activity and a diet of low energy density (low, fat, high fiber), promoted the maintenance of a very lean body weight and minimized insulin resistance. In contrast, for most Aborigines, western life-style is characterized by reduced physical activity and an energy-dense diet (high in refined carbohydrate and fat) that promotes obesity and maximizes insulin resistance. Intervention strategies aimed at prevention of insulin-resistance-related chronic disease should be directed at life-style modification. To be effective, such programs will have to be developed and controlled by Aboriginal communities.
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PMID:Westernization and non-insulin-dependent diabetes in Australian Aborigines. 166 99


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