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

Insulin resistance was evaluated in 807 middle-aged subjects at a health survey, with use of an index measured in 75 g oral glucose tolerance tests. The mean value of insulin resistance was higher in a hypertensive group than among the normotensives, independent of body mass index, physical activity, smoking sex, age, and thiazide treatment. One-third of the hypertensives had a high resistance value. Another third of the hypertensives, and also about one-third of the normotensives, had a slightly increased resistance. The remaining third of the hypertensives had a normal-low resistance. A high resistance was also independently related to obesity, low physical leisure time activity, and a family history of NIDDM, but not to a family history of hypertension. The statistical analysis implied a sequence of events: low physical activity might cause high resistance, which in turn might cause high blood pressure.
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PMID:Insulin resistance in the oral glucose tolerance test--a link with hypertension. 204 30

Hypertension is related to several conditions with abnormalities in carbohydrate and lipid metabolism, such as obesity and impaired glucose tolerance. However, perturbed metabolism is also seen in non-obese hypertensive individuals. In addition, hypertension is linked to impaired fibrinolysis and elevated levels of the plasminogen activator inhibitor of endothelial type (PAI-1). Insulin resistance and hyperinsulinaemia in essential hypertension may be an important cause of these metabolic and fibrinolytic abnormalities. Whether hyperinsulinaemia is the cause of hypertension is currently unknown. However, it is clear that the relationship between hypertension and insulin is complex, and further studies are required to clarify this association. Based on the evidence states, it is suggested that insulin resistance and hyperinsulinaemia play a role in hypertension. However, it is also clear that hyperinsulinaemia occurs in the absence of hypertension, which suggests that other factors, such as genetic susceptibility, may be important.
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PMID:Hypertension as a metabolic disorder--an overview. 204 18

Insulin regulates cellular metabolic reactions by its action on the plasma membrane, intracellular enzymes and the nucleus. The first stage in the propagation of the insulin signal is the coupling of insulin to specific receptors at the cell surface. The exact mechanism whereby the transmembrane signalling mechanism (s) results in different insulin-mediated cellular effects is not known. However, the insulin receptor tyrosine kinase, the expression of second messengers, and the action of protein kinase C may, either individually or in combination, mediate some of the insulin effects, such as translocation and activation of glucose transporter proteins. Insulin resistance in clinical conditions such as insulin-dependent diabetes mellitus (IDDM), non-insulin-dependent diabetes mellitus (NIDDM), hypertension and obesity may be acquired to a large extent, and is thus partially reversible. Regulatory factors in insulin sensitivity, such as free fatty acids, counterregulatory hormones and blood glucose level, play an important role in the metabolic control and pathogenesis of insulin resistance in man.
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PMID:Regulation of insulin action at the cellular level. 204 21

Diabetes mellitus is commonly associated with systolic/diastolic hypertension, and a wealth of epidemiological data suggest that this association is independent of age and obesity. Much evidence indicates that the link between diabetes and essential hypertension is hyperinsulinemia. Thus, when hypertensive patients, whether obese or of normal body weight, are compared with age- and weight-matched normotensive control subjects, a heightened plasma insulin response to a glucose challenge is consistently found. A state of cellular resistance to insulin action subtends the observed hyperinsulinism. With the insulin/glucose-clamp technique, in combination with tracer glucose infusion and indirect calorimetry, it has been demonstrated that the insulin resistance of essential hypertension is located in peripheral tissues (muscle), is limited to nonoxidative pathways of glucose disposal (glycogen synthesis), and correlates directly with the severity of hypertension. The reasons for the association of insulin resistance and essential hypertension can be sought in at least four general types of mechanisms: Na+ retention, sympathetic nervous system overactivity, disturbed membrane ion transport, and proliferation of vascular smooth muscle cells. Physiological maneuvers, such as calorie restriction (in the overweight patient) and regular physical exercise, can improve tissue sensitivity to insulin; evidence indicates that these maneuvers can also lower blood pressure in both normotensive and hypertensive individuals. Insulin resistance and hyperinsulinemia are also associated with an atherogenic plasma lipid profile. Elevated plasma insulin concentrations enhance very-low-density lipoprotein (VLDL) synthesis, leading to hypertriglyceridemia. Progressive elimination of lipid and apolipoproteins from the VLDL particle leads to an increased formation of intermediate-density and low-density lipoproteins, both of which are atherogenic. Last, insulin, independent of its effects on blood pressure and plasma lipids, is known to be atherogenic. The hormone enhances cholesterol transport into arteriolar smooth muscle cells and increases endogenous lipid synthesis by these cells. Insulin also stimulates the proliferation of arteriolar smooth muscle cells, augments collagen synthesis in the vascular wall, increases the formation of and decreases the regression of lipid plaques, and stimulates the production of various growth factors. In summary, insulin resistance appears to be a syndrome that is associated with a clustering of metabolic disorders, including non-insulin-dependent diabetes mellitus, obesity, hypertension, lipid abnormalities, and atherosclerotic cardiovascular disease.
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PMID:Insulin resistance. A multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia, and atherosclerotic cardiovascular disease. 204 34

The incidence of impaired glucose tolerance (IGT) in obese juvenile has not yet been well defined. Glycemic and insulin responses to OGTT were evaluated in 398 obese juveniles (and 70 healthy control subjects) to investigate possible correlations with age, body mass index (BMI) and obesity duration. Subjects were subdivided into two groups according to OGTT results: obese with normal glucose tolerance (OB-NGT) and obese with impaired glucose tolerance (OB-IGT). IGT was found in 11% of subjects but no correlations were observed in relation to age, BMI and obesity duration. There was no difference in the glycemic response to OGTT in terms of the biological parameters examined. Insulin plasma levels were twice as high in OB-NGT in comparison to control subjects and OB-NGT. Basal insulinemia increased with BMI in OB-IGT but not in OB-NGT.
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PMID:[Impaired glucose tolerance in obesity in children and adolescents]. 206 6

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.
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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 records of 303 females with gestational diabetes (GD) seen from 1977 to 1988 in the Hospital La Paz in Madrid were reviewed. In some respects, two periods were separately considered, period A from 1977 to 1983 and period B from 1983 to 1988, the latter corresponding to the activity of the Diabetes and Pregnancy Unit. Significant differences in fetal mortality (0.65%) with nondiabetic pregnant women or between periods A and B were not found. Macrosomic fetuses (the most common abnormality, 18.5%) were related with maternal age, a macrosomic fetus in previous pregnancies, degree of carbohydrate intolerance at the time of diagnosis of the diabetes and need for insulin therapy. This latter feature indicates a more severe degree of metabolic involvement. Regarding risk factors, the most common were older maternal age, family history of diabetes and obesity. The pancreatic reserve in nonobese women with GD (2.1 +/- 0.8 ng/ml) was lower than in obese women with GD (3.3 +/- 0.9 ng/l) (p less than 0.001), higher than in progestational diabetic women type II (1.1 +/- 0.7 ng/ml) and type I (0.15 +/- 0.1 ng/ml) (p less than 0.001), and it was not different from that in normal pregnant women (2.15 +/- 0.6 ng/ml). Insulin therapy for the control of diabetes was required in 24.5% of pregnant women. During the period B, termination of pregnancy by means of cesarean section (25.3%) was higher than in normal pregnant women (11.2%) (p less than 0.001). After pregnancy, 13.2% of patients in period A and 39.1% in period B (p less than 0.01) complied with the evaluation of carbohydrate metabolism. Overall, 26.2% had carbohydrate intolerance and 5.9% diabetes mellitus. Although the creation of the Diabetes and Pregnancy Unit has provided a better care and follow-up of the diabetic pregnant women, has not resulted in significant differences in fetal mortality.
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PMID:[Diabetes and pregnancy. Our experience in pregnancy diabetes (1977-1988)]. 208 8

Predominant fat distribution in the upper body segment evaluated by waist to hip circunference ratio (WHR) has been associated with diabetes mellitus and cardiovascular morbidity excess. To investigate metabolic alterations underlying this risk excess, we selected 2 groups of 10 obese women without history of hypertension, menstrual irregularities or oral contraceptives, matched according to age (mean +/- SD): 30.5 +/- 5.3 vs 30.6 +/- 5.8 years and BMI 35.5 +/- 6.5 vs 35.7 +/- 6.7 Kg/m2. Each matched pair had a difference in WHR superior to 0.15 (0.83 +/- 0.04 vs 1.02 +/- 0.05). Insulin and C peptide were determined during an oral glucose tolerance test (75 g). At 30, 60, 90 and 120 minutes differences were significant for glycaemia, insulinaemia and C peptide. Fasting triglycerides were 103 +/- 48 in the lower WHR group vs 164 +/- 84 mg/dl (p less than 0.05); total cholesterol 186.5 +/- 31 vs 215.2 +/- 29.4 mg/dl (p less than 0.05); LDL cholesterol/HDL cholesterol 2.46 +/- 0.89 vs 3.18 +/- 0.96 (p less than 0.05). No significant differences were found in androgenic activity. We conclude that preferential fat distribution in the upper segment is, by itself, an aggravating factor of metabolic alterations associated with obesity, particularly dyslipidaemia and hyperinsulinaemia.
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PMID:[Influence of body fat topography on glucose homeostasis and serum lipids]. 208 55

The association between arterial hypertension and obesity has been known for many years and demonstrated by epidemiological studies. The physiopathological mechanisms involved consist of increased extracellular volumes, hyperactivity of the sympathetic nervous system and the renin-angiotensin-aldosterone system, and abnormal ion exchanges between extra- and intracellular compartments. Recent studies have demonstrated an association between arterial hypertension and insulin resistance. Insulin resistance may well be the most important aetiological factor in this type of arterial hypertension as it stimulates both renal sodium reabsorption and sympathetic nervous system activity and reduces vascular Na-K-ATPase activity.
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PMID:[Arterial hypertension in patients with obesity. Role of hyperinsulinism and insulin resistance]. 209 34

The effects of two standard meals (meal A: 20 g proteins, 20 g lipids, 80 g maltodextrin; meal B: meal A plus 52 g lipids) on insulin and C-peptide secretion and on plasma levels of glucose and free fatty acids (FFA) was studied in 12 obese women separated into two groups according to the onset of obesity. One group (n = 6) developed into obesity after puberty (OP), the other (n = 6) became obese after pregnancy (OG). Meals A.--In OP women, the maximum insulin response was reached at 30 min after meal (141.8 +/- 14.2 microU/ml) and insulinaemia fell to the basal values at 180 min; in OG women the insulin response was linear in the interval 30-150 min after meal. The maximum secretion of C-peptide occurred between 30 min and 90 min in OP and between 60 min and 120 min in OG; the secretion rate was similar in the two groups. Blood glucose levels returned to the basal values at 120 min after meal in OP and at 180 min in OG. FFA levels significantly decreased after meal in both groups (p less than 0.01 vs basal values). Meal B.--Insulin secretion was decreased at 30 min after meal in OP and at 150 min in OG and the levels of C-peptide was not modified in both groups. The glycaemic response was unchanged in OP, but was lower in OG women (p less than 0.02). These results show that OP women present stronger and more rapid insulin response to meals than the OG women; this conclusion is supported by the analysis of the secretion of C-peptide. Blood glucose levels return to basal values faster in OP than in OG women. The blood level of FFA after the standard meals A and B are normal both in OP and OG women.
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PMID:[Insulin response to food in obese women]. 209 59


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