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Query: HUMANGGP:034761 (insulin)
 211,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A clinical and metabolic study of 61 patients with myoocardial infarct before the age of 40 yr showed a high frequency of familial involvement, particularly in subjects with type IIA and IIB hyperbetalipoproteinaemia. Excess weight and arterial hypertension were rare, while premonitory angina was absent in 59%. Four subjects were diabetic. Oral glucose tolerance was normal in 14 and of diabetic type in 26 of 40 patients examined; the insulin response pointed to insulin-resistance. Dyslipidaemia was noted in 45%, including type IIA and IIB hyperbetalipoproteinaemia in 27%. Distribution of the frequency of infarct in function of cholesterolaemia classes gave a bimodal curve indicative of distinct normo- and hypercholesterolaemic groups within the series. Reduced glucose tolerance was more frequent in patients with low blood cholesterol. This suggests that reduced tolerance and high blood cholesterol are independent risk factors in coronary disease. No relation between the clinical and metabolic data could be ascertained.
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PMID:[Clinical and metabolic aspects of juvenile myocardial infarct]. 99 98

Hyperinsulinemia and insulin resistance have been implicated to play a role in the development of hypertension and to contribute to the increased risk for cardiovascular disease in diabetic, obese, hypertensive, and normotensive salt-sensitive humans. Reviewed herein are the effects of nonpharmacological measures, including exercise, weight loss, diet, and changes in lifestyle, on insulin resistance. Based on the evidence from both experimental and clinical studies, regular exercise, moderate weight reduction, and a low-fat, high-carbohydrate, high-fiber diet can markedly improve insulin sensitivity. The possible mechanisms involved are discussed. Because these nonpharmacological measures have also been shown to lower blood pressure and correct dyslipidemia, they can contribute substantially to the reduction of major cardiovascular risk factors and should be implemented in all patients who may be at risk for cardiovascular disease.
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PMID:Effects of nonpharmacological intervention on insulin sensitivity. 128 41

Insulin resistance and hyperinsulinemia is now recognized in non-insulin-dependent diabetes, essential hypertension, obesity, atherosclerotic heart disease, dyslipidemia, heart failure, and in heavy smokers. Several mechanisms have been proposed to explain hyperinsulinemia, insulin resistance and its relationship to hypertension; reduced sodium excretion, activation of the sympathetic nervous system, increased activity of the sodium/hydrogen pump, and stimulation of cellular growth. Some of the nonpharmacological methods to control hyperinsulinemia are of benefit in the management of hypertension, most notably weight loss, exercise program, and reduced salt intake. High-fiber and reduced-protein diets also reduce hyperinsulinemia. Thiazide diuretics can result in insulin resistance, and insulin secretion may be inhibited, possibly associated with concomitant hypokalemia. beta-Blockers result in some reduction of glucose tolerance and mask some of the features of hypoglycemia. Angiotensin-converting enzyme (ACE) inhibitors and alpha-receptor blockers do not effect insulin resistance; probably the same is true for calcium antagonists. Although the effect on risk factors should not be discounted, it is the effect of treatment on hard end points, cerebrovascular accidents, myocardial infarction, or death that is most important. Evidence in hypertension is at present restricted to diuretics and beta-blocking drugs.
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PMID:Hypertension and insulin resistance. 128 47

In this article we have focused on the evolving pattern of nutritional management of the person with diabetes. Before the advent of insulin in 1922, it was sufficient to identify a meal plan that would keep people alive until they could be rescued from mortality due to diabetic ketoacidosis (the major killer of the era) by pharmacologic means. Now, the life expectancy of people with diabetes is close to that of the general population and focus has turned to combating the new threats of macrovascular disease and kidney failure. Over recent years the susceptibility of NIDDM patients to macrovascular events has been established and the twofold increase in risk of a heart attack in diabetic men is outshadowed by the four- to fivefold risk in diabetic women and the 13- to 17-fold greater risk in diabetics under the age of 30 years compared with their nondiabetic counterparts. The mechanism behind the susceptibility to macrovascular disease has generated a veritable plethora of investigations focusing on the atherogenic profile of diabetic dyslipidemia. Hyperinsulinemia, insulin resistance, and overtreatment of the diabetic with insulin have been claimed as contributors to the development of premature atherosclerosis. The hallmark of the diabetic dyslipidemia is the tendency to elevated VLDL triglyceride levels and the closely linked reduction in HDL cholesterol. Although there is some controversy on the relationship between triglyceride levels and the incidence of CAD, there is no doubt that HDL is an independent risk factor. It can now be safely said that elevated triglycerides are a risk factor in women and that in men elevated triglycerides constitute a risk factor if accompanied by a reduced HDL level. For these reasons, any approach to nutritional management of the diabetic must attempt not only to normalize glycemia but to make every effort to reduce the atherogenic profile. In the accompanying algorithm (Fig. 4), we consider the risk factors conducive to a reduction in life expectancy and offer a meal plan that is appropriate for the individual with diabetes. For the 80% of NIDDM patients who are obese, a diet with a reduction of 500 to 1000 kcal is in order and this may be achieved by a periodic VLCD. We examined carefully the controversy related to yo-yo dieting and support the notion that its effects in humans are not all that harmful. Ingestion of simple sugars in the high carbohydrate diet has negative effects both on carbohydrate and lipid metabolism.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The good, the bad, and the ugly in diabetic diets. 131 32

Insulin resistance is a frequently occurring abnormality. Although there can be insensitivity to any of insulin's actions, insulin resistance par excellence is a decreased insulin-mediated whole-body glucose disposal rate. A distinction is made between primary and secondary insulin resistance. Primary insulin resistance is of unknown origin, is only partially experimentally reproducible, and is essentially irreversible (spontaneously or by treatment). In addition, it is both pathway-specific (ie, glucose storage) and organ-specific (mostly skeletal muscle), and is compatible with a postreceptor defect in insulin action. Primary insulin resistance is found in a proportion (approximately 25%) of otherwise healthy people, in non-insulin-dependent diabetes mellitus, essential hypertension, and some forms of dyslipidemia. The idea of an insulin resistance syndrome derives from the striking pattern of overlap among these clinical conditions. Their tendency to cluster in the same individuals is evident from both cross-sectional and longitudinal observations. It is proposed that the insulin resistance syndrome is a large constellation of interrelated changes in metabolic, anthropometric, and hemodynamic variables centered around insulin resistance or hyperinsulinemia. There is a significant genetic component, a predisposing influence for non-insulin-dependent diabetes mellitus, hypertension, dyslipidemia, and possibly, a distinct atherogenic potential.
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PMID:The insulin resistance syndrome. 134 29

It is clearly recognized that patients with NIDDM have an increased risk for CHD. Recent data indicate that persons with glucose concentrations in the nondiabetic range also may be at higher risk for CHD. These associations may not represent cause and effect, however. Emerging data suggest that hyperglycemia and CHD may both arise from hyperinsulinemia/insulin resistance. In support of this hypothesis are studies showing that NIDDM and CHD have many risk factors in common, including age, elevated blood pressure, dyslipidemia, adiposity, and a central pattern of fat distribution. Moreover, these risk factors are frequent concomitants of hyperinsulinemia, itself a risk factor for CHD and perhaps for NIDDM. Although the duration of NIDDM has been infrequently related to risk of CHD, the authors hypothesize that duration of hyperinsulinemia/insulin resistance would be a more sensitive marker for risk of CHD. The relation of IDDM to CHD is a different situation. The etiological process leading to IDDM, namely the destruction of beta-cells in genetically predisposed persons, is not related to cardiovascular risk. However, IDDM patients still have an excess of CVD, the risk factors for which may vary according to the location of the diseases (e.g., LEAD vs. CHD). There is a strong relationship between proteinuria and CVD, which has led to a general theory of vascular complications in IDDM based on defective heparan sulfate metabolism (Steno hypothesis). Recent evidence challenges parts of this hypothesis, and the possibility is raised that a higher case-fatality rate in a subgroup of patients with both renal and CVD explains part of the renal connection, as does the general worsening of CVD risk factors.
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PMID:Diabetes mellitus and macrovascular complications. An epidemiological perspective. 139 12

Diabetes mellitus has become the leading cause of ESRF in the United States. Patients with diabetic nephropathy suffer high cardiovascular morbidity and mortality. Because only 40% of diabetic patients eventually develop diabetic kidney disease, it may be possible to devise primary prevention measures targeted at the subset of patients at risk. Recently, a predisposition to hypertension, a family history of diabetic nephropathy, and a family history of CVD disease each have been associated independently with the development of diabetic renal complication in IDDM. Risk factors for macrovascular damage, including raised arterial BP, dyslipidemia, and insulin resistance, can be detected early in the course of progression to diabetic nephropathy. These risk indicators recently have been shown to be already present at the stage of normoalbuminuria in those patients who eventually will progress to microalbuminuria. Treatment of established renal disease can only delay the onset of ESRF, and lowering of microalbuminuria has been shown to retard the onset of persistent proteinuria. However, no study to date has demonstrated prevention of renal disease in these patients. The ultimate aim should, therefore, be the prevention of the transition from normoalbuminuria to microalbuminuria in individuals who are at higher risk of diabetic renal disease and CVD.
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PMID:Diabetic nephropathy. Future avenue. 139 18

The insulin resistance syndrome ("syndrome X") consists of hyperinsulinemia, glucose intolerance, dyslipidemia, and hypertension, although the inclusion of hypertension has been challenged. Insulin has biological effects that could produce a hyperdynamic circulation. We therefore postulated that an insulin-induced hyperdynamic circulation is an early feature of the insulin resistance syndrome and that this circulatory abnormality leads to later fixed hypertension. The San Antonio Heart Study cohort, a population-based cohort of 3,301 Mexican Americans and 1,857 non-Hispanic whites, was used to define individuals who were hyperdynamic (pulse pressure and heart rate in the upper quartile of their respective distributions), intermediate, and hypodynamic (pulse pressure and heart rate in the bottom quartile). The characteristics of the insulin resistance syndrome were then examined according to these three hemodynamic categories. We also examined the 8-year incidence of hypertension and of type II diabetes according to these hemodynamic categories. A hyperdynamic circulation was associated with statistically significant increases in body mass index (BMI) (p < 0.001), subscapular-to-triceps skinfold ratio (p = 0.042), triglyceride (p = 0.002), 2-hour glucose (p = 0.002), and fasting and 2-hour insulin (p = 0.019 and 0.006). When hemodynamic status was examined separately in lean (BMI < 27 kg/m2) and obese (BMI > or = 27 kg/m2) individuals, the above effects persisted, although they were somewhat attenuated. The odds ratio for the hyperdynamic state as a predictor of future hypertension was 1.66, although this was not statistically significant (p = 0.304). The odds ratio for predicting future type II diabetes was 3.97, which was statistically significant (p = 0.047).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hyperdynamic circulation and the insulin resistance syndrome ("syndrome X"). 145 96

Insulin resistance and consecutive hyperinsulinemia in individuals with the metabolic syndrome are associated with dyslipidemia. This latter is characterised by hypertriglyceridemia and a diminishment of high-density lipoprotein (HDL) cholesterol in the plasma. In severe forms of insulin resistance, low density lipoprotein (LDL) cholesterol may also be elevated. Hypertriglyceridemia is due to an increase in the rate of synthesis of very low density lipoproteins (VLDL) in the liver, and a reduction in their breakdown by the lipoprotein lipase in non-hepatic tissue. Changes in VLDL metabolism are associated with a reduction in HDL concentrations. In addition, direct effects of insulin on the lipid metabolism have been described. Changes in lipid metabolism due to insulin resistance and hyperinsulinemia may be of significance for the atherosclerosis risk in patients with the metabolic syndrome.
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PMID:[Dyslipoproteinemia and metabolic syndrome. Effects of insulin resistance and hyperinsulinemia on lipid metabolism]. 148 17

Hypertension, dyslipidemia, insulin resistance, and hyperinsulinemia--acknowledged risk factors for coronary artery disease--are all more common in persons with non-insulin-dependent diabetes than in nondiabetic persons. The interrelationships of these risk factors are becoming increasingly recognized. This article discusses the dyslipidemias commonly seen in type II diabetes and describes their relationship to glucose metabolism.
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PMID:Lipid metabolism in type II diabetes. 149 73


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