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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Insulin resistance is associated with a variety of cardiovascular risk factors including hypertension, dyslipidemia, and non-insulin-dependent diabetes. In blacks, the relation between insulin resistance, hypertension, and atherosclerosis has been questioned. Most data collected on the Insulin Resistance Syndrome have been collected in nondiabetic subjects; therefore, no inference can be drawn to exogenous insulin use in diabetic subjects where improved glycemic control is usually associated with improved cardiovascular risk factors (especially dyslipidemia) in the absence of weight gain.
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PMID:Progress in population analyses of the insulin resistance syndrome. 932 38

Authors summarise their 5-year long experiences on 343 patients about diagnostic methods of metabolic syndrome X and offer a simple possibility for screening of the jeopardized individuals. In a group of patients with hypertension and central obesity (group I: with 2 insulin resistant condition), 229 (89%) out of 255 cases met the basic criteria of the syndrome X which were hypertension, central obesity and high insulin levels for the corresponding blood sugar levels during oral glucose tolerance test (probable insulin resistance). Dyslipidemia was missing in 20% of these people. Hyperinsulinism occurred in 85%, glucose intolerance in 53%, presumable insulin resistance in 90% of cases. Insulin resistance was characterised by late hyperinsulinism (90 and 120 min.) during oral glucose tolerance test. This was the case in people with "diabetoid" glucose responses too, suggesting an early failure of glucose tolerance and/or insulin secretion. Components of syndrome X were present with a lower frequency in 24 patients with obesity (group II), in 35 patients with hypertension (group III) and in 29 patients without obesity or hypertension (group IV), as well. According to central obesity and hypertension, syndrome X could be screened by a probability of 90%. This can be helpful in prevention of NIDDM and coronary heart disease.
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PMID:[The value of certain parameters in the diagnosis and detection of metabolic X syndrome]. 938 Mar 79

Insulin resistance is characterized principally by impaired insulin-mediated glucose uptake which provokes a compensatory increase in pancreatic beta-cell secretory activity. For a time this may produce well-controlled plasma glucose levels but as the insulin resistance worsens the augmented insulin production becomes inadequate to keep plasma glucose at euglycemia leading to the development of non-insulin dependent diabetes mellitus (NIDDM), accompanied by hyperinsulinemia and hyperglycemia. A number of metabolic defects are associated with NIDDM including obesity, hypercoagulability, cardiovascular disease risk factors such as hypertension and dyslipidemia and these constitute the insulin resistance syndrome. The identity of the biochemical factor that might link all these defects is not yet known. We have hypothesized that platelet-activating factor (1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine, PAF) may be such a link. In this study, we measured plasma acetylhydrolase (EC.1.1.48), which degrades PAF to the inactive metabolise lyso-PAF, as a surrogate for PAF activity in three groups of hypercholesterolemic subjects: lean controls (n = 9), non-diabetic obese (n = 6) and NIDDM subjects (n = 6). The ages and body mass indices of the subjects were 46 +/- 3.1 and 24.2 +/- 2.2 for the lean controls, 52 +/- 2.5 and 28.7 +/- 0.9 for the NIDDM subjects and 60 +/- 2 and 27.6 +/- 2.1 for the obese, non-diabetic subjects (mean +/- S.E.M.). The measurements were made before and after therapy with the cholesterol-lowering drug lovastatin, a 3-hydroxy 3 methylglutaryl (HMG) coenzyme. A reductase inhibitor (40 mg/day) for 3 months. Fasting plasma glucose (FPG) levels were 91 +/- 11, 96 +/- 3 and 146 +/- 11 mg/dl, for the lean, obese and NIDDM subjects, respectively, before therapy began. Lovastatin did not affect FPG in any of the three subject groups. Before treatment, the fasting plasma insulin (FPI) levels were 6.1 +/- 0.92, 10.83 +/- 2.03 and 14.68 +/- 3.64 mU/l for the lean, non-diabetic obese and NIDDM subjects, respectively. After lovastatin therapy only the obese group exhibited a significant change in FPI (15.35 +/- 2.47 mU/l) (P < 0.05). Total cholesterol levels were similar in all three groups both before and after lovastatin therapy but within each group lovastatin therapy significantly reduced the total cholesterol by 32, 29 and 34% in the lean, obese and NIDDM subject groups respectively (P < 0.0001). Lovastatin therapy reduced LDL-cholesterol levels by 40, 32 and 46% in the lean, obese and NIDDM subjects, respectively, but produced no significant effect on HDL or triglyceride levels. Before therapy, the plasma acetylyhydrolase activities were 104 +/- 7, 164 +/- 7 and 179 +/- 7 nmol/ml per min in the lean, obese and NIDDM subjects, respectively. Lovastatin therapy reduced plasma acetylhydrolase levels to 70 +/- 7, 87 +/- 6 and 86 +/- 7 nmol/ml per min in the lean, obese and NIDDM subjects, respectively. Plasma acetylhydrolase activity was predominantly (> 80%) associated with LDL cholesterol both before and after lovastatin treatment. Also, plasma acetylhydrolase activity significantly correlated with fasting plasma insulin levels before lovastatin therapy but not after. Taken together, this study clearly implicates PAF metabolism in three defects associated with the insulin resistance syndrome: hypercholesterolemia, obesity and NIDDM. Additionally, we conclude that chronic hyperinsulinemia may play a significant role in the production of plasma acetylhydrolase.
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PMID:Plasma PAF acetylhydrolase in non-insulin dependent diabetes mellitus and obesity: effect of hyperinsulinemia and lovastatin treatment. 945 36

Insulin resistance or compensatory hyperinsulinemia has been associated with hypertension and dyslipidemia in cross-sectional studies. In contrast, evidence from prospective population-based studies, which could establish the time order of the relationship, is sparse and inconsistent. Therefore, we investigated the associations of hyperinsulinemia with the incidence of hypertension and dyslipidemia in the Kuopio Ischemic Heart Disease Risk Factor Study, a population-based 4-year follow-up study of middle-aged men from eastern Finland. Out of 975 men who had no diabetes, 543 had resting systolic blood pressure (sBP) of < 165 mmHg and resting diastolic blood pressure (dBP) of < 95 mmHg at baseline and were not taking antihypertensive medication, and 764 had serum triglycerides of < 2.3 mmol/l and HDL cholesterol of > or =1.0 mmol/l at baseline. In logistic regression models adjusted for age, baseline resting blood pressure, baseline lipids, obesity, weight change, and other risk factors, men with hyperinsulinemia (fasting insulin in the highest quintile, > or =12.0 mU/l) at baseline had a 2.0-fold (95% CI 1.1-3.5, P = 0.025) incidence of hypertension (sBP of > or =165 or dBP of > or =95 mmHg), a 2.1-fold (95% CI 1.3-3.4, P = 0.002) incidence of dyslipidemia (serum HDL cholesterol of < 1.0 mmol/l or serum triglycerides of > or =2.3 mmol/l), and a 2.6-fold (95% CI 1.1-6.3, P = 0.028) incidence of the combination of these disorders in 4 years, compared with normoinsulinemic men. These findings demonstrate the role of hyperinsulinemia in incident hypertension and dyslipidemia and suggest that both hypertension and dyslipidemia are associated with insulin metabolism disturbance, independently of obesity and body weight.
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PMID:Hyperinsulinemia is associated with the incidence of hypertension and dyslipidemia in middle-aged men. 951 24

Insulin sensitivity varies greatly within the general population; factors contributing to this variability include genetic pre-disposition, obesity, unfavorable body fat distribution, and lack of physical activity. Impaired insulin sensitivity may lead to impaired glucose tolerance and, even in individuals with modest insulin deficiency, to the development of type 2 diabetes mellitus. Of equal concern in patients with impaired insulin sensitivity is the development of the insulin resistance syndrome, in which hypertension, dyslipidemia, and impaired glucose tolerance form a cluster of risk factors for cardiovascular disease. Treatment of insulin resistance includes metformin and the thiazolidinedione troglitazone. Both drugs have been shown to be effective in the treatment of insulin resistance, one of the central abnormalities in type 2 diabetes mellitus. The purpose of this study was to review the current understanding of insulin resistance and its implications for the treatment of type 2 diabetes mellitus. To do this, a MEDLINE search of the clinical literature was conducted and the content analyzed.
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PMID:Insulin resistance: current concepts. 958 14

Millions of Americans are at risk for cardiovascular morbidity and mortality related to disorders of glucose intolerance--particularly type 2 diabetes and prediabetic conditions, including the insulin resistance, or "cardiovascular dysmetabolic," syndrome. The latter is apparently more intricately associated with macrovascular disease--myocardial infarction, stroke, and peripheral vascular disease. In some situations the risk of cardiovascular disease might be reduced by the prevention of diabetes and also by prevention or treatment of the cardiovascular dysmetabolic syndrome. Studies have shown that intensive glycemic control can delay the development of microvascular complications in type 1, and possibly type 2, diabetes. Several longitudinal observational studies have demonstrated a relationship between glycemic control and the development of cardiovascular disease. Prospective clinical intervention trials to address this issue are underway. Insulin may have a role in atherogenesis, both directly and by promoting development of such risk factors as hypertension and dyslipidemia. Genetic factors and mechanisms promoting or discouraging development of glucose intolerance are also under investigation. Lifestyle changes--dietary and exercise modification, weight loss, and smoking cessation--have been shown to have a positive effect on cardiovascular disease risk. Clinical trials suggest that oral antidiabetic agents--particularly the new noninsulin secretagogues (including troglitazone and metformin, which act on the liver and on skeletal muscle)--may be useful in delaying or preventing development of type 2 diabetes and the cardiovascular dysmetabolic syndrome, as well as in their treatment, when present. Both agents, acting primarily by different mechanisms of action, have also demonstrated potential beneficial effects on serum lipid profiles and other cardiovascular risk factors and may be useful in patients with cardiovascular dysmetabolic syndrome who do not yet meet the criteria for diabetes.
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PMID:Type 2 diabetes care: the role of insulin-sensitizing agents and practical implications for cardiovascular disease prevention. 970 64

Insulin resistance and hypertension, as well as dyslipidemia, frequently cooccur. Evidence that nitric oxide (NO) plays a crucial role in the long-term regulation of systolic blood pressure led us to examine whether enhanced vasoconstriction and hypertension induced by NO synthase inhibitor could lead to insulin and lipid disorders. NG-Nitro-L-arginine methyl-ester (L-NAME), an inhibitor of NO synthase, was given for 4 weeks in drinking water (100 mg/kg/day) to 12 Sprague-Dawley rats. Another nine rats received both L-NAME and verapamil (100 mg/kg/day), whereas 12 animals fed rat chow only served as controls. Systolic blood pressure was measured weekly by the indirect tail cuff method. Blood samples were taken at the beginning of the experiment, and after 2 and 4 weeks from all rats. The samples were assayed for insulin, glucose, and triglyceride concentrations. L-NAME treatment resulted in a marked and sustained increase in systolic blood pressure from 130+/-7 to 171+/-3 mm Hg by the second week, which was succeeded by a significant elevation in insulin level at the end of 4 weeks, from 2.3+/-1.8 to 5.4+/-2.0 ng/mL. Triglycerides and glucose were unaffected throughout the experiment. The combination of L-NAME and the NO-independent vasodilator, verapamil, attenuated the hypertension induced by L-NAME and prevented the following rise in insulin level. Data suggest that chronic elimination of NO after chronic inhibition of NO synthase may lead to a state of hyperinsulinemia, possibly as an outcome of insulin resistance.
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PMID:Chronic hypertension leads to hyperinsulinemia in Sprague-Dawley rats treated with nitric oxide synthase inhibitor. 975

The prevalence of insulin resistance in the most common metabolic disorders is still an undefined issue. We assessed the prevalence rates of insulin resistance in subjects with impaired glucose tolerance (IGT), NIDDM, dyslipidemia, hyperuricemia, and hypertension as identified within the frame of the Bruneck Study. The study comprised an age- and sex-stratified random sample of the general population (n = 888; aged 40-79 years). Insulin resistance was estimated by homeostasis model assessment (HOMA(IR)), preliminarily validated against a euglycemic-hyperinsulinemic clamp in 85 subjects. The lower limit of the top quintile of HOMA(IR) distribution (i.e., 2.77) in nonobese subjects with no metabolic disorders (n = 225) was chosen as the threshold for insulin resistance. The prevalence of insulin resistance was 65.9% in IGT subjects, 83.9% in NIDDM subjects, 53.5% in hypercholesterolemia subjects, 84.2% in hypertriglyceridemia subjects, 88.1% in subjects with low HDL cholesterol, 62.8% in hyperuricemia subjects, and 58.0% in hypertension subjects. The prevalence of insulin resistance in subjects with the combination of glucose intolerance (IGT or NIDDM), dyslipidemia (hypercholesterolemia and/or hypertriglyceridemia and/or low HDL cholesterol), hyperuricemia, and hypertension (n = 21) was 95.2%. In isolated hypercholesterolemia, hypertension, or hyperuricemia, prevalence rates of insulin resistance were not higher than that in nonobese normal subjects. An appreciable number of subjects (n = 85, 9.6% of the whole population) was insulin resistant but free of IGT, NIDDM, dyslipidemia, hyperuricemia, and hypertension. These results from a population-based study documented that 1) in hypertriglyceridemia and a low HDL cholesterol state, insulin resistance is as common as in NIDDM, whereas it is less frequent in hypercholesterolemia, hyperuricemia, and hypertension; 2) the vast majority of subjects with multiple metabolic disorders are insulin resistant; 3) in isolated hypercholesterolemia, hyperuricemia, or hypertension, insulin resistance is not more frequent than can be expected by chance alone; and 4) in the general population, insulin resistance can be found even in the absence of any major metabolic disorders.
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PMID:Prevalence of insulin resistance in metabolic disorders: the Bruneck Study. 975 5

Insulin resistance is characterized by impaired responsiveness to endogenous or exogenous insulin and often results in the insulin resistance syndrome, a clustering of cardiovascular risk factors that includes abdominal obesity, hypertension, dyslipidemia, glucose intolerance, and hyperinsulinemia. Although the mechanism responsible for insulin resistance has not been completely defined, it is likely due to defective insulin receptor signaling and results in decreased use of glucose. Troglitazone, the first in a new class of drugs, directly decreases insulin resistance by improving insulin-mediated glucose disposal and reduces plasma insulin concentrations. Glycemic control achieved with troglitazone monotherapy is equivalent to that with sulfonylurea and metformin, and when combined with these agents offers additional plasma glucose reduction. Studies are necessary to determine the effect of thiazolidinediones on morbidity and mortality of patients with type 2 diabetes and insulin resistance.
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PMID:The role of troglitazone in treating the insulin resistance syndrome. 975 9

The study purpose was to explore the association between dyslipidemia and insulin resistance in three ethnic groups. The Insulin Resistance Atherosclerosis Study (IRAS) is a multicenter epidemiologic study conducted at four clinical centers in California, Texas, and Colorado. The study population for this analysis consisted of 931 non-Hispanic white, African American, and Hispanic men and women (aged 45 to 64 years) without diabetes. The IRAS clinical examinations included lipoprotein measures, a 75-g glucose tolerance test, and the frequently sampled intravenous glucose tolerance (FSIGT) test. The results show a consistent relationship between insulin-mediated glucose disposal and dyslipidemia in African American, Hispanic, and non-Hispanic white men and women. Further, LDL size was inversely associated with insulin resistance in all three ethnic groups. These findings indicate that dyslipidemia is a fundamental part of the insulin resistance syndrome in all of the ethnic groups studied.
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PMID:Relationships between insulin resistance and lipoproteins in nondiabetic African Americans, Hispanics, and non-Hispanic whites: the Insulin Resistance Atherosclerosis Study. 978 17


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