Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Familial dyslipidemic hypertension (FDH) is a syndrome recently described from sibships selected for early familial hypertension and found to have one or more of three fasting lipid abnormalities [high triglycerides, low high density lipoprotein (HDL) cholesterol, high low density lipoprotein (LDL) cholesterol]. In further analyses of these same 131 hypertensive subjects, apolipoprotein A-I and B, fasting plasma insulin (adjusted for body mass index), and detailed anthropometrics were different in two subgroups of FDH. Of 63 FDH patients, 19 met the criteria for familial combined hyperlipidemia (FCHL); 44 did not, but still had high triglyceride and/or low HDL cholesterol levels. When compared to 20 normolipidemic hypertensive patients, the 19 hypertensive patients with FCHL had 196% higher very low density lipoprotein cholesterol (p = 0.0001), 33% higher apolipoprotein B (p = 0.0002), smaller LDL particles (p = 0.007), and 73% higher fasting insulin (p = 0.003), but no significant differences in body mass index or skinfold thicknesses. The other 44 FDH patients without FCHL had 33% lower HDL (p = 0.0001), with only 8% lower apolipoprotein A-I levels (p = 0.20); significantly higher subscapular skinfolds (p = 0.02), weights (p = 0.002), body mass index (p = 0.006), knee widths (p = 0.0007), and wrist circumferences (p = 0.0009); smaller, denser LDL subfractions (p = 0.001); and increased apolipoprotein B levels (p = 0.01) compared to the normolipidemic hypertensive group. Increased fasting insulin levels were similar to the normolipidemic group and significantly lower than the FCHL group after adjustment for body mass index, suggesting a relationship between obesity and fasting insulin levels only in the non-FCHL group. We conclude that FDH consists of at least two subgroups: 1) FCHL with high apolipoprotein B, small LDL particles, and increased fasting plasma insulin levels, and 2) a less well-defined residual having upper central obesity with low HDL cholesterol and high triglyceride levels. Elevated insulin levels found in both groups, but possibly originating through different physiological mechanisms, may provide the pathophysiological connections between dyslipidemia, obesity, and hypertension.
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PMID:Apolipoprotein, low density lipoprotein subfraction, and insulin associations with familial combined hyperlipidemia. Study of Utah patients with familial dyslipidemic hypertension. 249 19

The metabolic and cardiovascular complications of obesity are dependent upon the distribution of body fat excess: predominantly abdominal or "android" obesity is more pathogenic than "gynoid" obesity which predominates in the lower part of the body. Adipose tissue overloads localized to the abdomen are associated with hypermortality from vascular diseases, even in patients who are not overweight. The metabolic characteristics of abdominal adipocytes, which have increased lipolytic capacity, might account for this situation, as they would facilitate hyperinsulinism, insulin resistance and such-metabolic disturbances as arterial hypertension, diabetes mellitus and dyslipidemia. Androgens seem to play a key role in the development of obesity morphotypes. These notions have important practical applications: an excess of body fat is not necessarily pathogenic; as regards vascular and metabolic risks, body fat distribution seems to be more important than overweight.
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PMID:[Influence of the distribution of body fat on vascular risk]. 295 Apr 48

Coronary artery disease (CAD) is the leading cause of death among whites with non-insulin-dependent diabetes mellitus (NIDDM). Several risk factors--dyslipidemia induced by NIDDM, obesity, hypertension and hyperglycemia--likely contribute to accelerated atherosclerosis. The dyslipidemia in NIDDM is characterized by abnormalities in composition and metabolism of very low density lipoproteins, low-density lipoproteins (LDL) and high-density lipoproteins (HDL). However, because of the lack of long-term prospective epidemiologic studies, the relative importance of lipoprotein risk factors in the causation of CAD in diabetic patients is not clear. The World Health Organization Multinational Study of vascular disease in diabetics observed increased prevalence of CAD in diabetic populations with relatively high levels of plasma cholesterol and supports the concept that lowering cholesterol levels may significantly reduce coronary risk in NIDDM. To determine the effectiveness of lovastatin, an inhibitor of HMG CoA reductase, for lowering cholesterol levels, 16 patients with NIDDM and mild to moderate increases in plasma cholesterol were given lovastatin (20 mg twice daily) in a randomized, double-blind, placebo-controlled manner for 4 weeks. Compared with the placebo, lovastatin reduced concentrations of total cholesterol (233 +/- 10 vs 172 +/- 7 mg/dl [standard error of the mean], p less than 0.001), LDL cholesterol (140 +/- 9 vs 101 +/- 6 mg/dl, p less than 0.001), and LDL apolipoprotein-B (108 +/- 16 vs 80 +/- 16 mg/dl, p less than 0.001). Plasma triglycerides and very low density lipoprotein cholesterol levels also decreased by 31 and 42%, respectively. Although HDL cholesterol levels did not increase, the total cholesterol/HDL cholesterol ratio decreased significantly with lovastatin therapy. No adverse effects were noted and glycemic control was well-maintained.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment of dyslipidemia in non-insulin-dependent diabetes mellitus with lovastatin. 305 23

Serum lipoproteins are important risk factor variables for coronary artery disease (CAD). Studies of a large population of young individuals show changes in lipoproteins in childhood are race- (black-white) and sex-specific and certain changes occur during growth phases. White boys show adverse changes in lipoprotein levels during sexual maturation that mark them at high risk for CAD. Further, low-density lipoprotein particles are relatively apolipoprotein B enriched in white children, especially boys, a characteristic associated with low levels of high-density lipoprotein cholesterol. The impact of apolipoprotein E genotype on serum lipoproteins seen in adults is already apparent in children, which may be helpful in identifying a high-risk group. Observations of child-parent associations in terms of parental myocardial infarction and levels of lipoprotein variables in the offspring suggest that childhood profiles of lipoprotein (a), apolipoprotein A-I, and apolipoprotein B may be helpful as markers of future CAD. Clustering of increased levels of truncal fat, insulin, and blood pressure is often seen in young adults with an adverse lipoprotein profile. This clustering is related to subtle abnormalities in carbohydrate and lipid metabolism and obesity in childhood. The fact that lipoprotein levels persist from childhood to young adulthood underscores the importance of detection and management of dyslipidemia early in life.
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PMID:Childhood lipoprotein profiles and implications for adult coronary artery disease: the Bogalusa Heart Study. 750 26

Reviewed herein are data supporting the hypothesis that insulin and the sympathoadrenal system are involved in the pathogenesis of hypertension in the obese. Data from the Normative Aging Study, a population-based cohort followed in Boston, confirm other epidemiologic reports of a direct relationship between upper-body obesity, hyperinsulinemia, and hypertension. Because insulin is known to stimulate the sympathetic nervous system (SNS), the possibility that insulin-mediated sympathetic stimulation contributed to hypertension in the obese was investigated by the analysis of 24-h urinary norepinephrine (NE) excretion in this group. Urinary NE was directly correlated with body mass index and waist/hip ratio, supporting increased SNS activity in the obese. Epinephrine excretion, an index of adrenal medullary activity, was inversely related to obesity, and both high insulin and low epinephrine levels were independently correlated with lower levels of high-density lipoprotein cholesterol and higher levels of triglycerides. These results are consistent with the hypothesis that insulin-mediated sympathetic stimulation results in hypertension from concomitant sympathetic stimulation of the heart, vessels, and kidney. Reciprocal changes in adrenal medullary function contribute to the associated dyslipidemia. Therapeutic strategies aimed at diminishing insulin resistance and lowering insulin levels, and antagonizing the effects of sympathetic stimulation on the heart, the vessels, and the kidneys, would appear to have a solid physiological rationale in the obese.
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PMID:Pathophysiology of obesity-related hypertension: role of insulin and the sympathetic nervous system. 751 90

So-called insulin resistance is a frequent phenomenon and a marker of increased risk for both type II diabetes mellitus and atherosclerosis. Today, insulin resistance is widely understood as a tissue- and pathway-specific defect of insulin-stimulated glucose uptake into skeletal muscle that is compensated for by hyperinsulinemia, leading to a cluster of undesirable hypertensiogenic, diabetogenic, and atherogenic processes. Additional defects of insulin-stimulated muscle blood flow and cellular kation balance are presently attracting increasing awareness. Clinical and experimental evidence suggests that angiotensin-converting enzyme (ACE) inhibition ameliorates both insulin-stimulated skeletal-muscle glucose uptake and blood flow in insulin-resistant states by a direct stimulation of cellular glucose uptake, which appears to be kinin-mediated. This improvement of insulin sensitivity could mean not only improvement of glucose metabolism, but also reduction of chronically elevated serum insulin and the ensuing atherogenic consequences (hyper- and dyslipidemia, sympathetic overactivity, growth of vascular smooth-muscle cells, hypertension, etc.). Ca(2+)-channel blockers that do not increase heart rate appear to exert direct antiatherogenic effects while being metabolically neutral. Thus, the combination of Ca(2+)-channel blockade by sustained release verapamil and ACE inhibition by trandolapril in insulin-resistant type II diabetic patients with essential hypertension appears to be promising in terms of possible synergistic effects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Possible synergistic effect of ACE inhibition and calcium-channel blockade on insulin sensitivity in insulin-resistant type II diabetic hypertensive patients. 751 94

Hypertension is associated with insulin resistance and dyslipidemia in a syndrome named X. Epidemiologic evidence also supports a link between hyperinsulinemia and blood pressure (BP), independent of obesity and non-insulin-dependent diabetes mellitus. To assess the possible role of insulin receptors in this syndrome, we studied insulin binding by erythrocyte ghosts in patients with moderate essential hypertension with or without fasting or postglucose hyperinsulinemia. We measured plasma glucose and insulin before and at 30, 60, and 120 min after administration of 75 g glucose in 62 hypertensive patients and 20 matched normotensive controls. Both groups had comparable age (mean 45 years) and waist/hip ratios (mean 0.88). Patients undergoing antihypertensive treatment did not receive antihypertensive medication for 3 weeks. Patients with fasting or postglucose hyperglycemia were excluded from the study. Insulin binding to erythrocyte ghosts was significantly decreased (p < 0.001) to almost half the values of controls (6.5% specific binding) in both patients with hyperinsulinemic (3.2% specific binding) and those with normoinsulinemic (3.9% specific binding) hypertension. Scatchard analysis demonstrated that this was due to a lesser number of insulin receptors. These data indicate that patients with essential hypertension can show decreased erythrocyte insulin receptors without detectable hyperinsulinemia.
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PMID:Diminished insulin receptors on erythrocyte ghosts in nonobese patients with essential hypertension independent of hyperinsulinemia. 752 93

Insulin resistance and dyslipidemia have been described in women with polycystic ovary syndrome (PCOS), a disorder characterized by hyperandrogenism and oligomenorrhea. Although oral contraceptives (OC) are often instituted to regulate menses and suppress HA in women with PCOS, their use has been postulated to cause a deterioration in insulin sensitivity and to adversely affect circulating lipids. To investigate these effects, 9 women with PCOS and 10 age- and weight-matched control women were studied before and during the third month of therapy with a low-dose norethindrone-containing triphasic combination OC using the hyperglycemic clamp technique. At baseline, the PCOS group had higher androgen, triglyceride, and glycosylated hemoglobin concentrations, with a greater insulin response to oral glucose and a lower insulin sensitivity index (ISI) than controls. During OC therapy, a reduction in ISI was observed in both groups, whereas an increase in triglycerides was observed only in controls, removing any observed difference between the two groups in ISI or lipids. In women with PCOS, an increase in insulin concentrations during hyperglycemia accounted for the decline in ISI (P = 0.026), whereas in control women the decrease in ISI was attributable to a decrease in glucose disposal (P = 0.004). In conclusion, PCOS is characterized by insulin resistance in the untreated state. Short-term therapy with a triphasic OC results in a further decline in ISI in women with PCOS, without inducing additional adverse effects on lipids. A more pronounced decline in ISI together with an elevation in triglyceride levels occurs in normal women with OCs. The mechanisms leading to this decrease in ISI are different for each group.
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PMID:Metabolic effects of oral contraceptives in women with polycystic ovary syndrome. 759 46

Arterial hypertension is a chronic condition regarded as one of the main risk factors for development of coronary atherosclerosis. As dyslipidemia and reduced glucose tolerance are also risk factors for coronary disease, it is considered important to use antihypertensive drugs having no negative effects on lipid and glucose metabolism when diabetic patients are treated for hypertension. Lacidipine, a new dihydropyridine-like calcium antagonist, has been shown in in vivo and in vitro preclinical studies to possess potent, long-lasting antihypertensive activity. The present study compared the efficacy and safety of once-daily treatment with lacidipine versus nifedipine SR given twice-daily in non-insulin-dependent diabetic patients. Results have shown a similar efficacy of the two treatments: 6 months later, both drugs had reduced blood pressure values [lacidipine from 184.8/105.2 mm Hg to 144.4/87.1 mm Hg; nifedipine slow-release (SR) from 182.3/106.8 mm Hg to 143.6/89.4 mmHg]. However, lacidipine exhibited a lower incidence of adverse events (particularly ankle edema and tachycardia) than nifedipine SR. Finally, both treatments showed no negative effect on metabolic parameters (total cholesterol, high-density lipoprotein cholesterol, triglycerides, and blood glucose).
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PMID:Calcium antagonist antihypertensive treatment of non-insulin-dependent diabetics: efficacy and safety of lacidipine versus nifedipine SR. 760 94

Several risk factors for the development of microalbuminuria such as: blood glucose unbalance, high blood pressure, dyslipidemia, genetic susceptibility have been described and discussed. The object of this study was to ascertain the importance of these factors. To this end albuminuria was measured using MICRAL-test in two groups of subjects: 100 diabetics (43 type I (insulin-dependent) and 57 type II (non insulin-dependent), and 54 controls. According to diabetes duration, the cases were divided into four sub-groups (less than 5 years; 5-9 yrs; 10-19 yrs; over 20 yrs). The mean values of albuminuria were assessed in the two groups (diabetics and controls) and also for each subgroup of diabetes duration. It was found that in insulin-dependent diabetes mellitus (IDDM), the duration of the disease is an important determinant of albuminuria, a significant increase in its values being observed after 10 yrs of diabetes evolution. The importance of diabetes duration, glucose unbalance and high blood pressure (BP) as possible determinants of microalbuminuria was assessed by comparing the micro- and normoalbuminuric diabetics. Our results are similar to those reported by many other authors, showing that these are important risk factors for microalbuminuria, especially in IDDM.
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PMID:Determinants of microalbuminuria in diabetics. 761 2


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