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)

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

Diabetes mellitus and hypertension each confer increased cardiovascular risk. That risk is much greater when the diseases coexist and is further magnified by their frequent association with dyslipidemia and central obesity. Insulin resistance appears to be an important common component to these four entities, whether or not the relationship is truly cause and effect. Increased renal tubule absorption of sodium and increased sympathetic nervous system stimulation from insulin have been said to be the mechanisms by which elevated levels of insulin cause hypertension. However, animal experiments suggest that these are short-term effects only and that long-term insulin may actually increase peripheral blood flow and reduce blood pressure. Experiments in humans suggest that the insulin resistant state in obese patients and type II diabetics is associated with a decrease of the usual vasodilatory effect of insulin. Antihypertensive drugs have differing effects on insulin resistance. Angiotensin converting enzyme inhibitors, alpha-adrenergic blockers, and dihydropyridines appear to improve insulin sensitivity. Other calcium channel blockers appear to be neutral, as is furosemide. Thiazide diuretics, spironolactone, and beta-adrenergic blockers impair insulin sensitivity. The drugs that increase insulin sensitivity also tend to improve dyslipidemia or remain lipid neutral. In contrast, those drugs that tend to impair insulin sensitivity also tend to worsen dyslipidemia.
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PMID:Hypertension in patients with diabetes mellitus. 884 91

Insulin resistance and/or compensatory hyperinsulinemia are associated with hypertension, obesity, dyslipidemia, and glucose intolerance. Insulin resistance and hyperinsulinemia are considered to increase blood pressure through sympathetic nervous system activation, renin-angiotensin system stimulation, and vascular smooth muscle cell proliferation. Leptin, magnesium ions, nitric oxide, endothelin, peroxisome proliferator-activated receptor gamma, and tumor necrosis factor-alpha also modulate blood pressure. Decreasing insulin resistance by lifestyle modification including diet, weight loss, and physical exercise has been shown to reduce blood pressure. Angiotensin-converting enzyme inhibitors have a beneficial effect on insulin resistance. On the other hand, the angiotensin II antagonist, losartan, does not affect insulin sensitivity. The selective alpha1-blockers have a favorable metabolic profile producing increases in insulin sensitivity. A short-acting type calcium channel blocker seems to decrease insulin sensitivity. On the other hand, long-acting type calcium channel blockers improve insulin sensitivity. Thiazide diuretics and most of the beta-blockers decrease insulin sensitivity. Vasodilatory beta-blockers have been reported to improve insulin sensitivity. Use of low-dose diuretics avoids the adverse effects seen with conventional doses.
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PMID:Hypertension and insulin disorders. 1241 78

Thiazide diuretics and beta-blockers are first-line therapies for hypertension unless there are compelling indications for other drug classes. Diuretics and beta-blockers, however, may worsen dyslipidemia and glucose tolerance whereas antihypertensive agents in other drug classes may have neutral or beneficial effects. Initial clinical trials of antihypertensive regimens suggested that blood pressure lowering was the most important aspect of therapy and that the adverse effects on lipids and glucose tolerance did not impact clinical outcomes. Newer trials, however, question this finding and implicate these pleotropic effects as contributing to the results of the trials. Patients with cardiometabolic risk factors may have compelling indications for agents that inhibit the renin-angiotensin-aldosterone system, relegating diuretics and beta-blockers to third-line therapy.
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PMID:Lipid effects of antihypertensive medications. 2203 72