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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is now well established that non-insulin dependent diabetes mellitus is characterized by insulin resistance. Independent data have suggested that essential hypertension also is associated with abnormal glucose tolerance and an impairment of insulin action. These observations have led to the hypothesis that insulin resistance and/or hyperinsulinaemia may provide a common pathophysiological basis for the high concordance of these two diseases in many individuals. The relationship between insulin resistance, diabetes and hypertension assumes additional importance when one considers that many antihypertensive medications may impair insulin sensitivity or insulin secretion, thus leading to a further impairment of glucose tolerance or deterioration of glycaemic control. In the present review, the epidemiological and pathophysiological evidence supporting this hypothesis will be examined and the implications for treating hypertension in the patient with diabetes will be discussed.
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PMID:Insulin sensitivity and the effects of antihypertensive agents: implications for the treatment of hypertension in the patient with diabetes mellitus. 307 96

During the last several years, the pharmacist has acted as a primary-care provider for patients with selected chronic illnesses at an urban county health department. The pharmacist's responsibilities include examining patients, ordering laboratory tests and X-rays, and adjusting or prescribing medication. In order to comply with health department regulations requiring the use of protocols by non-physician practitioners, and to better define the pharmacist's role, pharmacy protocols for the treatment of essential hypertension and type II diabetes mellitus have been developed. The protocols provide specific guidelines for the pharmacist involved in primary patient care. In addition, they describe a procedure for the selection and referral of patients. These protocols can serve as a sound foundation by which other pharmacists involved with primary patient care treat essential hypertension and type II diabetes mellitus. They can easily be modified to suit a pharmacist's particular needs and situation.
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PMID:Protocols for the treatment of essential hypertension and type II diabetes mellitus by pharmacists in ambulatory care clinics. 360 99

The authors conducted a clinical investigation in twenty-five patients affected with essential hypertension of mild or moderate grade associated with type II diabetes mellitus, the purpose being to assess the effect of 8 weeks of combined treatment with atenolol (100 mg) and chlorthalidone (25 mg) on arterial blood pressure, heart rate, and glycaemia. It is, indeed, generally known that both beta-blockade agents and diuretics can interfere with carbohydrate metabolism. The results indicate that 92% of the patients treated in this trial had significant reduction of systolic and diastolic blood pressure readings, in the absence of bradycardia or other adverse effects. Glycaemia values were lower at the end of treatment, probably as a result of better diet control during the trial, as suggested by the general tendency to body-weight reduction.
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PMID:Hypotensive effect of the association atenolol-chlorthalidone in hypertensive diabetics. 650 Jan 67

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

To investigate the metabolic and renal effects of the nonsulfhydryl, tissue-active ACE inhibitor quinapril in diabetes and in hypertension, we studied 30 essential hypertensives and 24 non-insulin-dependent (type II) diabetic (NIDDM) subjects with hypertension. Systolic and diastolic blood pressures, plasma glucose, and insulin responses to an oral glucose load (75 g), lipid profile, and urinary albumin excretion were evaluated before and after 8 weeks' administration of quinapril (10 to 40 mg/day). Quinapril produced a significant and comparable reduction of arterial blood pressure in both groups. Mean arterial pressure decreased from 114.8 +/- 0.9 to 94.2 +/- 1.1 (-17.9 +/- 1.5%) in the essential hypertensive group and from 118.4 +/- 1.6 to 96.2 +/- 1.4 (-18.4 +/- 1.6%) in the diabetic hypertensive group. In both essential hypertensives and diabetic-hypertensive subjects with microalbuminuria, quinapril significantly and comparably reduced the urinary albumin excretion rate (UAE); UAE decreased from 32.5 +/- 5.5 micrograms/min to 14.7 +/- 3.7 micrograms/min (P < .05 v baseline) in the diabetic-hypertensive group and from 27.5 +/- 3.0 micrograms/min to 11.6 +/- 2.7 micrograms/min (P < .05 v baseline) in the essential hypertensives. Altogether, a direct correlation was found between the initial level of UAE and the UAE reduction after quinapril (delta UAE) (r = 0.706, p < .05). Insulin and glucose responses to an oral glucose tolerance test and the lipid profiles were not modified by quinapril treatment. The results confirm that quinapril is an effective antihypertensive agent that additionally reduces microalbuminuria in both hypertensive diabetics and in patients with essential hypertension, without altering insulin sensitivity and lipid profiles.
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PMID:Quinapril reduces microalbuminuria in essential hypertensive and in diabetic hypertensive subjects. 757 97

Mortality and morbidity from coronary heart disease (CHD), diabetes mellitus (DM) and essential hypertension (HTN) are higher in people of South Asian descent than in other groups. There is evidence to believe that essential fatty acids (EFAs) and their metabolites may have a role in the pathobiology of CHD, DM and HTN. Fatty acid analysis of the plasma phospholipid fraction revealed that in CHD the levels of gamma-linolenic acid (GLA), arachidonic acid (AA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are low, in patients with HTN linoleic acid (LA) and AA are low, and in patients with non-insulin dependent diabetes mellitus (NIDDM) and diabetic nephropathy the levels of dihomo-gamma-linolenic acid (DGLA), AA, alpha-linolenic acid (ALA) and DHA are low, all compared to normal controls. These results are interesting since DGLA, AA and EPA form precursors to prostaglandin E1, (PGE1), prostacyclin (PGI2), and PGI3, which are potent platelet anti-aggregators and vasodilators and can prevent thrombosis and atherosclerosis. Further, the levels of lipid peroxides were found to be high in patients with CHD, HTN, NIDDM and diabetic nephropathy. These results suggest that increased formation of lipid peroxides and an alteration in the metabolism of EFAs are closely associated with CHD, HTN and NIDDM in Indians.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Essential fatty acid metabolism in patients with essential hypertension, diabetes mellitus and coronary heart disease. 764 60

The effect of essential hypertension at baseline on the development of NIDDM within 6 years was investigated in 465 Chinese nondiabetics with or without hypertension. The age, sex adjusted 6 year incidence of NIDDM in hypertensive group (BP > 18.7 +/- 12. okPa (140/90 mmHg) or treated with antihypertensives) at baseline was significantly higher than that in normotensive group (44.6%, n = 325, P < 0.05) at baseline. Multivariate regression analysis showed the hypertensive group had higher risk of worsening to diabetes compared with normotensives (OR: 1.82, 95% Ci: 1.03-3.21, P < 0.05) after the adjustment for two other important risk factors for NIDDM, the fasting plasma glucose and BMI. Further more the increasement of SBP by 20 mmHg at baseline significantly increase the risk for NIDDM in the followup period in the blood-lowering-drug-free group (OR: 1.54, 95% Ci: 1.05-2.24, P < 0.05). Thus it confirmed that hypertension at baseline was an independent predictor for NIDDM. In addition, our observation showed that some antihypertensive drugs appears also to play an unfavorable role in the occurrence of NIDDM.
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PMID:[Essential hypertension: a predictor of the 6 year-incidence of NIDDM in 465 non-diabetics]. 771 8

Gastric inhibitory polypeptide (GIP) is one of the strongest insulinotropic gut factors. Its secretion is induced by oral (but not intravenous) glucose and it has been implicated in the pathogenesis of hyperinsulinemic states (NIDDM, obesity). To determine its relevance to hypertension, 54 subjects were studied: 26 normotensives (12 with and 14 without family history of essential hypertension), and 28 essential hypertensive subjects. Plasma glucose, serum insulin (IRI), and GIP were evaluated after a mixed meal containing a total of 82 g of carbohydrates, and 2 g sodium chloride. Venous blood was collected at baseline and every 15 min during a 3-h period. Baseline levels of glucose, IRI, and GIP were comparable in the three groups. At 30 min, however, IRI and GIP were higher in normotensives with a family history of hypertension and in established hypertensive versus control subjects. Both in normotensive and in hypertensive groups, glucose, IRI, and GIP responses to the meal were significantly correlated. Our data suggest the contribution of altered GIP secretion in the pathogenesis of hyperinsulinemia in essential hypertension.
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PMID:Hyperinsulinemia and hypertension. Do intestinal hormones play a role? 775 55

Insulin resistance is the major pathogenetic link of atherosclerosis development and progression. The clinical diagnosis is made on the basis of analysis of glycemic and insulinemic response during the oral glucose tolerance test. Insulin resistance prevalence is constant in NIDDM and advanced renal failure, and almost 50% in early stages of essential hypertension and kidney diseases. Its prevention and therapy are effective. The increase of free Ca and decrease of free Mg concentrations participate both in insulin resistance and hemodynamic changes in diseases of the Reaven's syndrome. The intracellular mineral dysbalance is caused by the alteration of Na+,H(+)-antiporter. (Fig. 1, Tab. 4, Ref. 51.).
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PMID:[Insulin resistance: its clinical importance and trends in modern research]. 781 48

Obesity is the most common reason for insulin resistance with consequent hyperinsulinemia. Other reasons for hyperinsulinemia are type II diabetes mellitus and a genetic predisposition with a family history of hypertension. Hyperinsulinemia is considered to cause blood pressure elevation and is generally accepted as an independent risk factor for atherosclerosis. However, insulin per se does not elevate blood pressure, but rather reduces total peripheral vascular resistance in experimental studies. Blood pressure might be elevated by other mechanisms secondary to hyperinsulinemia, however, such as enhanced renal sodium retention, elevated intracellular free calcium, and increased activity of the sympathetic nervous system. Indeed, subjects whose blood pressure is salt-sensitive exhibit hyperinsulinemia after glucose loading, and normotensive subjects with glucose-induced hyperinsulinemia will develop hypertension within 5 years more often than normoinsulinemic subjects. In primary hypertension, the incidence of insulin resistance and hyperinsulinemia is much higher than in normotensive controls. However, not all reported studies show a relationship between hyperinsulinemia and blood pressure elevation, and in some experimental studies no blood pressure elevation could be induced by prolonged hyperinsulinemia. Therefore, it is still unclear whether hyperinsulinemia induces hypertension or is only casually associated with it. Nevertheless, treatment of hyperinsulinemia is recommended to avoid secondary complications. Treatment should begin with weight reduction and physical exercise, which will improve insulin resistance. Hypertension benefits more from weight reduction than from exercise. If drug therapy of hypertension is required, angiotensin-converting enzyme (ACE) inhibitors and calcium-channel blockers are the drugs of first choice. In addition, beta-blockers and centrally acting drugs appear to be of certain benefit. However, diuretics must be used carefully, because they ameliorate insulin resistance, induce dyslipoproteinemia, and stimulate the sympathetic nervous system.
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PMID:Hyperinsulinemia, insulin resistance, and hypertension. 789 93


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