Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 43 patients with non-insulin dependent diabetes mellitus (NIDDM) associated with hypercholesterolemia, the effect of pravastatin, a potent HMG CoA-reductase inhibitor, on serum lipids, apolipoproteins and lipoprotein (a) was examined. After 1 to 3 months administration of 10 mg per day of pravastatin, the serum levels of total cholesterol, triglycerides and low-density lipoprotein cholesterol (LDL-C) were significantly decreased, while the serum level of high density lipoprotein cholesterol (HDL-C) was significantly increased in patients with NIDDM. The levels of apolipoproteins B (apo B) and E were significantly decreased, while apolipoprotein AI (apo A-I) was not changed by the administration of pravastatin. The atherogenic indices (LDL-C/HDL-C and apo B/apo A-I) were significantly decreased by the administration of this drug. The serum lipoprotein (a), which was increased in the diabetic patients, was not affected by the pravastatin treatment. Plasma glucose and hemoglobin A1c levels were not affected by the treatment. We concluded that pravastatin is a potentially useful agent in the treatment of hypercholesterolemia in patients with NIDDM.
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PMID:Effect of pravastatin on serum lipids, apolipoproteins and lipoprotein (a) in patients with non-insulin dependent diabetes mellitus. 153 40

Changes of glucose and lipid metabolism in NIDDM hypertensive patients during treatment with a new dihydropyridine derivative, nilvadipine, were examined by a randomized, crossover study comparing the results with those elicited by captopril in 18 patients for 12 weeks each. Nilvadipine (8 mg per day) and captopril retard (75 mg per day) caused a sufficient decrease in blood pressure without changing the pulse rate. Nilvadipine and captopril did not significantly change fasting plasma glucose, hemoglobin A1c, serum cholesterol, triglycerides, high-density lipoprotein cholesterol or apoprotein A-I, A-II and B levels in either of the 12-week treatments. In 75-g oral glucose tolerance tests carried out three times in each patient (before treatment and after 12 weeks of treatment with each drug), changes in plasma glucose and serum insulin levels were not significantly different among the three tests. These results demonstrate that nilvadipine as well as captopril are antihypertensive drugs without adverse effects on glucose and lipid metabolism in hypertensive patients with NIDDM.
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PMID:Comparison of the effects of nilvadipine and captopril on glucose and lipid metabolism in NIDDM patients with hypertension. 160 Aug 52

Resistance to insulin-stimulated glucose uptake is associated with an increased rate of synthesis and secretion of VLDL-triglycerides and, in the absence of adequate removal capacity, with hypertriglyceridemia. Subjects with a low glucose disposal rate or a high degree of insulin resistance (as measured by the euglycemic hyperinsulin clamp technique) have also decreased HDL cholesterol levels. The recent developments in the chemistry of lipoproteins indicate that the physicochemically defined lipoproteins such as VLDL, IDL, LDL or HDL are both chemically and metabolically heterogeneous. According to the Alaupovic concept, the plasma lipoprotein system consists of a mixture of particles, each of which is characterized by a unique apolipoprotein composition. Using enzyme-linked differential antibody immunosorbent assay and differential electroimmunoassay, we have discovered that the determination of lipoprotein particle profiles is essential for further clarification of the diagnostic value of measuring apo B and apo A-I. The metabolism of apo B and apo A-I containing lipoprotein particles seems to be affected primarily by their corresponding apolipoprotein composition. Some particular subpopulations of apo B containing lipoprotein particles, such as LpB containing only apo B, LpB:E containing apo B and (a) have been identified as important risk factors in atherosclerosis. We have also recently demonstrated that the protective effect of HDL is due to particles containing apo A-I but not apo A-II (LpA-I), while have little or have no effect those containing apo A-I and apo A-II (LpA-I:A-II). Non-insulin-dependent diabetic patients (NIDDM) are characterized by increased concentrations of cholesteryl ester rich LpB and triglyceride rich LpB:C-III and LpB:E.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Insulin-resistance and lipoprotein abnormalities. 193 84

In diabetic patients, hyperglycaemia results in the non enzymatic glycation of many proteins. We studied the glycation of HDL of patients with either type 1 or type 2 diabetes compared with that of control subjects. Although a basal glycation was detectable in HDL of normal individuals, this increased by about 400% in HDL of both groups of diabetic patients. The degree of HDL glycation was positively correlated with blood glucose concentration. All the HDL apoproteins were glycated but the glycation of apo A-I represented about 80% of the total HDL. These data were compared to those obtained in vitro after incubation of normal apo A-I either as free molecular species or as phospholipid/apo A-I complex, in the presence of glucose (0 to 80 mmol/l) at 37 degrees C. The resulting apo A-I glycation was dependent upon both time of incubation and glucose concentration and was largely increased in the presence of phospholipids. These data suggest that the in vivo glycation of HDL apoproteins might depend upon glucose concentration but might also be partly influenced by their lipid environment.
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PMID:Characterization of the non enzymatic glycation of high density lipoprotein in diabetic patients. 313 9

We investigated the effects of omega-3 fish oil (FO) supplementation on lipid metabolism, glycemic control, and blood pressure (BP) in patients with type II diabetes mellitus. In 22 diabetic patients without overt hyperlipidemia, serum triglyceride, total cholesterol, high density lipoprotein (HDL)-cholesterol, HDL2-cholesterol, HDL3-cholesterol, and apolipoprotein A-I (apo A-I) levels did not change during omega-3 FO supplementation for 8 weeks. The mean serum apo B concentration increased significantly [baseline, 2.56 +/- 0.11 (+/- SEM) mmol/L; 4 weeks, 2.82 +/- 0.13 mmol/L; 8 weeks, 2.80 +/- 0.13 mmol/L; P less than 0.01]. The mean plasma postheparin lipoprotein lipase activity increased transiently during the fourth week (baseline, 168 +/- 17 U/mL; 4 weeks, 182 +/- 18 U/mL; P less than 0.05), whereas postheparin hepatic triglyceride lipase activity did not change. Glycemic control worsened transiently during the fourth week, (baseline, 7.7 +/- 0.4%; 4 weeks, 8.4 +/- 0.3%; P less than 0.05). Both systolic and diastolic BP decreased significantly throughout the study (systolic BP: baseline, 142 +/- 5 mm Hg; 8 weeks, 128 +/- 5 mm Hg; diastolic BP: baseline, 88 +/- 4 mm Hg; 8 weeks, 80 +/- 3 mm Hg; P less than 0.01). These findings suggest that in type II diabetics without overt hyperlipidemia, omega-3 FO supplementation does not improve either the glycemic control or serum lipids, and it is associated with a potentially detrimental rise in serum apo B concentrations. Until more information is available, use of such supplementation should be discouraged.
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PMID:Effects of omega-3 fish oils on lipid metabolism, glycemic control, and blood pressure in type II diabetic patients. 337 25

Serum concentrations of apolipoproteins A-I, A-II, B, C-I, C-II, C-III and E were determined by electroimmunoassay in 56 patients with chronic renal failure (CRF) in the predialytic phase. The results were compared with those obtained in asymptomatic normolipidemic subjects, patients with type IV hyperlipoproteinemia, and patients with type II diabetes mellitus. CRF patients had reduced concentrations of ApoA-I and ApoA-II, normal levels of ApoB and ApoC-I, and increased concentrations of ApoC-II and, in particular, of ApoC-III. There was a significant reduction in the levels of ApoE, especially in male patients. In comparison with type IV, hyperlipoproteinemic patients, CRF patients had lower concentrations of ApoA-I, ApoA-II, ApoB, ApoC-I and, particularly, ApoE; there was no difference in ApoC-III levels reflecting the hypertriglyceridemia common to both disorders. Similar but less marked differences were also found in comparison with type II diabetics. The findings suggest that in CRF, the accumulation of ApoC-III-enriched lipoprotein particles accompanied by a moderate hypertriglyceridemia may be caused more probably by an impaired catabolism than overproduction of triglyceride-rich lipoproteins. CRF patients with vascular disease tended to have higher serum concentrations of triglycerides, cholesterol and ApoB and lower ApoA-I/ApoC-III and ApoA-I/ApoB ratios than patients without vascular disease.
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PMID:Serum apolipoprotein profile of patients with chronic renal failure. 366 95

Plasma triglycerides, cholesterol, high-density lipoprotein (HDL) cholesterol, and apolipoproteins (apo) A-I, A-II, C-II, and C-III were determined and analyzed in 170 diabetic patients and 46 age-matched healthy normal subjects. The diabetics were separated into two groups: insulin-dependent diabetes mellitus (IDDM, n = 78) and noninsulin-dependent diabetes mellitus (NIDDM, n = 92). Significantly increased triglycerides, low HDL cholesterol, and normal cholesterol levels were found in the diabetics. The lipid profiles were similar in the IDDM and NIDDM groups. Plasma apo A-I, but not apo A-II, was low in both groups of diabetics. However, only in the IDDM subjects was there a statistically significant decrease in apo A-I when compared to normal subjects. The decreased apo A-I level negatively correlated with plasma triglycerides. Apo C-II and apo C-III were slightly increased in the diabetics compared to normal subjects. Apo C-II and apo C-III levels significantly correlated with plasma triglycerides (apo C-II, r = 0.70, P less than 0.0001; apo C-III, r = 0.71, P less than 0.0001). Only apo C-II correlated with total cholesterol. Thirty-eight to forty-two percent of the IDDM and NIDDM subjects had a clinical diagnosis of coronary artery disease (CAD) and/or peripheral arteriovascular disease (PAD). In the IDDM subjects, but not in the NIDDM subjects the incidence of CAD and/or PAD was associated with the decreased apo A-I levels as evaluated by a univariate analysis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Analysis of plasma lipids and apolipoproteins in insulin-dependent and noninsulin-dependent diabetics. 641 12

The aim of the present study was to determine if low-density lipoproteins (LDLs) and red blood cell (RBC) membranes from diabetic patients present an increased susceptibility to lipoperoxidation, which might be related to the increased incidence of atherosclerosis in diabetes. LDLs and RBC membranes were isolated from 11 insulin-dependent (IDDM) and 18 non-insulin-dependent diabetic (NIDDM) patients and exposed to a peroxidative stress by incubation with phenylhydrazine. The susceptibility to peroxidation was determined by measuring the production of thiobarbituric acid-reactive substances (TBARS) after the incubation. The following parameters were also evaluated: plasma glucose, triglycerides (TG), phospholipids (PL), total and high-density lipoprotein (HDL) cholesterol, apolipoprotein (apo) A-I, apo B, hemoglobin A1c (HbA1c), LDL PL and cholesterol, LDL fatty acid composition, and RBC membrane PL and cholesterol. Although they were apparently normolipidemic, diabetic patients showed an increased susceptibility to peroxidation in LDLs and erythrocyte membranes as compared with control subjects. The amount of arachidonic acid in LDLs and the PL concentration of RBC membranes from diabetic patients were significantly higher than in normal subjects. The increased lipoperoxidability of both RBC membranes and LDLs might play a central role in the pathogenesis of the vascular complications of diabetes mellitus.
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PMID:Increased susceptibility to lipid oxidation of low-density lipoproteins and erythrocyte membranes from diabetic patients. 799 Jun 98

Twenty patients (18 men, 2 women) with non-insulin dependent diabetes mellitus (NIDDM) were randomized to receive either gemfibrozil 1200 mg daily or placebo for 3 months in a double-blind study. The effect of gemfibrozil on plasma HDL subfraction distribution was studied with sequential and density gradient ultracentrifugation and in gradient gel electrophoresis. The concentrations of apo A-I, apo A-II, Lp A-I and Lp A-I:A-II particles were measured. Postheparin plasma lipoprotein lipase (LPL) and hepatic lipase (HL) activities and plasma cholesteryl ester transfer protein (CETP) activities were also determined. Gemfibrozil increased the concentration of HDL cholesterol (P < 0.01), which was due to the rise of HDL3 cholesterol (+16%), while in the placebo group these values remained unchanged. Gemfibrozil increased the concentrations of apo A-I(+12.6%, NS), apo A-II (+28.2%, P < 0.01) and Lp A-I:A-II particles (+21.6%, P < 0.06) but there were no changes in the placebo group. Neither gemfibrozil nor placebo had any effect on the concentration of Lp A-I particles. As determined by density-gradient ultracentrifugation, gemfibrozil increased the concentration of cholesterol in the most dense HDL fractions (mean density 1.193 g/ml, +22%, P < 0.05 and mean density 1.158 g/ml, +19.3%, P < 0.05). In gradient gel electrophoresis, the gemfibrozil-induced elevations of the cholesterol and protein were most pronounced in the HDL3a (8.8-8.2 nm) region. Gemfibrozil increased LPL and HL activities by 14.7% (P < 0.05) and by 18.8% (P < 0.01), respectively, while in the placebo group LPL and HL activities remained unchanged. Plasma CETP activity was also increased during gemfibrozil treatment while in the placebo group it remained unchanged. We conclude that gemfibrozil causes multiple changes in plasma HDL metabolism. The gemfibrozil-induced elevation of HDL3 and dense HDL subpopulations may reflect the concerted action of LPL, HL and CETP on plasma HDL metabolism.
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PMID:Effect of gemfibrozil on high density lipoprotein subspecies in non-insulin dependent diabetes mellitus. Relations to lipolytic enzymes and to the cholesteryl ester transfer protein activity. 825 55

In 98 Japanese patients with Type 2 diabetes mellitus, serum total cholesterol, triglyceride, high density lipoprotein cholesterol (HDL-C), free fatty acid (FFA), and apolipoproteins (apo) A-I, A-II, B, C-II, C-III, and E were determined. The data were compared with those in 47 normolipidaemic normal controls. The total cholesterol value of the diabetic patients was also compared to that of a general population (n = 2227). The diabetic patients were separated into those with cardiovascular disease (n = 20) and without it (n = 78) and a comparison of clinical characteristics and dyslipidaemia was also performed. The diabetic patients had slightly but significantly higher FFA, LDL-C, apo B, C-II, C-III, E, and B/A-I, and lower apo A-I and A-II compared to the normal controls. The total cholesterol level of the diabetic patients (5.17 +/- 0.96 mmol-1) was not significantly higher than that of the general population (5.12 +/- 0.91 mmol-1). By multivariate stepwise discriminant analyses, only total cholesterol significantly discriminated the patients with and without cardiovascular disease. In Japanese patients with Type 2 diabetes, a diabetic population with a very low prevalence of cardiovascular disease, high total cholesterol is a risk factor for developing cardiovascular disease. Nevertheless, a markedly low prevalence of cardiovascular disease in Japanese with Type 2 diabetes compared to Caucasian counterparts may partly be due to the mildness of dyslipidaemia.
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PMID:Possible link between a low prevalence of cardiovascular disease and mild dyslipidaemia: a study in Japanese patients with type 2 diabetes. 833 22


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