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 order to examine relationships between albuminuria, insulin resistance, and dyslipidaemia in non-insulin-dependent diabetes (NIDDM), we studied 164 Chinese patients (68 men, 96 women), treated with diet or oral hypoglycaemic agents, on three occasions during a 6-week period. Antihypertensive treatment, if previously prescribed, was withdrawn for at least 2 weeks before the study period. Insulin resistance was calculated from simultaneous fasting plasma glucose and insulin concentrations using the homeostasis model assessment (HOMA) method. Based on two of three 24 h urinary collections, 87 (53%) patients had normoalbuminuria, 46 (28%) microalbuminuria, and 31 (19%) macroalbuminuria. Despite similar glycaemic control, patients with abnormal albuminuria had higher mean arterial pressure, fasting plasma total cholesterol, triglyceride and serum apo B concentrations and were more insulin resistant than normoalbuminuric patients. Albuminuria correlated with mean arterial pressure (r = 0.31, p < 0.001), triglyceride (r = 0.36, p < 0.001), total cholesterol (r = 0.28, p = 0.001), apolipoprotein B (apo B) (r = 0.25, p = 0.003), and insulin resistance (r = 0.25, p < 0.002). These close associations may contribute to the increased cardiovascular risk in Chinese NIDDM patients with abnormal albuminuria.
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PMID:Albuminuria, insulin resistance and dyslipidaemia in Chinese patients with non-insulin-dependent diabetes (NIDDM). 864 Nov 20

This review is aiming to study the values of apolipoprotein AI and B and plasma lipid levels (total cholesterol, HDL cholesterol, LDL cholesterol and triglyceride) in well-treated diabetic patients, and their possible relationship with hemoglobin A1, body mass index and insulin levels. The study groups were 26 insulin-dependent diabetic (IDDM) patients, 30 non-insulin-dependent diabetic (NIDDM) subjects and 20 non diabetic subjects (controls). Apolipoprotein AI concentrations were similar in the three groups, but apolipoprotein B values and apo B/apo AI ratio were significantly higher in IDDM as related to NIDDM patients (p < 0.001) and to non-diabetic subjects (p < 0.001). We were not able to find significant differences concerning plasma lipid values between the three groups. We found a weak correlation between apo B and hemoglobin AI in IDDM (r = 0.45; 0.02 < p < 0.05), but not in NIDDM patients. Body mass index was not related to the values of apolipoproteins AI and B. We found a positive but weak correlation between insulin levels and triglyceride (r = 0.42), and an inverse one with HDL cholesterol (r = 0.57; 0.02 < p < 0.05) in non-diabetic subjects only, while in NIDDM patients these associations were even less significant. Plasma insulin values strongly correlate to body mass index in both NIDDM (r = 0.64; p < 0.001) and in control subjects (r = 0.73; 0.001 < p < 0.001).
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PMID:Apolipoproteins AI and B and plasma lipid values in well-treated diabetic patients from Romania. 864 98

Hypertriglyceridemia is the most frequent form of hyperlipidemia seen in diabetes. Because hypertriglyceridemia and hyperinsulinemia often coexist in the general population and because patients with NIDDM generally are hyperinsulinemic, we have undertaken a series of in vivo studies to examine the effects of hyperinsulinemia on VLDL production. These studies showed that chronic hyperinsulinemia is accompanied by increased VLDL production and that this occurs even when plasma free fatty acid (FFA) levels have fallen. By contrast, acute hyperinsulinemia is accompanied by a reduction in VLDL production, and this reduction is, at least in part, mediated by an associated reduction in the availability of plasma FFAs as a substrate for VLDL-triglyceride (TG). The studies also raise the possibility that the difference in the dependence of VLDL production on plasma FFAs in acute versus chronic hyperinsulinemia results from an increase in hepatic lipogenic enzymes and from the availability of an alternate substrate such as fructose. The overall effect of hyperinsulinemia on VLDL production is postulated to reflect both the effect of insulin on apolipoprotein B production and the hepatic synthesis of TG from either plasma FFAs or newly made fatty acids.
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PMID:Hyperinsulinemia and triglyceride-rich lipoproteins. 867 84

In view of their known high incidence of noninsulin dependent diabetes (NIDDM), we sought to determine whether Native American (Plains Indian) children and adolescents show evidence of risk factors for both NIDDM and cardiovascular disease. Children and adolescents between the ages of 4 and 19 y were recruited, and field days were organized for data collection, which included height, weight [to compute body mass index (BMI)], waist and hip circumference, family histories, quantum of Native American ancestry, and blood sampling for fasting lipids, apolipoproteins, insulin, and glucose. BMI increased with age in boys and girls and tended to be higher than in Caucasian children. The difference was significant in 5-9-y-old (p < 0.05) and 10-14-y-old (p < 0.05) boys and 10-14-y-old girls (p < 0.001). Ten- to 14-y-old girls in the highest quartile for BMI had higher triglyceride levels (p < 0.05) and lower HDL cholesterol (p < 0.001) when compared with those in the lower quartiles. In contrast, 15-19 y olds in the highest quartile for BMI had higher cholesterol, LDL cholesterol, and apolipoprotein B (p < 0.001). The mean fasting insulin levels were not related to BMI. The data suggest that, within this Plains Indian population, obesity associated with elevated lipid levels tends to begin at an early age in Native American children. Insulin levels do not appear to be related to BMI, a putative index of adiposity, in this population of children known to be prone to NIDDM in adult life.
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PMID:Lipoprotein changes in relation to body mass index in Native American adolescents. 879 50

Serum lipoprotein (a) concentrations (Lp(a)) are largely under genetic control, and are strong predictors of coronary heart disease. It has been hypothesised that Lp(a) may contribute to the increased risk of coronary heart disease in familial Type 2 diabetes mellitus. We therefore examined the Lp(a) concentrations and the apolipoprotein (a) (apo(a)) phenotypes in 126 normoglycaemic first degree relatives from families with two or more living Type 2 diabetic patients. These were compared with 147 sex matched normoglycaemic control subjects with no family history of diabetes. Lp(a) concentrations were measured using an enzyme-linked immunosorbent assay (ELISA), and apo(a) isoforms were determined and classified according to the relative mobility of apo(a) on sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE), relative to that of apolipoprotein B-100. There were no significant differences in Lp(a) concentrations between the relatives (R) and controls (C): 11.2 (R) vs. 11.1 (C) mg/dl (median). The distribution of apo(a) phenotypes was not significantly different between groups 0.65 (R) vs. 0.67 (C). These results show that first degree relatives at risk of developing Type 2 diabetes do not have abnormal Lp(a) concentrations or apo(a) phenotypes.
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PMID:Lipoprotein (a) concentrations and apolipoprotein (a) phenotypes in normoglycaemic relatives of type 2 diabetic patients. 880 Apr 99

The 75-g oral glucose tolerance test was performed in 38 normoglycaemic (World Health Organization criteria) non-diabetic volunteers, aged 31-40 years, of whom 20 had a non-insulin-dependent diabetic (NIDDM) mother and 18 had an NIDDM father. At the time of the study the offspring of NIDDM mothers had a somewhat higher body mass index (BMI) (males: 26.5 +/- 1.0 (mean +/- SEM), females: 27.5 +/- 1.5 kg/m2) than the offspring of NIDDM fathers (males: 23.4 +/- 0.9, females: 24.2 +/- 1.2 kg/m2). There was no difference in the time-course of glycaemia; however the serum concentrations of immunoreactive insulin (IRI), C-peptide and proinsulin were significantly higher in offspring of NIDDM mothers than in offspring of NIDDM fathers: area under the curve (AUC) serum IRI: 0.928 +/- 0.091 vs 0.757 +/- 0.056 nmol.l-1.h-1, p = 0.019; serum C-peptide: 6.379 +/- 0.450 vs 4.753 +/- 0.242 nmol.l-1.h-1, p = 0.004; serum proinsulin: 172 +/- 40 vs 51 +/- 7 pmol.l-1.h-1, p = 0.008). Serum IRI correlated with BMI, but C-peptide and proinsulin did not, and after accounting for BMI by covariance analysis they remained significantly higher in offspring of NIDDM mothers. In this group serum proinsulin was significantly higher in male than in female offspring (AUC serum proinsulin: 289 +/- 68 vs 77 +/- 27 pmol.l-1.h-1, P = 0.015). Male offspring of NIDDM mothers also had significantly higher serum triglyceride levels than females of the same group and than offspring of NIDDM fathers. The offspring (male and female) of NIDDM mothers had slightly lower serum apolipoprotein A-I levels than the offspring of NIDDM fathers. Significant correlations were found between serum triglycerides, HDL-cholesterol and apolipoprotein B, and serum concentrations of pancreatic beta-cell peptides, mostly in the offspring of NIDDM mothers; however, they did not display unequivocal association with gender within this group. The data are consistent with clinical observations of a greater risk of NIDDM transmission from the mother than from the father, and may suggest that male offspring are more exposed to this risk than female offspring.
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PMID:Difference in the influence of maternal and paternal NIDDM on pancreatic beta-cell activity and blood lipids in normoglycaemic non-diabetic adult offspring. 881 8

Disturbances in lipid metabolism and in blood fibrinolytic system may play a role in pathogenesis of vascular complications of diabetes mellitus. The aim of the study was to evaluate fibrinolytic parameters (antigen of tissue plasminogen activator-tPA, its inhibitor-PAI, tPA/PAI complexes measured by enzyme immunoassays, euglobulin clot lysis time-ECLT), cholesterol, triglycerides, lipoprotein (a) and apolipoproteins (AI, AII, B) in diabetic patients with and without diabetic nephropathy. The studies were performed in 25 patients with type II diabetes mellitus (age range 42-69), 31 patients with diabetic nephropathy (age range 46-76) and healthy volunteers (age range 31-66). There were no significant differences among the groups studies in tPA:Ag, tPA/PAI complexes, total PAI:Ag and free PAI. ECLT was slightly prolonged in patients with diabetic nephropathy when compared to controls. Cholesterol and triglycerides were significantly elevated in patient with diabetic nephropathy and without nephropathy when compared to healthy volunteers. Triglicerides levels were higher in patients with diabetic nephropathy when compared to subjects without it. Apolipoprotein AI and AII were significantly lower, whereas lipoprotein (a) and apolipoprotein B were significantly higher in patient with diabetic nephropathy when compared to healthy volunteers and diabetic subjects without nephropathy. Lipid metabolism disturbances and impairment in fibrinolysis might contribute to the progression of atherosclerosis and nephropathy in diabetic patients.
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PMID:[Lipid metabolism and fibrinolysis in diabetic nephropathy in the course of diabetes type II]. 883 26

The role of the intestine in cholesterol metabolism in human diabetes is unclear, although abnormalities have been demonstrated in cholesterol synthesis and absorption in diabetic animals. This study examines the relationship between fasting and post-prandial apolipoprotein B-48 in type 2 (non-insulin-dependent) diabetic and non-diabetic subjects. Eight type 2 diabetic patients and ten healthy non-diabetic control subjects were given a high-fat meal (1300 kcal), and the triglyceride-rich lipoprotein fraction was isolated by ultracentrifugation (d < 1.006 g/ml) from fasting and post-prandial plasma. Apolipoprotein B-48 and apo B-100 were separated on 4%-15% gradient gels and quantified by densitometric scanning with reference to a purified low-density lipoprotein (LDL) apo B-100 preparation. Diabetic patients had significantly higher concentrations of apo B-48 and apo B-100 in both the fasting (P < 0.05) and post-prandial (P < 0.001) triglyceride-rich lipoprotein samples compared with non-diabetic subjects. The diabetic patients also exhibited a significantly different post-prandial profile for apo B-48 and apo B-100, with a prolonged increase and a later post-prandial peak, than the non-diabetic subjects (P < 0.01). These results suggest that the raised fasting triglyceride-rich lipoproteins, often found in diabetes, are associated with apo B-48 and may be derived from increased intestinal chylomicron production. The post-prandial pattern suggests an abnormality in intestinal production as well as hepatic clearance of apo B-48 in type 2 diabetes.
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PMID:Elevated triglyceride-rich lipoproteins in diabetes. A study of apolipoprotein B-48. 890 26

Abdominal obesity has emerged as a strong and independent predictor for non-insulin dependent diabetes mellitus (NIDDM). Adiposity located centrally in the abdominal region, and particularly visceral as opposed to subcutaneous fat, is also distinctly associated with hyperlipidemia, compared with generalized distributions of body fat. These lipoprotein abnormalities are characterized by elevated very low density lipoprotein (VLDL) and low density lipoprotein (LDL) levels, small dense LDL with elevated apolipoprotein B levels, and decreased high density lipoprotein2b (HDL2b) levels. This is the same pattern seen in both familial combined hyperlipidemia and NIDDM. The pronounced hyperinsulinemia of upper-body obesity supports the overproduction of VLDL and the increased LDL turnover. We have proposed that an increase in the size of the visceral fat depot is a precursor to the increased lipolysis and elevated free fatty acid (FFA) flux and metabolism and to subsequent overexposure of hepatic and extrahepatic tissues to FFA, which then, in part, promotes aberrations in insulin actions and dynamics. The resultant changes in glucose/insulin homeostasis, lipoprotein metabolism, and vascular events then lead to metabolic morbidities such as glucose intolerance, NIDDM, dyslipidemia, and increased risk for coronary heart disease.
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PMID:Intra-abdominal fat: is it a major factor in developing diabetes and coronary artery disease? 896 90

Fibrates and HMG CoA reductase inhibitors are commonly used in the treatment of diabetic dyslipidaemia. However, these two groups of drugs have not been compared in diabetic patients in a randomized controlled trial. Therefore, a multicentre study was performed in 73 subjects with non-insulin-dependent (Type 2) diabetes mellitus (NIDDM) and combined hyperlipidaemia (serum cholesterol 6.2-10.0 mmol l(-1), serum triglycerides 2.3-10.0 mmol l(-1)), comparing the efficacy of 400 mg bezafibrate with 10 mg simvastatin in a double-blind fashion. Treatment with bezafibrate during 12 weeks reduced serum triglycerides significantly more than simvastatin (-41% vs -22%, p < 0.001) and increased HDL cholesterol more (bezafibrate: + 17% vs simvastatin: + 9%, p < 0.05). LDL cholesterol levels decreased by 14% (p < 0.001) during simvastatin and increased by 21% (p < 0.01) during bezafibrate. This increase in LDL cholesterol was positively correlated with fasting serum triglycerides (p < 0.001) and was associated with a reduction of the serum apolipoprotein B concentration, suggesting an increase in LDL particle size. Metabolic control of diabetes (fasting glycaemia; HbA1c) and insulin secretion (C-peptide levels) were unaffected by both treatments. The incidence of side-effects during treatment was similar for both drugs. Thus, 400 mg bezafibrate mainly increases HDL cholesterol and lowers serum triglycerides but at the expense of an increase in LDL cholesterol; 10 mg simvastatin lowers LDL cholesterin more effectively but has a smaller effect on HDL cholesterol and triglycerides.
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PMID:Comparison of bezafibrate and simvastatin in the treatment of dyslipidaemia in patients with NIDDM. 922 86


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