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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

High density lipoprotein subfraction 2 (HDL1)-cholesterol level is usually decreased in Type 2 (non-insulin-dependent) diabetes. A study was carried out in 251 Type 2 diabetic patients (106 males [M], 145 females [F]) and in 120 non diabetic controls in order to determine the influence of hypertriglyceridaemia and obesity on the HDL2-cholesterol level and to analyse the relationship between HDL2-cholesterol level and atherosclerosis (coronary heart disease, peripheral atherosclerosis or cerebral vascular disease), in Type 2 diabetes. Influence of hypertriglyceridaemia and obesity on HDL2-cholesterol level was studied by comparing the mean values of HDL2-cholesterol between diabetics and controls, after controlling for hypertriglyceridaemia and obesity, and by a multiple linear regression test. A stepwise logistic regression was performed to analyse the association between the prevalence of atherosclerosis and several variables: age, duration of diabetes, hypertension, cigarette smoking, body mass index, mean glycaemia, total cholesterol, triglyceride, HDL-cholesterol, HDL2-cholesterol and HDL3-cholesterol levels. In both men and women, when both of the factors (hypertriglyceridaemia and obesity) were present of when only one was, HDL2-cholesterol level was significantly lower in the diabetic population, compared with controls. But when obesity and hypertriglyceridaemia were absent, HDL2-cholesterol level, in the diabetic population, was not significantly different from controls (M: 17.9 +/- 13.3 vs 20.5 +/- 13.8 mg/dl: NS; F: 30.1 +/- 21.5 vs 27.6 +/- 14.2 mg/dl: NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of obesity and hypertriglyceridaemia on the low HDL2-cholesterol level and on its relationship with prevalence of atherosclerosis in type 2 diabetes. 145 17

The objective of this study was to determine whether a less favorable risk factor pattern for cardiovascular disease among persons with impaired glucose tolerance could be explained by fasting insulin, obesity, and/or a central distribution of body fat. Between 1984 and 1988, cardiovascular risk factors were examined cross-sectionally in Hispanic and non-Hispanic white participants in the San Luis Valley Diabetes Study who had either impaired (n = 173) or normal (n = 1,107) glucose tolerance. Sex-specific analysis of covariance models were constructed to adjust risk factor levels for age, age and insulin, and age, insulin, body mass index, and centrality index. Both males and females with impaired glucose tolerance had higher age-adjusted mean diastolic blood pressures, heart rates, uric acid levels, and triglyceride levels and lower levels of high density lipoprotein (HDL) cholesterol and HDL3 cholesterol than normal subjects; differences were significant for all risk factors except HDL cholesterol and HDL3 cholesterol in males. Differences in diastolic blood pressure in males, and differences in heart rate and triglyceride in both sexes, remained significant after adjustment for all covariates. However, differences in uric acid in males and differences in diastolic blood pressure and HDL3 cholesterol in females were attenuated to borderline significance levels. Differences in uric acid and HDL cholesterol in females were diminished to nonsignificant levels, especially after adjustment for obesity-related measures. With few exceptions, fasting insulin did not appear to play a major role in accounting for differences in these risk factors. With adjustment, ethnic differences (Hispanic vs. non-Hispanic white) were smaller and were statistically significant less often than differences observed between impaired and normal glucose tolerant groups. The authors concluded that hyperinsulinemia, obesity, and a central body fat distribution accounted for some, but usually not all, of the less favorable cardiovascular risk factor pattern found in subjects with impaired glucose tolerance.
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PMID:The roles of insulin, obesity, and fat distribution in the elevation of cardiovascular risk factors in impaired glucose tolerance. The San Luis Valley Diabetes Study. 146 70

Normolipidemic patients of both sexes with insulin-dependent diabetes mellitus have the same pervasive changes in lipoprotein surface and core lipid composition. The disproportionate increase observed in their lipoprotein free (unesterified) cholesterol relative to the predominant surface phospholipid lecithin (phosphatidylcholine) is reflected by elevation of the FC-L ratio in their whole plasma, VLDL, HDL2, and HDL3. As a possible consequence of this qualitative disturbance, cholesteryl ester transfer is pathologically increased and the mass of cholesteryl ester transferred from HDL to VLDL + LDL is significantly greater in IDDM patients than in control subjects at 1, 2, and 4 hr (P less than 0.001). Consistent with accelerated CET in vivo, the TG-CE core lipid ratio was decreased in VLDL from six subjects (IDDM 9.5 +/- 0.8 vs. control 12.9 +/- 3.4; P less than 0.01) and increased in their HDL (diabetic 0.55 +/- 0.11 vs. control 0.42 +/- 0.04: P less than 0.025). These abnormalities in lipoprotein composition and CET do not correlate with glycemic control and persist after intensive management with s.c. insulin. They may be related to the peripheral hyperinsulinemia that is an unavoidable consequence of conventional s.c. insulin administration because preliminary studies indicate that these disturbances in lipoprotein composition and function are reversed when systemic insulin levels are lowered and insulin is delivered into the portal circulation from an i.p. catheter connected to an implanted programmable s.c. insulin pump.
Diabetes 1992 Oct
PMID:Effects of insulin treatment on lipoprotein composition and function in patients with IDDM. 152 28

The chemical composition, subpopulation distribution and peak hydrated density of high-density lipoprotein (HDL) were examined in 18 morbidly obese women with either normal glucose tolerance or with non-insulin-dependent diabetes mellitus (NIDDM), and in 15 age-matched lean control subjects. Similar measurements were made in the morbidly obese subjects after gastric bypass surgery for weight loss. In the diabetic group, HDL was relatively protein-enriched and cholesterol- and cholesterol ester-poor compared with the lean controls. The same trend was seen in the nondiabetic group, although the cholesterol ester difference was not significant. In both cases, both electrophoretic and density gradient analysis showed that plasma HDL contained more of the HDL3 and less of the HDL2 subfractions than that for the lean controls. Following surgery in the diabetic group, the protein percentage of HDL decreased, and that of cholesterol ester increased; for the nondiabetic group, the protein decreased and phospholipid increased. In the diabetic group, a shift of the electrophoretic HDL subpopulation distribution toward more HDL2 accompanied these changes. Average hydrated peak density of HDL shifted from the HDL3 to the HDL2 range for the diabetic group following surgery; for the nondiabetic group the peak density also decreased but still remained within the HDL3 range. In all cases, the differences seen were more pronounced among the diabetic patients. These changes in the properties of HDL after gastric bypass surgery may favorably influence the risk for coronary heart disease usually associated with diabetes.
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PMID:Influence of morbid obesity and non-insulin-dependent diabetes mellitus on high-density lipoprotein composition and subpopulation distribution. 153 44

The predictors of premature coronary atherosclerosis were examined in 203 patients (99 men aged less than or equal to 50 years, and 104 women aged less than or equal to 60 years) undergoing elective diagnostic coronary arteriography. Age, cigarette smoking, hypertension, obesity, diabetes, positive family history of premature coronary artery disease (CAD), and plasma levels of total cholesterol, triglyceride, lipoproteins (i.e., very low, intermediate-, low-, and high-density [HDL] lipoproteins and their subfractions [HDL2 and HDL3], and lipoprotein [a]) and apolipoproteins (apoA-1, apoA-2 and apoB, respectively) were examined using univariate analyses and multivariate logistic regression. In men, age (p less than 0.05), smoking (p less than 0.05), and plasma triglyceride (p less than 0.02) and apoA-1 (p less than 0.05) levels were independently associated with CAD. In women, smoking (p less than 0.001) and plasma apoB levels (p less than 0.04) were the strongest variables independently associated with CAD. It is concluded that the "nontraditional" risk factors (plasma apoA-1 and apoB levels) are better predictors of premature CAD than are plasma lipoproteins and that smoking is the strongest of the traditional nonlipid risk factors.
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PMID:Comparison of the plasma levels of apolipoproteins B and A-1, and other risk factors in men and women with premature coronary artery disease. 156 71

We studied serum thromboxane (TXB2), the prostacyclin metabolite, 6-keto-PGF1 (6KPGF1) glucose, insulin, and lipid/lipoprotein profiles in 27 patients with non-insulin-dependent diabetes mellitus (NIDDM) who were switched from therapy with glibenclamide (GLB) (with [GLBH] or without phenformin) to gliclazide for 3 months. We found that therapy with gliclazide was followed by a decrease in serum TXB2 (281.8 +/- 128.3 to 149.1 +/- 77.0 mg/L, P less than .001) and an increase in serum 6KPGF1 (60.5 +/- 19.1 to 96.0 +/- 40.3 mg/L, P less than .001). This was accompanied by a decrease in total and low-density lipoprotein (LDL) cholesterol and an increase in high-density lipoprotein (HDL) cholesterol, within the HDL3 cholesterol fraction. These changes were seen despite the fact that neither fasting plasma glucose nor insulin changed with therapy. These findings suggest that gliclazide may have beneficial actions on cardiovascular risk factors in these NIDDM patients.
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PMID:Thromboxane/prostacyclin balance in type II diabetes: gliclazide effects. 157 13

This study was conducted to determine whether changes in the levels of plasma apolipoproteins (apo) A-I, A-II, B, C-II, and C-III, along with cholesterol and triglycerides, could provide additional information on these parameters in relation to the control of glycemia. Plasma and lipoprotein lipids and apolipoprotein levels were measured in 123 insulin-dependent diabetic children (4- to 12-years-old), classified into good, fair, and poor diabetic control based on HbA1c and fructosamine levels, and in 62 comparable healthy controls. Total cholesterol, very low density lipoprotein cholesterol, and low density lipoprotein cholesterol, as well as total triglycerides, very low density lipoprotein, low density lipoprotein, and high density lipoprotein (HDL) triglycerides, and apo B and apo C-III were increased significantly in children with fair and poor diabetic control. While in diabetic children with good control, only very low density lipoprotein cholesterol was elevated significantly compared with healthy control subjects. Conversely, the levels of cholesterol in HDL, HDL2, HDL3, and apo A-I were decreased significantly in the three diabetic groups, but apo A-II and apo C-II did not change. We conclude that in children with insulin-dependent diabetes mellitus, abnormalities in plasma lipid, lipoprotein, and apolipoprotein levels occur, the extent of which depends on the degree (extent) of glycemic control (the poorer the control the more substantial the abnormality). We suggest that measurement of apo C-III level along with apo B and apo A-I in these patients may be a sensitive indicator to alterations in glycemic control.
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PMID:Apolipoprotein A-I, A-II, B, C-II, and C-III in children with insulin-dependent diabetes mellitus. 157 7

The excess risk of atherosclerosis that is associated with diabetes mellitus cannot be completely accounted for by other known risk factors. Recent studies have suggested that increased glycation of high density lipoproteins (HDL) at high glucose concentrations causes functional abnormalities that might contribute to accelerated atherosclerosis. Other investigators also have shown that elevated glucose concentrations can stimulate the activity of protein kinase C in cultured cells. Because protein kinase C appears to be involved in HDL receptor-mediated efflux, the hypothesis that a high glucose concentration in vitro might modulate HDL-mediated efflux of cholesterol from human fibroblasts was tested. These studies indicate that a high glucose level alone does not affect the interaction of normal HDL3 with cultured human skin fibroblasts.
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PMID:High glucose levels do not directly impair cellular binding of HDL3 or HDL-mediated efflux of cholesterol from human skin fibroblasts. 166 7

This double-blind cross-over study was performed to investigate whether the lipoproteins in plasma were different on furosemide (Lasix Retard) and thiazide (hydrochlorthiazide) treatment in patients suffering from type II diabetes. Twenty-four patients were randomly allocated to either furosemide-hydrochlorthiazide (LR-HCT) or HCT-LR treatment. The treatment period was 12 months: 6 months on each sequence. After inclusion, the patients were seen every second month. Laboratory data were recorded at each visit. The only significant treatment effect was observed for high-density-lipoprotein3 cholesterol concentration (HDL3 cholesterol concentration), which was higher when patients were on furosemide therapy (p less than 0.05). We conclude from the present study that blood-glucose HbA1c, and the concentration of lipoproteins connected to development of atherosclerosis is unaffected whether type II diabetes patients are treated with HCT or furosemide.
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PMID:Lipoproteins and diuretics in type II diabetes. 183 Mar 13

Previous studies have shown that nonenzymatic glycosylation of high-density lipoprotein (HDL) inhibits high-affinity binding to cultured cells and the candidate HDL-receptor protein. Because binding of HDL to its receptor is required for HDL-receptor-mediated cholesterol efflux from cells, we hypothesized that glycosylated HDL3 would have reduced ability to remove cholesterol from cells. HDL3 was glycosylated in vitro to achieve up to 40-50% reductions in free-lysine residues. Glycosylated HDL3 had a slightly greater ability than control HDL3 to sequester cholesterol directly from the plasma membrane, as predicted by changes in lipid composition. This process is independent of HDL-receptor binding and should not be influenced by reduced binding of HDL3. In contrast, efflux of intracellular cholesterol from cells, which is HDL-receptor dependent, was reduced 25-40%. The ability of glycosylated HDL3 to diminish cholesterol esterification was significantly reduced, indicating reduced net cholesterol efflux. Steady-state efflux of LDL-derived cholesterol was also markedly reduced. These findings suggest that nonenzymatically glycosylated HDL is functionally abnormal and might contribute to the accelerated development of atherosclerosis in patients with diabetes mellitus.
Diabetes 1991 Mar
PMID:Nonenzymatic glycosylation of HDL and impaired HDL-receptor-mediated cholesterol efflux. 184 86


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