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

A diet high in carbohydrates with high glycemic indexes (GI) and glycemic load were linked to risk of coronary heart disease development in women in a large prospective study. Two cross-sectional studies showed that low-GI diets are associated with high HDL-cholesterol concentrations, especially in women. In a tightly controlled study of patients with type 2 diabetes, serum total cholesterol, LDL cholesterol, and apolipoprotein B concentrations fell more significantly after a low-GI diet than after a high-GI diet. In the same study, plasminogen activator inhibitor-1 concentrations were reduced by 58% after the low-GI diet. Insulin-stimulated glucose uptake by adipocytes was significantly higher in patients undergoing coronary artery bypass graft surgery after 4 wk of consuming a low-GI diet than after consuming a high-GI diet. The effects of low-GI diets may be mediated by changes in postprandial fatty acid concentrations or by hormonal signals from adipocytes, but a possible association of low-GI diets with some other dietary factor such as chromium must not be excluded. Proof of the clinical value of low-GI diets awaits prospective trials, which should include short-term observations covering periods of metabolic stress induced by surgery as well as long-term trials with clinical endpoints.
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PMID:Glycemic index and heart disease. 1208 53

To investigate the association of oxidized low-density lipoprotein (ox-LDL) with the development of diabetic nephropathy, plasma levels of ox-LDL were measured in 70 patients with type 2 diabetes mellitus. A sandwich enzyme-linked immunoadsorbent assay (ELISA) using the mouse monoclonal antibody FOH1a/DLH3, which specifically recognizes oxidized phosphatidylcholine, and a horseradish peroxidase (HRP)-labeled goat anti-human apolipoprotein B IgG was used to measure ox-LDL levels. The mean age of the patients was 57.0+/-1 3.4 years, and the mean duration of diabetes was 13.4+/-8.5 years. Plasma ox-LDL levels were similar in patients with normoalbuminuria (13.7+/-3.9 U/ml), patients with microalbuminuria (12.8+/-3.9 U/ml), and normal controls (12.5+/-4.2 U/ml). However, the plasma ox-LDL level in patients with macroalbuminuria (16.8+/-7.5 U/ml) was significantly higher than those in the other groups (P<0.05). Hemoglobin A1c (HbA1c) levels were similar in diabetic patients with normoalbuminuria (8.2+/-2.2%), microalbuminuria (7.8+/-1.3%), or macroalbuminuria (7.2+/-1.4%). There was no significant correlation between the ox-LDL level and the HbA1c level. The significantly elevated plasma ox-LDL levels in patients with macroalbuminuria suggest that ox-LDL may play an important role in the progression of diabetic nephropathy.
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PMID:Association between plasma oxidized low-density lipoprotein and diabetic nephropathy. 1221 52

This study evaluated the effects of rosiglitazone therapy on lipids and the efficacy and safety of rosiglitazone in combination with atorvastatin in patients with type 2 diabetes mellitus. Three-hundred thirty-two patients entered an 8-week, open-label, run-in treatment phase with rosiglitazone 8 mg/day, and 243 were randomized to a 16-week, double-blinded period of continued rosiglitazone plus placebo, atorvastatin 10 mg/day, or atorvastatin 20 mg/day. With rosiglitazone alone, a modest increase in low-density lipoprotein (LDL) cholesterol (9%), a shift in LDL phenotype from dense to large buoyant subfractions (52% of patients), and an increase in total high-density lipoprotein (HDL) cholesterol levels (6%), predominantly in HDL(2) levels (13%), occurred from week 0 to week 8. When atorvastatin was added, there was a further increase in HDL(3) (5%) and expected significant reductions (p <0.0001) in LDL cholesterol (-39%), apolipoprotein B (-35%), and triglyceride levels (-27%). Glycemic control achieved with rosiglitazone alone was not adversely affected by add-on atorvastatin. The combination was well tolerated compared with placebo. To conclude, in addition to the beneficial effects of rosiglitazone on glycemic control, rosiglitazone and atorvastatin in combination achieved 2 goals: the reduction of LDL cholesterol to <100 mg/dl and the removal of small dense LDL in patients with type 2 diabetes mellitus.
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PMID:Effects of rosiglitazone alone and in combination with atorvastatin on the metabolic abnormalities in type 2 diabetes mellitus. 1239 60

The objective of this study was to determine the effect of slow-release (XL) fluvastatin on low density lipoprotein (LDL) subfractions in type 2 diabetes. A multicenter, double-blind, randomized, parallel-group comparison of fluvastatin XL 80 mg (n = 42) and placebo (n = 47), each given once-daily for 8 wk, in 89 patients with type 2 diabetes (HbA1c: 7.2 +/- 1.0%, LDL cholesterol (LDL-C): 3.4 +/- 0.7 mmol/liter, high density lipoprotein cholesterol: 1.1 +/- 0.3 mmol/liter, and triglycerides (TG): 2.4 +/- 1.4 mmol/liter). At baseline and on treatment, plasma lipoproteins were isolated and quantified. Eight weeks of fluvastatin treatment decreased total cholesterol (-23.0%, P < 0.001), LDL-C (-29%, P < 0.001) and TG (-18%, P < 0.001), compared with placebo. At baseline, there was a preponderance of dense LDL (dLDL) (apolipoprotein B in LDL-5 plus LDL-6 > 25 mg/dl) in 79% of patients, among whom fluvastatin decreased all LDL subfractions, reductions in dLDL being greatest (-28%, P = 0.001; cholesterol in dLDL -29%). In patients with low baseline dLDL (apolipoprotein B in LDL-5 plus LDL-6 </= 25 mg/dl), but a preponderance of buoyant LDL (LDL-1 through LDL-3), fluvastatin significantly decreased only these subfractions. Fluvastatin 80 mg XL, once daily, decreased total cholesterol and total LDL-C. In patients with atherogenic dLDL, absolute changes of dLDL were most pronounced, emphasizing the value of fluvastatin treatment in type 2 diabetes. The antiatherogenic potential of fluvastatin in type 2 diabetes may thus be greater than that expected from its effects on LDL-C and TG alone.
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PMID:Effect of fluvastatin slow-release on low density lipoprotein (LDL) subfractions in patients with type 2 diabetes mellitus: baseline LDL profile determines specific mode of action. 1246 41

Hypertension is often associated with insulin resistance, dyslipidemia and obesity, which indicate a prediabetic state and increased risk of cardiovascular disease. Pioglitazone treatment of patients with type 2 diabetes reduces insulin resistance and improves lipid profiles. The present double-blind placebo-controlled study is the first study to report effects of pioglitazone in non-diabetic patients with arterial hypertension. Following a one week run-in, 60 patients were randomized to receive either pioglitazone (45 mg/day) or placebo for 16 weeks. Insulin sensitivity (M-value) increased by 1.2 +/- 1.7 mg/min/kg with pioglitazone compared with 0.4 +/- 1.4 mg/min/kg (P = 0.022) with placebo. HOMA index was decreased (-22.5 +/- 45.8) by pioglitazone but not by placebo (+0.8 +/- 26.5; P < 0.001). Decreases in fasting insulin and glucose were significantly (P = 0.002 and P = 0.004, respectively) greater with pioglitazone than placebo. Body weight did not change significantly with either treatment. HDL-cholesterol was increased and apolipoprotein B was decreased to a significantly greater extent with pioglitazone. There was a significantly (P = 0.016) greater decrease from baseline in diastolic blood pressure with pioglitazone. These changes would suggest improved glucose metabolism and a possible reduction in risk of cardiovascular disease with pioglitazone treatment of non-diabetic patients with arterial hypertension.
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PMID:Effects of pioglitazone in nondiabetic patients with arterial hypertension: a double-blind, placebo-controlled study. 1246 45

LDL phenotype B is a component of diabetic dyslipidaemia, but its diagnosis is cumbersome. Our aim was to find easily available markers of phenotype B in a group of type 2 diabetic subjects. We studied 123 type 2 diabetic patients (67.5% male, aged 59.3+/-10.1 years, mean HbA1c 7.4%). Clinical features and fasting total cholesterol, triglyceride, HDL cholesterol, LDL cholesterol (LDLc, using Friedewald's equation and an alternative formula), apolipoprotein B (apoB), lipoprotein (a) and LDL particle size (on gradient polyacrylamide gel electrophoresis) were assessed. Patients with phenotypes A (predominant LDL size > or =25.5 nm) and B (<25.5 nm) were compared, and regression analysis was performed to find the best markers of LDL particle. Cut-off points were obtained and evaluated as predictors of phenotype B (kappa index). Patients with phenotype B (36%) showed higher total cholesterol, triglyceride and apolipoprotein B, and lower HDL cholesterol and LDLc/apoB ratio. Triglyceride was the best predictor of LDL particle size (r=-0.632, p<0.01), but an LDLc/apoB ratio below 1.297 mmol/g detected phenotype B best (sensitivity 65.9%, specificity 92.4%, kappa=0.611). Although triglyceride concentration is the best predictor of LDL size in type 2 diabetes, LDLcholesterol/apolipoproteinB ratio is the best tool to detect phenotype B.
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PMID:LDL-cholesterol/apolipoprotein B ratio is a good predictor of LDL phenotype B in type 2 diabetes. 1248 96

Spirulina, with its high concentration of functional nutrients, is emerging as an important therapeutic food. This study aimed to evaluate the hypoglycemic and hypolipidemic role of Spirulina. Twenty-five subjects with type 2 diabetes mellitus were randomly assigned to receive Spirulina (study group) or to form the control group. At baseline, the control and study groups were matched for various variables. The efficacy of Spirulina supplementation (2 g/day for 2 months) was determined using the preintervention and postintervention blood glucose levels, glycosylated hemoglobin (HbA(1c)) levels, and lipid profiles of the diabetic subjects. Two-month supplementation with Spirulina resulted in an appreciable lowering of fasting blood glucose and postprandial blood glucose levels. A significant reduction in the HbA(1c) level was also observed, indicating improved long-term glucose regulation. With regard to lipids, triglyceride levels were significantly lowered. Total cholesterol (TC) and its fraction, low-density lipoprotein cholesterol (LDL-C), exhibited a fall coupled with a marginal increase in the level of high-density lipoprotein cholesterol (HDL-C). As a result, a significant reduction in the atherogenic indices, TC:HDL-C and LDL-C: HDL-C, was observed. The level of apolipoprotein B registered a significant fall together with a significant increment in the level of apolipoprotein A1. Therefore, a significant and favorable increase in the ratio of A1:B was also noted. These findings suggest the beneficial effect of Spirulina supplementation in controlling blood glucose levels and in improving the lipid profile of subjects with type 2 diabetes mellitus.
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PMID:Role of Spirulina in the Control of Glycemia and Lipidemia in Type 2 Diabetes Mellitus. 1263 1

Elevated concentrations of circulating apolipoprotein B (apoB)-containing lipoproteins, other than low-density lipoprotein (LDL), have been implicated as causative agents for the development of atherosclerosis. A form of dyslipidemia, the atherogenic lipoprotein profile, that consists of elevated intermediate-density lipoprotein (IDL), triglycerides (TGs), dense LDL and dense very low density lipoprotein (VLDL), and low high density lipoprotein-2, occurs in 40% to 50% of patients with coronary artery disease (CAD). The recently released Adult Treatment Panel III guidelines suggest that because elevated TGs are an independent CAD risk factor, some TG-rich lipoproteins, commonly called remnant lipoproteins, must be atherogenic. Relevant to this series on diabetes, a number of studies have shown that in type 2 diabetes, the severity of CAD is positively related to the numbers of TG-rich particles in the plasma. Although less clear, other studies in type 2 diabetes suggest that elevated levels of lipoprotein (a) [Lp(a)] may also be independently associated with CAD. In this article, we summarize evidence for the role of apoB-containing lipoprotein particles other than LDL in the development of atherosclerosis and discuss methods of quantification and possible pharmacologic interventions for lowering their plasma concentrations. The particles reviewed include the TG-rich lipoproteins: VLDL and its remnants, chylomicron remnants and IDL, and the C-rich lipoprotein: Lp(a).
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PMID:The role of non-LDL:non-HDL particles in atherosclerosis. 1264 86

Microsomal triglyceride transfer protein (MTP) is rate limiting for the assembly and secretion of apolipoprotein B-containing lipoproteins. Elevated hepatic MTP mRNA level, presumably as a result of impaired insulin signaling, has been implicated in the pathophysiology of dyslipidemia associated with insulin resistance/type 2 diabetes. In this study, we showed that insulin decreases MTP mRNA level mainly through transcriptional regulation in HepG2 cells. We further characterized the corresponding signal transduction pathway, using chemical inhibitors and constitutively active and dominant negative forms of regulatory enzymes. We demonstrated that insulin inhibits MTP gene transcription through MAPK(erk) cascade but not through the PI 3-kinase pathway. Activation of ras through farnesylation is not a prerequisite for the inhibition. In addition, cellular MAPK(erk) and MAPK(p38) activities play a counterbalancing role in regulating the MTP gene transcription. These complex regulations may represent a means to fine-tuning MTP gene transcription in response to a diverse set of environmental stimuli and may have important implications for the onset and development of diabetes-associated dyslipidemia.
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PMID:Regulation of microsomal triglyceride transfer protein gene by insulin in HepG2 cells: roles of MAPKerk and MAPKp38. 1271 35

The effect of statin therapy on subclasses of LDL, VLDL and HDL lipoproteins is unclear. We compared changes in serum lipids, apolipoproteins and nuclear magnetic resonance (NMR) spectroscopy measured lipoprotein subclass concentration and average particle size over a minimum 6 months treatment period of atorvastatin 10 mg vs. placebo in 122 men and women. All subjects had type 2 diabetes and a modest dyslipidaemia (mean LDL-cholesterol 3.2 mmol/l and median triglycerides 1.8 mmol/l) and had a previous myocardial infarction. Compared with placebo, atorvastatin therapy was associated with a greater decrease in medium VLDL (median within person change -13.4 vs. -5.9 nmol/l, P<0.001 adjusted for baseline level), small VLDL (median change -17.8 vs. -8.1 nmol/l, P=0.002), large LDL (mean within person change -167.9 vs. -48.6 nmol/l, P<0.001) and medium LDL (median within person change -101.8 vs. -22.3 nmol/l, P=0.017). Atorvastatin therapy was also associated with a greater increase in large HDL than placebo (median change 1.40 vs. 0.80 micromol/l, P=0.02) and there was little change in small HDL so that average HDL particle size increased significantly with atorvastatin (P=0.04). In addition to reducing levels of (enzymatically measured) triglyceride, LDL-cholesterol and apolipoprotein B in diabetic patients, atorvastatin significantly reduces NMR measured medium and small VLDL and large and medium LDL, and increases large HDL.
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PMID:The effect of atorvastatin on serum lipids, lipoproteins and NMR spectroscopy defined lipoprotein subclasses in type 2 diabetic patients with ischaemic heart disease. 1281 7


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