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 the present study the effects of a short term intensive glycaemic control obtained with subcutaneous insulin therapy on lipids and apoprotein levels, platelet aggregation, platelet sensitivity to prostacyclin and platelet thromboxane production were investigated in 20 patients with type 2 diabetes and vascular disease. In 11 out of the 20 patients there was a significant improvement of glycaemic control (fructosamine reduction). Only with tight improvement of glycaemic control there was significant change in the concentration of ADP and collagen required to produce 50% of the maximum aggregation wave response, in the responsiveness of platelet to PGI2 and in the TxB2 synthesis. Lower Apo B levels were also shown in the tight control group suggesting that Apo B changes may have influenced platelet aggregation and thromboxane synthesis.
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PMID:Platelet function in patients with type 2 diabetes mellitus: the effect of glycaemic control. 266 42

The purpose of the present study is to elucidate the characteristics of lipoprotein disorders in diabetes mellitus. By analytical ultracentrifugation, non-insulin-dependent diabetic patients (NIDDM) with type IIa hyperlipoproteinemia (HLP) showed significantly higher incidence of multidisperse low density lipoprotein (LDL) than non-diabetics with type IIa HLP. Furthermore, LDL multidispersity in diabetic subjects seemed to be directly related to neither triglyceride (TG) levels in very low density lipoprotein (VLDL) nor the degree of glycemic control. Diabetics with multidisperse LDL had a lipoprotein profile that was different from the subjects with paucidisperse LDL as follows: (1) enrichment in the cholesterol content of VLDL, (2) TG-rich LDL with small flotation coefficient, (3) low cholesterol levels in high density lipoprotein2 along with enrichment in TG, and (4) high plasma concentrations of apoprotein B. Although the underlying mechanism behind the prevalence of multidisperse LDL in NIDDM with type IIa HLP remains unknown, it seems important that lipoprotein disorders in diabetics with multidisperse LDL were potentially atherogenic.
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PMID:Appearance of multidisperse low density lipoprotein and altered lipoprotein composition in non-insulin-dependent diabetes with type IIa hyperlipoproteinemia. 291 42

While guar gum has been shown to lower total cholesterol and low density lipoprotein cholesterol (LDL-C) in diabetic patients over the short-term, the long-term effects are less well studied and may be unpredictable. Granola bars with and without 6.6 g guar gum were developed and fed to 16 adult volunteers with Type II diabetes mellitus who had been randomized in a double-blind fashion into guar and placebo groups of equal size. Four to six bars were consumed daily with an ad lib diet over a 6-month period. Total cholesterol, total high density lipoprotein cholesterol (HDL-C), subfractions HDL2-C and HDL3-C, LDL-C, and beta-apoprotein were measured at 0 and 6 months. Although LDL-C was lower and triglycerides higher at 6 months than at baseline, these changes were of equal magnitude and direction in both guar and placebo groups. Using each subject as his own control, only the change in triglycerides was statistically significant (P less than 0.025). When male subjects alone were analyzed, the guar group showed a statistically significant decrease in LDL, while the placebo group did not. Other lipid parameters were not significantly changed during the study, despite a positive effect on carbohydrate metabolism from the guar bars. The data suggest either that the hypolipemic effects of guar gum in patients with Type II diabetes mellitus are not sustained for 6 months, or the effects occur only in men.
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PMID:Long-term effects of guar gum on blood lipids. 301 Oct 23

Plasma lipoproteins and apoproteins were compared among Chinese and American controls and non-insulin-dependent diabetic (NIDDM) subjects in the same laboratory. Apoprotein AI concentrations in Chinese subjects, both NIDDM subjects and controls (men, 147 and 158 mg/dl, respectively), were significantly higher than those in American subjects (men, 104 and 124 mg/dl, respectively). Apoprotein AII concentrations, however, were comparable between Chinese and American subjects. Chinese NIDDM subjects had lower high-density lipoprotein cholesterol (HDLC), higher low-density lipoprotein cholesterol (LDLC), and higher apoprotein B levels than Chinese controls. Chinese subjects with NIDDM had HDLC and LDLC levels similar to those of American controls but trends of higher HDLC and lower LDLC compared with American subjects with NIDDM. These differences may in part explain the relatively higher incidence of atherosclerotic vascular disease in Americans.
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PMID:Comparison of plasma lipoproteins and apoproteins in Chinese and American non-insulin-dependent diabetic subjects and controls. 374 15

Serum concentration of apoprotein A, high density lipoprotein (HDL)-cholesterol and HDL-phospholipids has been studied in thirteen consecutive episodes of diabetic ketoacidosis. In three patients with type I diabetes mellitus HDL2 and HDL3 subfractions were also measured. Patients with type I diabetes showed greatly decreased HDL-cholesterol concentration on admission which increased into the normal range after insulin treatment, while HDL-phospholipids decreased during treatment and apoprotein A remained almost unmodified. In three patients with type I diabetes a virtual absence of HDL2-cholesterol subfraction was observed, which rose to normal values during recovery. Conversely, in type II diabetes mellitus HDL-cholesterol was slightly reduced on admission, and tended to decrease during recovery. These findings imply the existence of abnormalities in the qualitative composition of HDL, and indicate that HDL-cholesterol can fluctuate much more rapidly than previously thought.
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PMID:High density lipoprotein changes during treatment of diabetic ketoacidosis. 392 72

Epidemiological studies have elucidated that diabetes mellitus (DM) is one of the risk factors of coronary heart disease and that DM often accompanies dyslipidemia. Dyslipidemia in DM can be classified as either quantitative or qualitative. Although dyslipdemia in DM is affected by the type of DM and glycemic conditions, the characteristics of dyslipidemia in DM, especially in NIDDM are the increase in triglycerides accompanied by the decrease in HDL-cholesterol level. Recently, new commercial kits for measurement of atherogenic lipoproteins which increase in DM are clinically available. The usefulness of these kits in DM was reviewed. Polyacrylamide electrophoresis can detect IDL and Lp(a) qualitatively. It has also become possible to estimate Lp(a) quantitatively by ELISA, TIA and LIA methods. Remnant lipoprotein can be measured in the fraction unbound to anti-apo A1 and anti-apo B100 antibodies by immunoaffinity gel analysis. Apoproteins, apoprotein E phenotype, post-heparin lipoprotein lipase, and Lp AI (HDL with apo AI and without apo AII) can be measured by the commercially available kits. Modified LDLs (glycated, oxidative) increase in DM, but their measurements remain complicated at the moment. Analysis of plasma fatty acids by gaschromatography is useful for dietary assessment. The measurement of these new markers seems to be useful to assess the extent of atherogenic risk in DM.
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PMID:[Plasma fatty acids, lipids, lipoprotein and macroangiopathy]. 778 61

The relationship between diabetic macroangiopathy or microangiopathy and apolipoprotein B (apoB) polymorphism was studied in 139 male and 129 female patients with non-insulin-dependent diabetes (NIDDM) mellitus, comprising consecutive patients with poor diabetic control (HBA1 13.2% +/- 2.7 (SD)) referred to our hospital. Plasma cholesterol and triglyceride concentrations were higher in the patients who were homozygous for the X2 allele (presence of XbaI cleavage site). Patients with the X1 allele (absence of XbaI cleavage site) tended to have a higher frequency of macroangiopathy, although the differences were not statistically significant. There was no difference in the prevalence of microangiopathy between the groups. In subjects with only an R1 allele (= R+; homozygous for the presence of EcoRI cleavage site) the prevalence of coronary heart disease (CHD) was observed to be high (61.9%) as compared to the subjects possessing an R2 allele (= R-; homozygous or heterozygous for the absence of the EcoRI cleavage site) (46.7%; p < 0.02). When the polymorphisms XbaI (subjects homozygous for the absence of the cutting site = X+; subjects homozygous or heterozygous for the presence of the cutting site = X-) and EcoRI were combined, the prevalence of macroangiopathy was observed to be high in X+R+ (80.0%) as compared with X+R- (44.2%), X-R+ (56.8%) and X-R- (50.0%) (p < 0.03). The prevalence of macroangiopathy tended to be particularly high in patients with the apoprotein E4 allele (phenotype E4/4 or E4/3), combined with either X+ or R+.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Apolipoprotein B gene DNA polymorphisms are associated with macro- and microangiopathy in non-insulin-dependent diabetes mellitus. 826 46

The effect of dietary fructose (20% of carbohydrate calories, 45-65 g day-1 for 4 weeks) on glycaemic control, serum lipid, lipoprotein and apoprotein A-I and A-II concentrations and on insulin sensitivity was studied in 10 type 2 diabetic patients. The study was done in a randomized, double-blind fashion with crystalline fructose or placebo administered evenly during 4 meals or snacks per day. The patients were hospitalized throughout the study periods. The fasting plasma glucose concentration decreased during the fructose (from 10.7 +/- 1.4 mmol l-1 to 8.0 +/- 0.8 mmol l-1, P < 0.02) and the control diet (from 10.1 +/- 0.9 mmol l-1 to 8.0 +/- 0.7 mmol l-1, P < 0.05). The mean diurnal blood glucose concentration also fell both during the fructose (from 10.8 +/- 0.5 mmol l-1 to 8.4 +/- 0.3 mmol l-1, P < 0.001) and the control diet (from 10.3 +/- 0.3 mmol l-1 to 8.8 +/- 0.9 mmol l-1, P < 0.01). The HbA1 concentration improved (P < 0.02) only during the fructose diet. Insulin sensitivity increased by 34% (P < 0.05) during the fructose diet, but remained unchanged during the control period. Serum insulin, triglyceride, apoprotein A-I and A-II concentrations, body weight, blood pressure and blood lactate remained unchanged during both diets. In conclusion, substitution of moderate amounts of fructose for complex carbohydrates can improve glycaemic control and insulin sensitivity in patients with type 2 diabetes.
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PMID:Fructose and insulin sensitivity in patients with type 2 diabetes. 843 75

Six patients with type 2 diabetes underwent detailed metabolic studies before and after a minimum of 3 months' glibenclamide therapy. Treatment was associated with a small but significant increase in body weight. Despite improvements in almost all the measured parameters of glucose homeostasis (plasma glucose, glycosylated haemoglobin (HbA1), hepatic glucose production and insulin-mediated glucose disposal) neither fasting serum triglycerides nor HDL cholesterol changed and apoprotein A1 concentrations actually decreased significantly. NEFA and glycerol in fasting plasma and during the clamp studies did not change significantly with treatment. Post-heparin lipoprotein lipase and hepatic lipase activity did not change significantly. Thus, despite substantial improvements in glycaemic control and insulin sensitivity with sulphonylurea therapy, several aspects of lipid and lipoprotein metabolism remain largely unaffected. This small study suggests either that lipoprotein concentrations in type 2 diabetes are not influenced by insulin sensitivity or that the improvement is offset by another change that occurs during this form of therapy. It also suggests that other forms of therapy will be required to improve these cardiovascular risk factors in type 2 diabetes.
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PMID:The effects of glibenclamide on glucose homeostasis and lipoprotein metabolism in poorly controlled type 2 diabetes. 845 16

Elevated levels of plasma triglycerides (TG) and reduced concentrations of HDL cholesterol are very common in patients with diabetes, particularly NIDDM. Although regulation of the plasma concentrations of VLDL, the major TG-rich lipoprotein is extremely complex, it is clear from in vivo kinetic studies that increased rates of secretion of VLDL into plasma is almost uniformly present in patients with NIDDM and hypertriglyceridemia. Recent studies at the cellular level indicate that increased fatty acid flux to the liver, also common in NIDDM (and other insulin-resistant states associated with elevated plasma TG levels), will stimulate the assembly and secretion of apoprotein (apo) B-containing lipoproteins by targeting apoB for secretion rather than intracellular degradation. Increased rates of secretion of VLDL into plasma appears to drive the exchange of TG from these lipoproteins for HDL cholesteryl ester. This exchange, which occurs in plasma, is facilitated by cholesteryl ester transfer protein, and generates a TG-enriched HDL that is a substrate for either hepatic lipase or lipoprotein lipase. When the TG in HDL is hydrolyzed, the resultant particle is smaller, and this appears to affect the binding of the major HDL protein, apoA-I. ApoA-I dissociates from the smaller, lipid-poor HDL, and the free apoA-I (molecular weight 28,000) can be filtered by the glomerulus in the kidney and most likely is degraded in renal tubular cells after reabsorption. Thus, increased free fatty acid transport in plasma, a common abnormality in insulin-resistant states, may be the underlying driving force for the two common lipid abnormalities seen in diabetes.
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PMID:Diabetic dyslipidemia: basic mechanisms underlying the common hypertriglyceridemia and low HDL cholesterol levels. 867 85


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