Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Utilization of percutaneous transluminal coronary angioplasty (PTCA) has dramatically expanded even in the management of elderly patients with coronary artery disease. However, restenosis after successful PTCA remains the major problem limiting the long-term efficacy of the procedure. Reported restenosis rates vary from 25 to 43%. In order to determine the relationship of restenosis to coronary risk factors in the elderly, we analyzed the data in 87 patients who had undergone PTCA and angiography before and 3 to 6 months after PTCA. Of these, 29 patients were 65 years of age or older (elderly group) and 58 were less than 65 years of age (younger group). Restenosis, defined as a luminal narrowing of greater than 50% at follow-up time, was found in 20 of the elderly group (69.0%), and in 26 (44.8%) of younger group (p < 0.0001). Total cholesterol, LDL cholesterol, apolipoprotein B (apo B), and the ratio of apoB/apoA1 in the elderly group were significantly lower than those in the younger group. HDL cholesterol levels were lower than 40 mg/dl in both groups (not significant). Each group was subdivided into two types; restenosis type and non-restenosis type. There were no significant differences in serum lipid, apolipoprotein, and lipoprotein(a) levels between the 2 subtypes in each group. The degree of coronary atherosclerosis calculated by Gensini's method, the number of damaged coronary vessels, diabetes mellitus, hypertension, and smoking did not appear to affect the rate of restenosis in either group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Restenosis after percutaneous transluminal coronary angioplasty in the elderly--risk factor analysis]. 750 May 52

Levels of lipoprotein(a) [Lp(a)], apolipoprotein (apo) B, and lipoprotein cholesterol distribution using density-gradient ultracentrifugation were measured as part of a cross-sectional study at the final follow-up examination (mean 6.2 years) in the Diabetes Control and Complications Trial. Compared with the subjects in the conventionally treated group (n = 680), those subjects receiving intensive diabetes therapy (n = 667) had a lower level of Lp(a) (Caucasian subjects only, median 10.7 vs 12.5 mg/dl, respectively; P = 0.03), lower apo B (mean 83 vs. 86 mg/dl, respectively; P = 0.01), and a more favorable distribution of cholesterol in the lipoprotein fractions as measured by density-gradient ultracentrifugation with less cholesterol in the very-low-density lipoprotein and the dense low-density lipoprotein fractions and greater cholesterol content of the more buoyant low-density lipoprotein. Compared with a nondiabetic Caucasian control group (n = 2,158), Lp(a) levels were not different in the intensive treatment group (median 9.6 vs. 10.7 mg/dl, respectively; NS) and higher in the conventional treatment group (9.6 vs. 12.5 mg/dl, respectively; P < 0.01). No effect of renal dysfunction as measured by increasing albuminuria or reduced creatinine clearance on Lp(a) levels could be demonstrated in the diabetic subjects. Prospective follow-up of these subjects will determine whether these favorable lipoprotein differences in the intensive treatment group persist and whether they influence the onset of atherosclerosis in insulin-dependent diabetes.
Diabetes 1995 Oct
PMID:Levels of lipoprotein(a), apolipoprotein B, and lipoprotein cholesterol distribution in IDDM. Results from follow-up in the Diabetes Control and Complications Trial. 755 61

Human serum paraoxonase is physically associated with HDL and has been implicated in the detoxification of organophosphates and possibly in the prevention of LDL lipid peroxidation. We investigated the serum activity and concentration of paraoxonase in 78 patients with type 1 diabetes mellitus, 92 with type 2 diabetes, and 82 nondiabetic control subjects. Paraoxonase activity was generally lower in diabetics than in control subjects. This decrease was unrelated to differences in paraoxonase phenotype distribution or its serum concentration. Rather, the difference in paraoxonase activity was explained by its specific activity, which was lower in diabetics, indicating either the presence of a circulating inhibitor or disturbance of the interaction of paraoxonase with HDL affecting its activity. Paraoxonase specific activity was lowest in patients with peripheral neuropathy, suggesting an association of paraoxonase with neuropathy. In control subjects but not patients with diabetes, paraoxonase correlated with HDL cholesterol and apolipoprotein A-1. Our results indicate that the low paraoxonase activity in diabetes is due to decreased specific activity. In other studies low serum paraoxonase activity has been associated with increased susceptibility to atherosclerosis, and the present results also suggest an association with peripheral neuropathy, which could be due to reduced capacity to detoxify lipid peroxides in diabetes.
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PMID:Serum paraoxonase activity, concentration, and phenotype distribution in diabetes mellitus and its relationship to serum lipids and lipoproteins. 758 60

As part of an ongoing search for diabetes susceptibility loci, we tested linkage with non-insulin-dependent diabetes mellitus (NIDDM) for 19 candidate loci or regions chosen for their potential to affect directly or indirectly the action of insulin. Loci were associated with insulin resistance, known effects on lipid metabolism, or effects on glucose metabolism or insulin action. Loci included the insulin-responsive (GLUT4) glucose transporter, hexokinase 2, glucagon, growth hormone, insulin receptor substrate 1 (IRS1), phosphoenolpyruvate carboxykinase, hepatic and muscle forms of pyruvate kinase, hepatic phosphofructokinase, the apolipoprotein B and the apolipoprotein A2 cluster, lipoprotein lipase, hepatic triglyceride lipase, the very-low-density-lipoprotein receptor, and the Pima insulin resistance locus on chromosome 4. For several candidates, no specific informative marker was available; consequently, we tested the surrounding region with highly informative markers. These regions included the diabetes-associated ras-like gene, rad, and the cholesterol ester-transfer gene, both mapped to chromosome 16. Additionally, we tested for linkage with markers at the tumor necrosis factor-alpha gene and the Friedreich's ataxia region. All regions were tested for linkage with microsatellite polymorphisms in > 450 individuals from a minimum of 16 Caucasian families under parametric (LINKAGE 5.1) and nonparametric (affected pedigree member) models.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1995 Nov
PMID:Linkage analysis of 19 candidate regions for insulin resistance in familial NIDDM. 758 21

To assess the alteration of apolipoprotein (apo) B mRNA editing in non-insulin-dependent diabetes mellitus (NIDDM), we measured plasma apoB-100 and apoB-48 levels and apoB mRNA editing efficiency in the liver and intestine from GK (Goto-Kakizaki) rats, a genetically NIDDM animal. Male GK rats and control littermates, aged 25 weeks, were used in this study. Ventromedial hypothalamus (VMH)-lesioned control rats were used as hyperinsulinemic models. VMH-lesioned GK rats (GK+VMH) were treated as an insulin-exhausted NIDDM model. Plasma cholesterol and triglyceride levels were increased in GK rats. Very low density lipoprotein (VLDL)-triglyceride and low density lipoprotein (LDL)-cholesterol concentrations were significantly higher in GK rats than in controls. The increase of VLDL-triglyceride was most marked in GK+VMH rats. Plasma apoB-48 levels, quantified by immunoblot, were increased in GK rats. However, apoB-100 levels were minimally elevated in GK rats. Therefore, the apoB-48/apoB-100 ratio was remarkably increased in GK rats. ApoB mRNA editing was analyzed by reverse transcriptase-polymerase chain reaction coupled with dideoxynucleotide chain termination assay. The ratio of apoB-48-type cDNA to apoB-100-type cDNA was significantly increased in the liver from GK rats compared with controls. Although the development of the VMH lesion increased plasma apoB-48 levels, it had no effect on the proportion of apoB-48-type to apoB-100-type cDNA in the liver from both GK and control littermates. ApoB mRNA in the intestine was almost totally edited (approximately 95%). Intestinal apoB-48/apoB-100 cDNA ratio showed no significant difference among the four groups. In conclusion, an enhanced apoB mRNA editing was indicated in the non-insulin-dependent diabetic rats, which might contribute to the increase of plasma apoB-48 levels.
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PMID:Increased proportion of plasma apoB-48 to apoB-100 in non-insulin-dependent diabetic rats: contribution of enhanced apoB mRNA editing in the liver. 759 89

The effects of fluvastatin treatment on lipid profile and apolipoproteins were assessed in a group of 31 Chinese patients with hypercholesterolemia, maintained on a constant low-fat diet. Some patients had the additional cardiovascular risk factors of hypertension and non-insulin-dependent diabetes mellitus, and 6 patients had familial hypercholesterolemia. Baseline lipid levels were measured after a 4-week placebo period, and these were repeated after 4 weeks of treatment with fluvastatin 20 mg daily, and after 4 weeks of treatment with fluvastatin 40 mg daily. Total cholesterol, low density lipoprotein cholesterol, and apolipoprotein (apo) B were each reduced to the same extent with the 2 doses of fluvastatin (-20%, -26%, and -20%, respectively). Triglycerides and very low density lipoprotein cholesterol were also reduced by about 12% with the 2 doses of fluvastatin. Apo A-I was increased by 7% and high density lipoprotein cholesterol (HDL-C) was increased by 10% with the 40 mg dose. The increase in HDL-C was due to increases in both HDL2-C (18%) and HDL3-C (7%). Lipoprotein(a) levels did not show any significant change with the 2 doses of fluvastatin in this short-term study. One patient developed reversible asymptomatic elevation of liver enzymes with the higher dose of fluvastatin; otherwise the drug was well tolerated and no patients had to be withdrawn from the study.
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PMID:Effects of fluvastatin on lipid profile and apolipoproteins in Chinese patients with hypercholesterolemia. 760 89

Lp(a) has atherogenic and thrombotic properties and is considered to be a major risk factor for the development of atherosclerotic disease. The risk of cardiovascular disease is increased in both insulin-dependent (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM), and Lp(a) has attracted attention as a potential risk factor in diabetic patients. Lp(a) levels are "probably" elevated in IDDM patients and related to altered metabolic control and increased urinary albumin excretion rate or renal insufficiency, although results are controversial. There appears to be a real difference between the Lp(a) of patients with proliferative diabetic retinopathy and those with or without background retinopathy. The plasma Lp(a) level may therefore be associated with microangiopathy in some IDDM patients. However, data relating Lp(a) to complications of diabetes are limited, and the literature is conflicting. The few available data suggest that Lp(a) is not elevated in NIDDM patients and that there is no strong link between blood glucose control and plasma Lp(a). There is no clear evidence as to whether Lp(a) is related to microalbuminuria in NIDDM patients. There is little evidence for a correlation between increased risk of cardiovascular disease and plasma Lp(a) among diabetic patients. However, some diabetic patients with coronary heart disease have elevated plasma Lp(a), which seems to be correlated with genetic factors (especially the isoforms of apolipoprotein a) rather than to diabetes per se. Lp(a) synthesis and catabolism could be influenced by insulin or by diabetes and its metabolic concomitants. The atherogenic and thrombogenic potential of Lp(a) could also be increased in diabetic patients. Plasma Lp(a) should be measured for both IDDM and NIDDM patients. If the Lp(a) level is elevated, it seems reasonable to check the other major vascular risk factors.
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PMID:[Lipoprotein (a) and diabetes mellitus]. 762 73

Three groups of age- and weight-matched men (aged 40 to 70 years) without diabetes were studied: controls (n = 10), plasma triglycerides (TG) less than 180 mg/dL and no cardiovascular disease (CVD); HTG-CVD (n = 11), hypertriglyceridemic (HTG) (TG > 240 mg/dL) without CVD; and HTG+CVD (n = 10), HTG (TG > 240 mg/dL) with documented CVD. HTG+CVD subjects had higher fasting and post-oral glucose tolerance test insulin levels than the other two groups, respectively. Very-low-density lipoprotein (VLDL)+chylomicrons (CMs), intermediate-density lipoprotein (IDL), low-density lipoprotein (LDL), and three high-density lipoprotein (HDL) subfractions (HDL-L, HDL-M, and HDL-D, from least to most dense) were isolated by gradient ultracentrifugation. Fasting lipoproteins were similar in HTG groups, except for higher VLDL lipid to apolipoprotein (apo) B ratios (P < .04) in the HTG+CVD group. Subjects were fed a high-fat mixed meal, and lipoprotein composition was determined at 3, 6, 9, and 12 hours postprandially. Postprandial responses of the core lipids (TG and cholesterol esters [CE]) in all of the lipoprotein subfractions were similar in the two HTG groups at each time point. However, both controls and HTG-CVD subjects had increases in HDL-M phospholipid (PL) at 9 and 12 hours with no change in HDL-D PL. The HTG+CVD group, on the other hand, had no increase in HDL-M PL and had a substantial reduction in HDL-D PL. These changes resulted in significant increases in HDL-M and HDL-D PL to apo A-I ratios in both controls and HTG-CVD subjects between 6 and 12 hours, whereas there was no increase seen in the HTG+CVD group. The HTG-CVD group also had a significantly greater increase in the VLDL+CM PL to apo B ratio (P = .038) at 3 hours than the HTG+CVD group. This diminished amount of surface lipid per VLDL particle may account for the late decrease in the HDL-D PL to apo A-I ratio seen in HTG+CVD patients. There were no other postprandial lipid or apolipoprotein differences between the two HTG groups. We conclude therefore that the major postprandial lipoprotein abnormality in these HTG+CVD patients was a failure to increase the PL content per particle in VLDL+CM, HDL-M, and HDL-D. This abnormality could prevent the usual increase in reverse cholesterol transport seen in postprandial plasma and therefore contribute to their increased incidence of CVD. The greater insulin resistance seen in these patients also appears to contribute significantly to their CVD.
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PMID:Postprandial lipoprotein responses in hypertriglyceridemic subjects with and without cardiovascular disease. 763 51

The type and degree of changes in the lipid transporting system of blood plasma and levels of hormonal provision of the regulatory processes in juvenile obesity of different degrees were under study. A single fat food loading was used to detect the precursors or latent forms of disorders in lipoprotein spectrum and their hormone regulators. A total of 35 obese patients aged 16 to 18 and 30 age-matched healthy youths were examined. Analysis of the baseline values showed increased levels of apolipoprotein B, cholesterol, triglycerides, insulin, and reduced levels of apolipoprotein A1, high-density lipoprotein cholesterol in obese youths vs. controls. A atherogenic pattern of changes in the lipoprotein and apolipoprotein spectra of the plasma obese youths was clearly seen under conditions of fat food loading, these changes being associated with disordered insulin reaction to intake if exogenous fat. The examinees suffering from obesity a varying degree, mainly from the abdominal variant, presented with a complex of interrelated metabolic disorders (hyperinsulinemia, insulin resistance, dyslipoproteinemias),--the metabolic X syndrome, this referring them to a group at risk of developing atherosclerosis, essential hypertension, diabetes mellitus irrespective of the degree of general obesity.
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PMID:[The lipid transport system and its hormonal regulators in youths suffering from obesity]. 774 31

Lipid analysis should be tailored to the likelihood of hyperlipidemia and atherosclerosis. In healthy individuals without a family history of hyperlipidemia, it is sufficient to obtain readings of total cholesterol and high-density lipoprotein (HDL) cholesterol. In patients with a family history of hyperlipidemia, in addition, triglycerides should be measured. In patients with manifest atherosclerotic disease, the lipid profile should always include plasma cholesterol and triglycerides as well as HDL cholesterol; if these do not explain presence or extent of atherosclerosis, apolipoprotein (a) should be measured. Patients with diabetes mellitus should undergo the same diagnostic work-up as those with atherosclerotic disease. An apolipoprotein B reading (together with triglyceride levels) is sometimes helpful in patients with diabetes mellitus, allowing to estimate the size of triglyceride-rich lipoproteins. In patients with pancreatitis, longitudinal assessment of plasma triglycerides and, if available, measurement of HDL triglyceride are useful to unmask underlying hyperlipidemia.
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PMID:[Lipid status in the physician's laboratory]. 777 Aug 20


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