Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The serum concentrations of apolipoproteins C-III, B, and A-I were determined in children with type I diabetes mellitus to establish whether they correlated with the level of glycosylated hemoglobin (Hb A1) and to determine whether these values differ between diabetic children and a population of normal children. Triglyceride (TG), total cholesterol (TC), and apolipoprotein (Apo) levels were studied in 95 children with type I diabetes; 51 of the children were attending a diabetes clinic and 44 were attending a diabetes summer camp. The level of Hb A1 correlated with Apo C-III (P less than .001) and TC (P less than .001) values in the clinic group, but not with Apo A-I or TG levels in either group. The Apo C-III level was higher in both groups of diabetic children (8.0 +/- 0.5 and 9.5 +/- 0.4 mg/dl) (P less than .01) than in normal subjects (6.1 +/- 0.2 mg/dl). We conclude that the Apo C-III level tends to be higher in diabetics than in normal subjects, even in the normotriglyceridemic camp group. The Apo C-III level correlated with both the TC level and Hb A1, suggesting that Apo C-III determinations in type I diabetic patients may permit early identification of atherosclerotic risk.
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PMID:Plasma apolipoprotein C-III levels in children with type I diabetes. 312 78

Serum levels of cholesterol (C), triglycerides (TG), lipoprotein-C and apolipoproteins (apo) A-I, A-II and B were measured in 30 children with type I diabetes mellitus (16 boys, 14 girls, aged 11-14 years) and in 26 healthy controls (15 boys, 11 girls, aged 10-13 years). For 19 diabetics controls matched for age, sex and relative body weight were selected. The diabetic patients were considered to be in fair metabolic control according to HbA1 levels and glycosylated serum protein concentrations. Mean serum apo A-I, A-II and B, C, TG, low density lipoprotein cholesterol (LDL-C) and high density lipoprotein cholesterol (HDL-C) did not differ significantly between diabetic nondiabetic children. Very low density lipoprotein cholesterol (VLDL-C) was significantly higher in diabetic children than in controls. Serum C and LDL-C levels showed close univariate linear correlations with glycosylated serum protein (LDL-C: r = 0.53, p less than 0.01, C: r = 0.58, p less than 0.01) in diabetics. The ratio LDL/HDL-C was significantly correlated to HbA1 levels (r = 0.47, p less than 0.01). By canonical and multiple linear correlation analysis significant relations of a selected set of variables concerning the control and therapy of diabetes (serum glucose, HbA1, glycosylated serum protein, insulin dose) with a set of lipoprotein variables (C, TG, VLDL-C, HDL-C, LDL-C, apo A-I, A-II, B) could be demonstrated. From these data we conclude that significant relations between atherogenic serum lipids and lipoproteins (C, LDL-C) and the degree of metabolic control exist in diabetic children, even in the absence of marked dyslipoproteinemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Apolipoproteins and lipoproteins in children with type I diabetes: relation to glycosylated serum protein and HbA1. 409 Sep 71

Plasma triglycerides, cholesterol, high-density lipoprotein (HDL) cholesterol, and apolipoproteins (apo) A-I, A-II, C-II, and C-III were determined and analyzed in 170 diabetic patients and 46 age-matched healthy normal subjects. The diabetics were separated into two groups: insulin-dependent diabetes mellitus (IDDM, n = 78) and noninsulin-dependent diabetes mellitus (NIDDM, n = 92). Significantly increased triglycerides, low HDL cholesterol, and normal cholesterol levels were found in the diabetics. The lipid profiles were similar in the IDDM and NIDDM groups. Plasma apo A-I, but not apo A-II, was low in both groups of diabetics. However, only in the IDDM subjects was there a statistically significant decrease in apo A-I when compared to normal subjects. The decreased apo A-I level negatively correlated with plasma triglycerides. Apo C-II and apo C-III were slightly increased in the diabetics compared to normal subjects. Apo C-II and apo C-III levels significantly correlated with plasma triglycerides (apo C-II, r = 0.70, P less than 0.0001; apo C-III, r = 0.71, P less than 0.0001). Only apo C-II correlated with total cholesterol. Thirty-eight to forty-two percent of the IDDM and NIDDM subjects had a clinical diagnosis of coronary artery disease (CAD) and/or peripheral arteriovascular disease (PAD). In the IDDM subjects, but not in the NIDDM subjects the incidence of CAD and/or PAD was associated with the decreased apo A-I levels as evaluated by a univariate analysis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Analysis of plasma lipids and apolipoproteins in insulin-dependent and noninsulin-dependent diabetics. 641 12

Fasting serum concentrations of high density lipoprotein cholesterol (HDLC) and apolipoprotein A-I (apo A-I) were determined in non-insulin dependent diabetes at diagnosis, diabetics treated by diet alone, diabetics treated by diet plus chlorpropamide, and normal controls matched for sex, age and body weight. Serum concentrations of HDLC and apo A-I were decreased in all groups of diabetics. There were no significant differences in HDLC and apo A-I concentrations between the diabetics at diagnosis and those treated by diet alone or diet plus chlorpropamide. Neither HDLC nor apo A-I concentrations were correlated with glucose concentrations. The results indicate that serum concentrations of HDLC and apo A-I are reduced in non-insulin dependent diabetics at diagnosis, and are not significantly affected by chronic diet and chlorpropamide therapy.
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PMID:High density lipoprotein cholesterol and apolipoprotein a-1 concentrations in non-insulin dependent diabetics treated by diet and chlorpropamide. 681 65

Arginine metabolism via nitric oxide (NO) synthase and other pathways was studied in coronary endothelial cells (EC) from the spontaneously diabetic BB rat, an animal model of human type I diabetes mellitus (IDDM). EC were prepared from insulin-treated diabetic BB (BBd) and non-diabetes-prone BB (BBn) rats. Basal NO synthesis was studied in EC cultured for 48 h in medium containing 0.4 mM L-arginine. At the end of the culture period, the medium was analyzed for nitrite and nitrate (two major end stable oxidation products of NO), and the cells were used to determine arginine uptake and metabolism and the activities of some arginine-degrading enzymes. For studies of arginine metabolism, cells were incubated at 37 degrees C for 1 h in Krebs-Henseleit bicarbonate buffer (pH 7.4) containing 1 mM L(-)[1-14C]arginine or L(-)[1-14C]ornithine. The rates of production of nitrite plus nitrate by BBd EC were only 15% of those of BBn cells. This impaired NO synthesis in BBd EC was not due to alterations in arginine uptake, NO synthase activity, or intracellular arginine concentrations but might have resulted from a limited intracellular availability of cofactors of NO synthase. In addition to the arginine-NO pathway, arginine was found to be metabolized to urea, ornithine, and, to a much lesser extent, CO2 via arginase and ornithine aminotransferase. The activities of arginase and the formation of ornithine and urea from arginine were decreased by 90% in BBd compared with BBn cells. These results, coupled with the reduced NO synthesis, indicate metabolic defects in arginine metabolism in BBd EC.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Impaired arginine metabolism and NO synthesis in coronary endothelial cells of the spontaneously diabetic BB rat. 748 63

The aim of the present study was to determine if low-density lipoproteins (LDLs) and red blood cell (RBC) membranes from diabetic patients present an increased susceptibility to lipoperoxidation, which might be related to the increased incidence of atherosclerosis in diabetes. LDLs and RBC membranes were isolated from 11 insulin-dependent (IDDM) and 18 non-insulin-dependent diabetic (NIDDM) patients and exposed to a peroxidative stress by incubation with phenylhydrazine. The susceptibility to peroxidation was determined by measuring the production of thiobarbituric acid-reactive substances (TBARS) after the incubation. The following parameters were also evaluated: plasma glucose, triglycerides (TG), phospholipids (PL), total and high-density lipoprotein (HDL) cholesterol, apolipoprotein (apo) A-I, apo B, hemoglobin A1c (HbA1c), LDL PL and cholesterol, LDL fatty acid composition, and RBC membrane PL and cholesterol. Although they were apparently normolipidemic, diabetic patients showed an increased susceptibility to peroxidation in LDLs and erythrocyte membranes as compared with control subjects. The amount of arachidonic acid in LDLs and the PL concentration of RBC membranes from diabetic patients were significantly higher than in normal subjects. The increased lipoperoxidability of both RBC membranes and LDLs might play a central role in the pathogenesis of the vascular complications of diabetes mellitus.
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PMID:Increased susceptibility to lipid oxidation of low-density lipoproteins and erythrocyte membranes from diabetic patients. 799 Jun 98

Chronic renal failure (CRF) in nondiabetics is associated with a number of lipoprotein abnormalities that place these patients at high risk for atherosclerosis. This study compared the lipoprotein composition of nondiabetic controls (n = 68) with that of patients with insulin-dependent diabetes mellitus ([IDDM] n = 13) and of patients with IDDM and CRF ([IDDM + CRF] n = 74). Six lipoprotein subfractions (very-low-density lipoprotein [VLDL], intermediate-density lipoprotein [IDL], low-density lipoprotein [LDL], high-density lipoprotein-light [HDL-L], HDL-medium [HDL-M], and HDL-dense [HDL-D]) were isolated by rapid gradient ultracentrifugation using a fixed-angle rotor. The apolipoprotein (by reverse-phase high-performance liquid chromatography [HPLC]) and lipid (by enzymatic assays) composition of each subfraction was determined. The only abnormalities found in IDDM patients were increases in IDL and HDL-L triglyceride (TG) levels and an increase in the HDL-L free cholesterol (FC) level. The IDDM + CRF group had multiple abnormalities including (1) elevated TG, apolipoprotein (apo) C-II, and apo C-III levels in all lipid subfractions; (2) elevated VLDL and IDL apo B, TG, FC, cholesterol ester (CE), and phospholipid (PL) levels (with an increased CE/TG ratio in VLDL only); (3) decreased HDL-M apo A-I, apo A-II, CE, and PL levels, but an increased HDL-D apo A-I level; and (4) decreased lecithin:cholesterol acyltransferase (LCAT) activity. Twenty-five of the IDDM + CRF patients underwent combined pancreas and kidney (P + K) transplantation, and 12 patients received only a kidney transplant. Lipoprotein composition was determined at 3, 6, and 12 months posttransplant. Both types of transplantation resulted in similar alterations in lipoprotein composition, even though there was essential normalization of blood glucose levels in most of the patients who received a pancreas transplant (hemoglobin A1C [HbA1C], 9.1% +/- 1.1% v 5.7% +/- 0.3% at 12 months, P < .01). These posttransplant changes included (1) no improvement in the elevated TG level in any lipid subfraction even though there was some reduction in apo C-III levels in VLDL; (2) reductions in levels of VLDL and IDL apo B but increases in LDL apo B; (3) increases in HDL apo C-III and FC concentrations despite an increase in LCAT activity; and (4) increases in apo A-I levels in HDL-L and HDL-M. The addition of a pancreas to a kidney transplant had no obvious impact on the lipoproteins.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Lipoprotein composition in insulin-dependent diabetes mellitus with chronic renal failure: effect of kidney and pancreas transplantation. 813 82

Lipoproteins, including intermediate density lipoproteins and lipoprotein(a), and apolipoproteins A-I, B, C-II, C-III and E, were studied in 13 newly-diagnosed type I diabetic patients with severe insulinopenia without dehydration or acidosis. At baseline, the main finding was a significant increase in serum triglycerides due to raised triglyceride concentrations in all lipoproteins, particularly triglyceride-rich lipoproteins. Cholesterol concentrations were slightly increased in lipoproteins and led to a significant increase in serum cholesterol. Two days after the start of insulin therapy, lipoprotein profiles had normalized except for the LDL triglyceride contents, which remained significantly increased on the fifth day of treatment. No significant modifications were observed in lipoprotein(a), apolipoproteins A-I and E concentrations throughout the study. However, serum apolipoproteins B, C-II and C-III were increased at baseline and fell to normal levels 2 days after the start of insulin therapy. On the other hand, apolipoprotein C-II/C-III ratios in high and very low density lipoprotein, showed no significant differences at baseline compared with controls, suggesting that an apolipoprotein C-II deficiency or apolipoproteins Cs imbalance can be ruled out. In conclusion, significant lipoprotein abnormalities were observed in the insulin-deficient state of type I diabetes mellitus; insulin therapy normalizes the lipoprotein profile in two days, except for low density lipoprotein triglyceride contents which remain increased at the fifth day.
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PMID:Lipoprotein composition in the insulin-deficient non-acidotic phase of type I diabetic patients and early evolution after the start of insulin therapy. 814 57

A reduction in total plasma cholesterol concentration has been reported in insulin-dependent diabetic (IDDM) pregnant women in early gestation. To determine if this reduction extends throughout gestation and which lipoprotein fractions may be responsible, we measured plasma triglyceride, cholesterol (C), high density lipoprotein cholesterol (HDL-C) and HDL2 and HDL3-C subfractions between 6 and 36 weeks' gestation in normal and IDDM women. Total plasma C was significantly lower in IDDM pregnant subjects between 20 and 36 weeks' gestation as compared to nondiabetic controls, while plasma triglyceride concentrations were not significantly different in this interval. Very low and low density lipoprotein (VLDL, LDL) C concentrations were not statistically significantly different from controls at any of the times studied, while HDL-C was lower throughout diabetic pregnancy as compared to controls, significantly so between 20 and 36 weeks' gestation. The lower HDL-C in IDDM women was associated with a significantly lower HDL3-C level. Plasma apoprotein A-I and A-II concentrations, markers of the HDL2 and HDL3 subclasses, respectively, were measured to corroborate the HDL subfraction changes. Apo A-I and A-II increased significantly between 12 and 28 weeks' gestation in control but not in diabetic pregnant subjects, consistent with a higher HDL3 in normal than in diabetic pregnant subjects. It appears that plasma triglyceride, VLDL and LDL-C, and HDL2-C concentrations are similar in IDDM and normal pregnancy, while total-C, HDL-C and HDL3-C and its associated apoproteins are lower than in normal subjects in late gestation. The mechanism of these changes and their significance for fetal growth and development deserve further study.
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PMID:Effect of insulin-dependent diabetes on plasma lipoproteins in diabetic pregnancy. 825 93

Insulin-dependent diabetes mellitus (IDDM) is characterized by altered composition of atherogenic lipoproteins, especially a depletion in choline-containing phospholipids (PL) of apolipoprotein (apo) B lipoproteins (LpB). To determine the effects of continuous intraperitoneal (IP) insulin infusion (CIPII) on this qualitative lipoprotein abnormality, we compared lipoprotein profiles of 14 IDDM patients treated by continuous subcutaneous insulin infusion (CSII) and at 2 and 4 months after treatment with CIPII using an implantable pump. IDDM patients were in fair metabolic control and were compared with 14 healthy control subjects matched for sex, age, body mass index, and plasma lipids. The following parameters were studies: hemoglobin A1c (HbA1c), monthly blood glucose, daily insulin dose (units per kilogram per day), total cholesterol (TC), triglycerides (TG), high-density lipoprotein (HDL) and low density lipoprotein (LDL) cholesterol, apo A-I, and apo B. Choline-containing PL were assessed in plasma and in apo B- and no-apo B-containing lipoprotein particles (LpB and Lp no B). As compared with the control group, plasma PL and LpB-PL were significantly lower in IDDM patients treated by CSII (2.95 +/- 0.26 v 3.30 +/- 0.45 mmol/L,P<.05, and 1.09 +/- 0.45 v 1.68 +/- 0.33 mmol/L,P<.01, respectively). No significant differences were observed for Lp no B lipid determinations between both groups. After initiation of CIPII, IDDM patients did not experience any significant changes in mean values for body mass index, HbA1c, and monthly blood glucose throughout the study. Daily insulin doses were identical to those observed before IP therapy. Lipid parameters remained unchanged in IDDM patients (TC, TG, HDL and LDL cholesterol, apo A-I, and apo B). A moderate but progressive elevation of plasma PL was noted, and after 4 months of CIPII, PL and LpB-PL levels were no longer significantly different between IDDM patients and controls. The increase in plasma and LpB choline-containing PL observed after 2 and 4 months of CIPII is not linked to changes in blood glucose control, body weight or daily insulin requirements. These changes may be related to the route of insulin administration, which may be accompanied by a reduction of lipoprotein lipase (LPL) activity and consequently a reduction of phospholipase activity. These results suggest that IP insulin delivery may be a more physiological route that increases the choline-containing PL content of LpB particles.
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PMID:Intraperitoneal insulin infusion improves the depletion in choline-containing phospholipids of lipoprotein B particles in type I diabetic patients. 860 27


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