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 activity of serum paraoxonase, an enzyme located on high-density lipoprotein, has been investigated in familial hypercholesterolaemia (FH) and insulin dependent diabetes mellitus (IDDM). Increases in total serum cholesterol and apolipoprotein B were present in both FH and IDDM compared to healthy controls and in the patients with IDDM, serum triglycerides were also raised. The serum HDL-cholesterol concentrations in controls and patients with FH and IDDM did not differ significantly. Serum paraoxonase activity was significantly lower in both the FH and IDDM populations than in controls (P less than 0.001 and P less than 0.01, respectively). 72% of the FH population and 67% of the IDDM population were in the lower half of the frequency distribution for serum paraoxonase (activity of less than 112 U/l). It is likely that the common factor related to low paraoxonase activity is hyperlipidaemia. It is possible that paraoxonase has a physiological role in lipid metabolism and that decreases in its activity may accelerate atherogenesis.
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PMID:Serum paraoxonase activity in familial hypercholesterolaemia and insulin-dependent diabetes mellitus. 165 32

The aim of the present study was to evaluate the serum and lipoprotein levels of choline--containing phospholipids (lecithin, lysolecithin and sphingomyelin) in a group of type I diabetic patients in fair metabolic control. Forty-eight male adult diabetic patients without macroproteinuria were compared with 48 healthy controls matched for age and body weight. Total cholesterol and phospholipids were assessed in plasma and in apolipoprotein B (apoB) and non apoB containing lipoprotein particles (Lp B and Lp non B particles) separated using precipitation with Concanavalin A. When compared to the control group, diabetic patients have significantly lower serum phospholipids and phospholipids and cholesterol content of LpB particles. All the other parameters studied were similar in the two groups. The phospholipids/cholesterol ratio, calculated in LpB particles is also significantly reduced in the diabetic group. These results strongly suggest a depletion in the choline containing phospholipid content of LpB particles and therefore an alteration of the surface components of atherogenic particles in type I diabetes mellitus.
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PMID:Depletion in choline containing phospholipids of LpB particles in adequately controlled type I insulin-dependent diabetes mellitus. 236 74

Complete acquired lipoatrophic diabetes (LD) is characterized by nonketotic insulin-resistant diabetes, elevated very low-density lipoprotein (VLDL) triglyceride (TG) levels, and absent subcutaneous fat. We studied a young child in whom LD atypically developed after the onset of type 1 diabetes mellitus. On uncontrolled home diet the patient had triglyceride levels over 1,000 mg/dL on multiple occasions. In order to demonstrate the effects of caloric and dietary-fat restriction on VLDL metabolism, 3H-glycerol and autologous 125I-VLDL were used to quantitate the turnover of VLDL-TG and VLDL-apolipoprotein B (apo B) during two periods of caloric restriction. Consumption of a 900-kcal 40-g fat diet resulted in a plasma triglyceride level of 1383 mg/dL (ten-fold elevation). This hypertriglyceridemia was associated with markedly increased production rates of both VLDL-TG (73.7 mg/kg/h) and VLDL-apo B (126.9 mg/kg/d). Consumption of a 900-kcal 25-g fat diet resulted in a plasma TG level of 663 mg/dL. This reduction in plasma TG was associated with a 40% decrease in VLDL-TG production rate (PR) (45.1 mg/kg/h). There was no change in the production rate (PR) of VLDL-apo B. The hypertriglyceridemia in this patient was due to marked over production of VLDL. Furthermore, the studies demonstrate: (1) the independent benefits of caloric and dietary-fat restriction in the treatment of LD, and (2) that fat restriction lowered plasma triglyceride by its effect on the VLDL-TG production rate.
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PMID:Very low-density lipoprotein metabolism in an unusual case of lipoatrophic diabetes. 638 60

Increased serum levels of lipoprotein (a) have been found to be an independent risk factor for coronary heart disease. The major protein constituents of lipoprotein (a) are apolipoprotein B 100 und apolipoprotein (a) (apo(a)). We determined the serum levels of apo(a) and several lipid (cholesterol, HDL- and LDL-cholesterol, triglycerides, apolipoproteins A, A1 and B) and glycaemic (HbA1c, fasting blood glucose) parameters in 40 patients with type 1 diabetes mellitus and in 103 age- and sex-matched control subjects. The median serum levels of apo(a) were significantly increased in the type 1 diabetic patients (142.7 vs. 80.0 U/L; P = 0.03), whilst HDL, LDL-cholesterol, and apolipoprotein A, A1 and B levels were lower (P < 0.01). No significant correlation was found between parameters of metabolic control and apo(a) levels. After subdivision of the diabetic patients according to different stages of diabetic nephropathy (DN), determined by urinary albumin excretion, significant relationships were found between DN and triglycerides (P = 0.04), LDL (P = 0.03) and apolipoprotein B (P = 0.008, Kruskal-Wallis test) levels. Apo(a) levels were significantly higher than normal values in patients without DN (P < 0.05), but unrelated to the degree of DN. Patients with diabetic macroangiopathy had significant higher levels of cholesterol (P = 0.0001), triglycerides (P = 0.026), LDL (P = 0.0003), and apoB (P = 0.002) than patients without. Apo(a) levels were unrelated to diabetic macroangiopathy. The significantly elevated levels of apo(a) even in patients without DN or macroangiopathy are noteworthy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Apolipoprotein (a) levels in patients with type 1 diabetes mellitus are unrelated to metabolic control or vascular disease. 785 76

Recent evidence suggests the rise in urinary albumin excretion preceding diabetic nephropathy may represent a continuum. We therefore studied factors relating to albumin excretion rate in children with insulin-dependent diabetes. Normal overnight albumin excretion rate was determined in 690 healthy schoolchildren. The 95th centile was 7.2 micrograms min-1. Patients included 169 children with IDDM aged 12.4 +/- 3.1 years who performed 4.8 +/- 0.4 overnight collections during 15 +/- 0.5 months and were analysed cross sectionally. They were stratified accordingly to mean albumin excretion rate: normal < 7.2 micrograms min-1, borderline 7.2-20 micrograms min-1, microalbuminuria 20-200 micrograms min-1; 96/169 patients performed 6.4 +/- 0.2 overnight collections during 24 months follow-up and were analysed longitudinally. Cigarette smoking was determined by history and urine cotinine levels. Smoking correlated with albumin excretion rate, independent of age and other variables, in cross-sectional and longitudinal analysis (p < 0.003). Smoking was more prevalent in the borderline albuminuria and microalbuminuria groups (p < 0.004, p < 0.001). Mean HbA1c during follow-up and mean HbA1c since diagnosis were significantly higher in the microalbuminuric group, compared with the normal patient group. HbA1c since diagnosis, mean blood pressure, lipoprotein(a), and apolipoprotein B did not correlate with albumin excretion rate, after controlling for other variables. Our findings highlight the continuing need for strategies to prevent smoking in this age group.
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PMID:Relationship of smoking and albuminuria in children with insulin-dependent diabetes. 795 92

In a prospective follow-up of 30 patients with type 1 diabetes and nephropathy, serum cholesterol, triglycerides, apolipoprotein Al and B, and lipoprotein(a) were determined to study their relationship to the rate of decline in glomerular filtration rate. The patients had proteinuria and advanced nephropathy with a mean +/- SD glomerular filtration rate of 39 mL/min/1.73 m2. The decline in glomerular filtration rate was determined during 2.5 +/- 0.5 years. High serum cholesterol, triglycerides, and apolipoprotein B were correlated to a more rapid deterioration in kidney function. The rate of decline in glomerular filtration rate was 1.0 +/- 2.5 mL/min/yr in the 10 patients with the lowest cholesterol level, compared with 4.5 +/- 3.2 mL/min/yr in the patients with the highest serum cholesterol (P = 0.015). The combined effect of the measured lipids, blood pressure, type of antihypertensive treatment, protein intake, proteinuria, and hemoglobin A1C on the rate of decline in glomerular filtration rate was assessed by multiple regression analysis. The measured factors together had a high explanatory power for the rate of decline in glomerular filtration rate. In this model, 73% of the variation in decline in glomerular filtration rate was explained by the measured variables (multiple r2 = 0.73). Low cholesterol and treatment with an angiotensin-converting enzyme inhibitor were the strongest predictors of a favorable renal prognosis. This suggests that hypercholesterolemia is an important risk factor for diabetic nephropathy.
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PMID:Cholesterol: a renal risk factor in diabetic nephropathy? 832 83

The effects of pravastatin on plasma lipid levels, in vitro oxidizability of the non-HDL fraction, metabolic control, urinary albumin excretion, and four serum enzymes (SGPT, SGOT, GT and CPK) were studied in 20 insulin-dependent diabetic patients (IDDM) with incipient nephropathy. The patients were divided into two groups and the study was carried out by a crossover design. After 12 weeks pravastatin treatment (20 mg daily), plasma cholesterol, LDL-cholesterol and apolipoprotein B (Apo B) decreased by 22, 19 and 15%, respectively. The thiobarbituric acid reactive substances (TBARS) formation and the oxidation lagtime of the non-HDL fraction during the in vitro incubation with copper were not changed before and after treatment. The HbA1c and blood glucose levels, urinary albumin excretion, SGOT, SGPT and GT were not influenced by pravastatin treatment. CPK activity was elevated after 12 weeks of pravastatin treatment, and this elevation persisted even after the 12 weeks placebo period. So, pravastatin could be used as an effective drug for IDDM patients with incipient nephropathy, but close monitoring of the CPK activity is recommended.
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PMID:Effects of pravastatin on lipid levels, in vitro oxidizability of non-HDL lipoproteins and microalbuminuria in IDDM patients. 859 12

This review is aiming to study the values of apolipoprotein AI and B and plasma lipid levels (total cholesterol, HDL cholesterol, LDL cholesterol and triglyceride) in well-treated diabetic patients, and their possible relationship with hemoglobin A1, body mass index and insulin levels. The study groups were 26 insulin-dependent diabetic (IDDM) patients, 30 non-insulin-dependent diabetic (NIDDM) subjects and 20 non diabetic subjects (controls). Apolipoprotein AI concentrations were similar in the three groups, but apolipoprotein B values and apo B/apo AI ratio were significantly higher in IDDM as related to NIDDM patients (p < 0.001) and to non-diabetic subjects (p < 0.001). We were not able to find significant differences concerning plasma lipid values between the three groups. We found a weak correlation between apo B and hemoglobin AI in IDDM (r = 0.45; 0.02 < p < 0.05), but not in NIDDM patients. Body mass index was not related to the values of apolipoproteins AI and B. We found a positive but weak correlation between insulin levels and triglyceride (r = 0.42), and an inverse one with HDL cholesterol (r = 0.57; 0.02 < p < 0.05) in non-diabetic subjects only, while in NIDDM patients these associations were even less significant. Plasma insulin values strongly correlate to body mass index in both NIDDM (r = 0.64; p < 0.001) and in control subjects (r = 0.73; 0.001 < p < 0.001).
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PMID:Apolipoproteins AI and B and plasma lipid values in well-treated diabetic patients from Romania. 864 98

The physicochemical modifications (composition and conformation) of lipoproteins containing apolipoprotein B-100 (apo B-100) were studied in normocholesterolaemic adequately controlled Type 1 insulin-dependent diabetic patients. Thirty-one normocholesterolaemic (serum cholesterol < 6.50 mmol/l) diabetic male patients and 31 age-and body mass index-adjusted healthy normolipaemic male controls were studied. Cholesterol and choline-containing phospholipids were measured in total serum and in two lipoprotein subfractions containing or not apo B (LpB and LpnoB respectively). These subfractions were separated by precipitation with concanavalin A. Total apo B-100 and two lipoprotein particles defined according to their apo B-100 epitope accessibility were determined using respectively anti-apo B polyclonal and two monoclonal antibodies that reacted with specific epitopes on the apo B molecule. Despite a classical lipid profile (cholesterol and triglyceride levels), which was quite normal in plasma from patients as compared to controls, a depletion of choline-containing phospholipid content in serum and more specifically in LpB particles was observed in diabetic patients. Decreased cholesterol content was also observed in LpB particles. Immunological analysis demonstrated an increased number of lipoprotein particles (a condition previously related to coronary artery disease) and decreased immunoaccessibility of a conformationally expressed apo B-100 epitope. These conformational changes were correlated with modifications of the surface phospholipid environment of LpB particles. It is concluded that subtle abnormalities in the composition and conformation of atherogenic apo-B-containing lipoproteins occur in Type 1 diabetes mellitus. These structural modifications may be one factor accounting for the increased rate of atherosclerosis in diabetes, despite the existence of a normal classical lipid profile.
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PMID:Accessibility of human apolipoprotein B-100 epitopes in insulin-dependent diabetes: relation with the surface lipid environment of atherogenic particles. 869 5

Non-insulin dependent diabetes (NIDDM) is associated with an increased risk of peripheral vascular disease (PVD), but within the diabetic population the relationship between lipid profile and PVD has not been clearly defined. In this study we examined the association of lipid parameters and in particular low density lipoprotein (LDL) particle size, with the presence of PVD in subjects with and without NIDDM. 41 NIDDM patients and 31 non-diabetic subjects with PVD in the absence of rest pain or ulceration, defined by ankle-brachial index measurements and duplex scanning, were compared with 41 NIDDM and 31 euglycemic control subjects of comparable age and sex, without PVD. In both groups those with PVD were found to have significantly elevated triglycerides (2.7 [2.2-3.3] versus 1.9 [1.6-2.2] mmol/l; P < 0.05 in the diabetic group and 2.0 [1.6-2.3] versus 1.4 [1.1-1.5] mmol/l; P < 0.05 in the non-diabetic group), decreased apolipoprotein A1 (124 +/- 3 versus 139 +/- 5 mg/dl; P < 0.01 in the diabetic group and 133 +/- 4 versus 147 +/- 4 mg/dl; P < 0.05 in the non-diabetic group) and decreased LDL particle size (25.4 +/- 0.1 versus 25.8 +/- 0.1 nm; P < 0.01 in the diabetic group and 26.0 +/- 0.1 versus 26.3 +/- 0.1 nm; P < 0.05 in the non diabetic group). In the non-diabetic group apolipoprotein[a] (365 [239-554] versus 184 [17-266] U/l; P < 0.01), total cholesterol (6.3 +/- 0.2 versus 5.6 +/- 0.2 mmol/l; P < 0.05), LDL cholesterol (4.1 +/- 0.2 versus 3.6 +/- 0.2 mmol/l; P < 0.05) and apolipoprotein B (146 +/- 8 versus 117 +/- 5 mg/dl; P < 0.05) were also found to be associated with PVD although these associations were not observed in the group with diabetes. In addition, 11 NIDDM subjects and 11 non-diabetic subjects with rest pain or ulceration were compared to the corresponding groups with uncomplicated PVD and had lipid profiles with significantly lower levels of total cholesterol and LDL cholesterol. We conclude that the dyslipidemic profile characterized by increased triglyceride level, decreased apolipoprotein A1 level and small dense LDL is associated with uncomplicated PVD in both NIDDM and non-diabetic subjects.
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PMID:Lipid levels and peripheral vascular disease in diabetic and non-diabetic subjects. 954 25


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