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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

On the basis of the available data (much of which is contradictory), I suggest that the following might summarize the role of Lp(a) in diabetes currently. 1. Lp(a) in IDDM: Concentrations are probably elevated. Concentrations are probably related to metabolic control. Concentrations are increased with microalbuminuria. 2. Lp(a) in NIDDM: Concentrations are not elevated. Concentrations do not change with metabolic control. Too few data exist to make an assessment of relation of Lp(a) to microalbuminuria in NIDDM. 3. Lp(a) and CHD in diabetes: Little current evidence shows that Lp(a) is a risk factor for CHD in diabetes. More studies--especially prospective studies with larger numbers of subjects--need to be done.
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PMID:Lipoprotein(a) and diabetes. An update. 849 27

Variations of serum Lp(a) concentrations were studied in a large population of insulin-treated diabetic patients in relation to the type of diabetes, insulin treatment and long-term complications. Lp(a) concentrations were measured by immunonephelometry in 740 diabetic patients [493 insulin-dependent diabetic (IDDM) patients and 247 insulin-treated Type 2 diabetic (ITD) patients]. Concentrations and distributions were compared with those of 128 non-diabetic controls. Correlations were investigated with lipidic and glycaemic parameters, daily lipid intake, body mass index (BMI), macrovascular and nephropathic complications, and insulin therapy. Both groups of insulin-treated patients (IDDM and ITD) displayed significantly higher Lp(a) concentrations when compared to controls. No relationship was found with macrovascular complications and nephropathy, except in IDDM patients in whom Lp(a) was elevated when creatinine concentration was above 120 mumol/L. Mean variations of Lp(a) were correlated with BMI and triglyceride variations in IDDM patients and only with triglycerides in ITD patients. These results suggest a direct and/or indirect (via serum triglycerides) potential role of exogenous insulin in the modulation of serum Lp(a) concentrations. BMI and lipid daily fat intake could be considered as additional modulating factors of Lp(a) serum concentrations in ITD patients.
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PMID:Influence of endogenous and environmental factors on variations of serum lipoprotein (a) concentrations in a large population of insulin-treated diabetic patients. 959 36

To investigate plasma concentrations of lipoprotein(a) [Lp(a)] and apolipoprotein(a) [apo(a)] polymorphism in relation to the presence of microvascular and neurological complications in type 1 diabetes mellitus, 118 young diabetic patients and 127 age-matched controls were recruited. Lp(a) levels were higher in patients than in controls, but the apo(a) isoforms distribution did not differ between the two groups [higher prevalence of isoforms of high relative molecular mass (RMM) in both groups]. Microalbuminuric patients had Lp(a) levels significantly greater than normoalbuminuric patients, and normoalbuminuric patients showed higher Lp(a) levels than controls. Patients with retinopathy or neuropathy showed similar Lp(a) levels to those without retinopathy or neuropathy. No differences in apo(a) isoforms frequencies were observed between subgroups with and without complications (higher prevalence of isoforms of high RMM in every subgroup). However, among patients with retinopathy, those with proliferative retinopathy had higher Lp(a) levels and a different apo(a) isoforms distribution (higher prevalence of isoforms of low RMM) than those with non-proliferative and background retinopathy (higher prevalence of isoforms of high RMM). Our data suggest that young type 1 diabetic patients without microalbuminuria have Lp(a) levels higher than healthy subjects of the same age. Lp(a) levels are further increased in microalbuminuric patients. High Lp(a) levels and apo(a) isoforms of low RMM seem to be associated with the presence of proliferative retinopathy, but have no relation to neuropathy.
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PMID:Lipoprotein(a) levels and apolipoprotein(a) polymorphism in type 1 diabetes mellitus: relationships to microvascular and neurological complications. 962 84

The aim of this multicentre study was to investigate the effect--in everyday life--of long term administration of acarbose on parameters of glycaemic control, daily insulin requirements, lipid parameters and tolerability in ambulant type 1 diabetic subjects insufficiently controlled with diet and insulin. Furthermore, effects on lipid parameters were to be studied. A total of 16 patients withdrew from the study, 13 of these during the acarbose medication period. For four of these 13 patients the adverse event started during the placebo run-in period. The data of 62 patients (35 men and 27 women, mean age 38 (range 18-64) years, median duration of diabetes 10 (range 1-40) years) were valid for statistical analysis. The median daily dose of acarbose at the final assessment (i.e. after 16 weeks of active treatment) was 200 (range 75-300) mg. During the placebo run-in period HbA1c levels tended to decrease from 8.9 +/- 1.1 to 8.5 +/- 0.9%. After 8 and 16 weeks of acarbose treatment the mean level had decreased further to 8.1 +/- 0.9 and 8.2 +/- 0.9%, respectively (both P < 0.001). After stopping acarbose HbA1c levels increased again to a mean level of 8.6 +/- 0.9%. Mean levels of HbA1c per centre followed the same profile. Seven-point blood glucose profiles followed the same pattern. None of these changes over time reached statistical significance except for a significant drop during acarbose treatment of the time-point 90 min after lunch (P < 0.01). After stopping acarbose treatment values returned to pre-study levels. For total cholesterol, HDL-cholesterol, triglycerides, Apo A1 and Apo B, and Lp(a) no significant changes were observed. Daily insulin dose was 48 (range 26-92) U at the start of the study and did not change. The most frequent reported adverse events were flatulence (43%), diarrhoea (27%), and abdominal pain (11%). We conclude that acarbose up to 3 x 100 mg/day can be a valuable adjunct to insulin in improving metabolic control in persons with type 1 diabetes.
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PMID:Effects of acarbose (Glucobay) in persons with type 1 diabetes: a multicentre study. 978 20

Raised plasma lipoprotein(a) (lp(a)) concentrations have been reported in patients with Type I (insulin-dependent) diabetes mellitus, which were lowered by insulin therapy. To investigate the biochemical background of these changes, we studied the effect of insulin on apolipoprotein(a) (apo(a)) synthesis and mRNA levels in primary cultures of cynomolgus monkey hepatocytes. Low concentrations of insulin (10 nmol/l) had a small but significant decreasing effect (p < 0.046) on apolipoprotein(a) secretion (-16%). Maximum inhibition (-33%) was obtained after incubation for 72 h with 1000 nmol/l insulin. Apolipoprotein B-100 secretion was 30%-36% decreased when using 10-1000 nmol/l and no change was observed for the secretion of apolipoprotein A-1 and albumin which were measured as control proteins. Steady state apolipoprotein(a) mRNA concentrations paralleled the decrease in apolipoprotein(a) synthesis (-29% after incubating the cells for 48 h with 100 nmol/l insulin) indicating that the decreased synthesis is regulated at the (post)-transcriptional level. Concentrations of apolipoprotein B-100 and apolipoprotein A-1 mRNA were not changed after incubation with insulin. We conclude that high concentrations of insulin suppress apolipoprotein(a) synthesis in monkey hepatocytes at the (post)-transcriptional level. These data may provide an explanation for the increased plasma concentrations of lipoprotein(a) as found in patients with insulin dependent diabetes mellitus.
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PMID:Insulin suppresses apolipoprotein(a) synthesis by primary cultures of cynomolgus monkey hepatocytes. 1044 Jan 36

High levels of plasma lipoprotein(a) [Lp(a)] represent an independent risk factor for cardiovascular morbidity; however, Lp(a) has not yet been identified as a risk factor for type 1 diabetic patients. Results from the limited number of available studies on plasma Lp(a) levels in relation to renal function in type 1 diabetes mellitus are inconclusive. We hypothesized that only type 1 diabetes mellitus patients with impaired renal function show increased plasma Lp(a) levels, due to decreased urinary apolipoprotein(a) [apo(a)] excretion. We therefore measured urinary apo(a) levels in 52 type 1 diabetes mellitus patients and 52 matched controls, and related the urinary apo(a) concentration to the plasma Lp(a) level, kidney function, and metabolic control. Our findings indicate that patients with incipient diabetic nephropathy as evidenced by microalbuminuria (20 to 200 microg/min) exhibit significantly higher plasma Lp(a) levels (median, 15.6 mg/dL) in comparison to normoalbuminuric patients (median, 10.3 mg/dL) and healthy controls (median, 12.0 mg/dL). Urinary apo(a) normalized to creatinine excretion was significantly elevated in both normoalbuminuric (median, 22.3 microg/dL) and microalbuminuric type 1 diabetic patients (median, 29.1 microg/dL) compared with healthy subjects (median, 16.0 microg/dL) and correlated significantly with Lp(a) plasma levels in both patient and control groups (P < .003). No correlation existed between the Lp(a) plasma level or urinary apo(a) concentration and metabolic control in type 1 diabetes mellitus patients. From these studies, we conclude that urinary apo(a) excretion is significantly increased in type 1 diabetic patients and correlates with plasma Lp(a) levels, and only type 1 diabetic patients with microalbuminuria have higher plasma levels of Lp(a) compared with patients with normoalbuminuria and healthy controls.
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PMID:Urinary excretion of apolipoprotein(a) fragments in type 1 diabetes mellitus patients. 1009 15

Lipoprotein(a) is a highly atherogenic particle. The plasma concentrations of this lipoprotein are strongly related to a genetically determined size polymorphism of apolipoprotein(a). This article reviews some pathogenetic characteristics of the apolipoprotein(a) polymorphism besides its known effect on the lipoprotein(a) plasma concentrations. Those are the relation of the apolipoprotein(a) phenotype with atherogenesis, the apolipoprotein(a) phenotype-specific elevation of lipoprotein(a) in hemodialysis patients and the advantages of this polymorphism for the atherosclerosis risk evaluation in high-risk patients. It furthermore discusses the observed association between the low molecular weight apolipoprotein(a) phenotype and Type I diabetes mellitus.
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PMID:[Genetic-epidemiological studies of apolipoprotein(a) polymorphism and its significance in nephrological diseases and type I diabetes mellitus]. 1151 90

Atherosclerotic cardiovascular diseases are the major causes of morbidity and mortality in patients with diabetes mellitus. Both quantitative and qualitative abnormalities of lipo-proteins are associated with the development of atherogenesis. In this study, the prevalence of dyslipidemia and the relative levels of glycosylated lipoproteins in 20 children and adolescents with type 1 diabetes mellitus were determined. Lipid profile, apolipoproteins A-I and B, Lp(a) and LpA-I in plasma were assayed. LpB and glycosylated HDL and LDL were evaluated by ELISA. Diabetic patients and controls had normal lipid profiles, but the diabetic group showed significantly higher LpA-I and lower LpA-I:A-II concentrations than controls. The diabetic group showed a significantly higher glycosylation level of HDL than controls and did not show a statistical difference for glycosylated LDL. No significant correlation between glycosylated lipoproteins, glycemia or HbA1c was found. In conclusion, these results suggest that type 1 diabetic patients develop important qualitative lipid abnormalities.
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PMID:Lipoprotein composition in children and adolescents with type 1 diabetes mellitus. 1581 4


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