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)

Dietary cod-liver oil containing eicosapentaenoic acid is effective on microvascular albumin leakage in diabetic patients with albuminuria. We determined the long-term effects of oral pure eicosapentaenoic acid ethyl (EPA-E: 900 mg/day) administration on diabetic nephropathy in non-insulin dependent diabetic (NIDDM) patients. The effects of EPA-E were determined by observing the changes of the index of urine albumin excretion level/urine creatinine (Cr) excretion level (UAI), the ratio of beta 2-microglobulin excretion level/urine Cr excretion level (beta 2-MG/Cr) and the ratio of N-acetyl-D-glucosaminidase excretion level/urine Cr excretion level (NAG/Cr) at 3, 6 and 12 months after the start of the treatment. Oral EPA-E administration immediately improved the increased UAI at 3 months after the start of treatment. A significant improvement of the UAI by EPA-E was sustained 12 months later. EPA E administration also tended to decrease the urine beta 2-MG/Cr ratio from 6 months, but the difference was statistically not significant. However, the urine NAG/Cr ratio was not changed by EPA-E administration. EPA-E administration did not affect blood pressure levels, glycemic control and lipid metabolism in these patients. The present data indicated that EPA-E administration improved increased albumin excretion in NIDDM patients with nephropathy and its effects on albuminuria sustained for at least 12 months after the start of treatment. However, tubular factors were not influenced by EPA-E administration.
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PMID:Long-term effect of eicosapentaenoic acid ethyl (EPA-E) on albuminuria of non-insulin dependent diabetic patients. 758 10

There are few data on the risk factors for diabetic nephropathy in the Asian Indian population, although several studies have shown a high prevalence of the disease in this ethnic group. This study also aimed to assess the role of hyperglycaemia and hypertension in the causation and course of nephropathy in this population, which has low rates of obesity. Retrospective analysis of two groups of non-insulin dependent diabetic (NIDDM) patients, one without proteinuria (< 100 mg/day, n = 25) and the other with proteinuria (> or = 500 mg/day, n = 25), matched for age, sex, duration of diabetes and body mass index (BMI) was done to study the factors predisposing to proteinuria and also its progression during a 2 year follow-up. Logistic regression analysis showed that the factors contributory to proteinuria were initial HbA1 and initial systolic blood pressure. The average proteinuria during the follow-up was dependent on the initial and average systolic and diastolic blood pressure values. No correlation was seen between cholesterol or triglyceride values and the change in proteinuria. Creatinine clearance deteriorated in the proteinuric group and this was related to the presence of proteinuria and initial diastolic blood pressure. This study emphasizes the importance of blood pressure in the progression of diabetic nephropathy, even in people who have low BMI. Therefore, good control of blood pressure has an important role to play in the management of this condition.
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PMID:Proteinuria in NIDDM in south India: analysis of predictive factors. 758 11

Thickening of the glomerular basement membrane (GBM) and expansion of the mesangial matrix are hallmarks of human diabetic nephropathy. Renal tissues from 15 patients with type II (non-insulin-dependent) diabetes (NIDDM) were studied by immunofluorescence (IF) and immunogold electron microscopy (IEM) for the distribution of 2 type IV collagen peptides [alpha 3(IV) noncollagenous (NC) domain and alpha 4(IV) NC domain] and 2 classical type IV collagen chains [alpha 1(IV) NC domain and alpha 2(IV) domain]. There was intense staining for alpha 3(IV) NC and alpha 4(IV) NC domain in the GBM but not in the mesangial matrix of patients with overt diabetic nephropathy. In contrast, staining with antibodies to alpha 1(IV) NC and alpha 2(IV) NC domain reacted with mesangial matrix but was significantly decreased in the GBM in the patients with overt diabetic nephropathy. IEM confirmed the IF findings. These data suggest that expansion of the mesangial matrix and thickening of GBM in NIDDM involves separate and distinct type IV collagen components and that the site-specific matrix alterations in NIDDM and type I (insulin-dependent) diabetes are parallel.
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PMID:Differential distribution of type IV collagen chains in patients with diabetic nephropathy in non-insulin-dependent diabetes mellitus. 761 16

Mortality and morbidity from coronary heart disease (CHD), diabetes mellitus (DM) and essential hypertension (HTN) are higher in people of South Asian descent than in other groups. There is evidence to believe that essential fatty acids (EFAs) and their metabolites may have a role in the pathobiology of CHD, DM and HTN. Fatty acid analysis of the plasma phospholipid fraction revealed that in CHD the levels of gamma-linolenic acid (GLA), arachidonic acid (AA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are low, in patients with HTN linoleic acid (LA) and AA are low, and in patients with non-insulin dependent diabetes mellitus (NIDDM) and diabetic nephropathy the levels of dihomo-gamma-linolenic acid (DGLA), AA, alpha-linolenic acid (ALA) and DHA are low, all compared to normal controls. These results are interesting since DGLA, AA and EPA form precursors to prostaglandin E1, (PGE1), prostacyclin (PGI2), and PGI3, which are potent platelet anti-aggregators and vasodilators and can prevent thrombosis and atherosclerosis. Further, the levels of lipid peroxides were found to be high in patients with CHD, HTN, NIDDM and diabetic nephropathy. These results suggest that increased formation of lipid peroxides and an alteration in the metabolism of EFAs are closely associated with CHD, HTN and NIDDM in Indians.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Essential fatty acid metabolism in patients with essential hypertension, diabetes mellitus and coronary heart disease. 764 60

In patients with type 1 diabetes an association has been found between an insertion/deletion (I/D) polymorphism in the gene for angiotensin I converting enzyme and the presence of diabetic nephropathy. Our objective was (i) to assess this association in a large cohort of patients with type 1 diabetes and (ii) to examine whether this finding also applies to type 2 diabetes. We examined 247 patients with type 1 diabetes of more than 10 years duration (135 patients > or = 20 years): Nephropathy was present in 114 and absent in 133 patients. Furthermore we separately analyzed 455 patients with type 2 diabetes of more than 10 years duration (158 patients > or = 20 years). Nephropathy was present in 247 and absent in 208 patients. Nephropathy was defined by confirmed presence of albuminuria > 30 mg/day (or > 20 micrograms/min). The I/D polymorphism was analyzed with PCR technique and alleles were visualized on 2% agarose gels after ethidium staining. Allele frequencies in the overall diabetic population did not differ significantly from the normal population. Distribution of genotypes was not significantly different between type 1 patients with and without nephropathy (P = 0.377). Also, no significant difference in genotype distribution was found between type 2 diabetic patients with and without nephropathy (P = 0.948). We conclude that no significant association between I/D polymorphism and nephropathy was demonstrable in either type 1 or type 2 diabetes, despite considerable statistical power of the patient sample and adequate duration of diabetes for nephropathy to become manifest.
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PMID:Association of ACE gene polymorphism and diabetic nephropathy? The Diabetic Nephropathy Study Group. 778 16

Progression of diabetic nephropathy from the stage of macroproteinuria with near-normal renal function until start of dialysis was compared in 16 patients with type I and 16 patients with type II diabetes mellitus. The mean creatinine clearance at the beginning of the study was 89 +/- 13 ml/min/1.73 m2 in patients with type I and 81 +/- 6 ml/min/1.73 m2 in those with type II diabetes. Dialysis was started after a mean interval of 77 (44-133) months, when creatinine clearance had decreased to 8 +/- 2 ml/min/1.73 m2 in type I diabetic patients. The respective figures for type II diabetic patients were 81 (40-124) months and 7 +/- 2 ml/min/1.73 m2. The mean rate of decrease in creatinine clearance was 1.05 +/- 0.45 ml/min/month in type I and 0.91 +/- 0.41 ml/min/month in type II diabetes. The mean rate of decrease was 1.46 +/- 0.30 ml/min/month in type I diabetic patients with a systolic BP > 160 mmHg versus 0.80 +/- 0.42 ml/min/month with < 160 mmHg (P < 0.01). In the type II diabetics the respective figures were 1.38 +/- 0.40 ml/min/month versus 0.78 +/- 0.15 ml/min/month (P < 0.01). During the observation period the prevalence of coronary heart disease increased from 6 to 50% in type I and from 31 to 87% in type II diabetes. In conclusion, the rate of progression of diabetic nephropathy during the predialytic phase is similar in type I and type II diabetes; BP adversely affects the rate of progression to the same extent in both groups.
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PMID:Similar rate of progression in the predialysis phase in type I and type II diabetes mellitus. 780 Feb 7

Diabetic nephropathy is the only increasing cause of renal failure in the Western world. It affects a large proportion of both insulin-dependent (IDDM) and non-insulin-dependent diabetic (NIDDM) patients. A critical stage in the development of diabetic renal disease is the onset of microalbuminuria, defined as an albumin excretion rate of 30 to 300 mg/day. Microalbuminuria predicts progression to renal failure and early cardiovascular mortality in both IDDM and NIDDM patients. Microalbuminuria is associated with a constellation of other risk factors for small and large vessel damage which include raised blood pressure, poor glycemic control, plasma lipid and clotting factor abnormalities, left ventricular hypertrophy, and insulin resistance. Treatment with angiotensin-converting enzyme inhibitors corrects microalbuminuria and prevents progression to persistent proteinuria. Good blood glucose control significantly reduces the risk of progression from normoalbuminuria to microalbuminuria. The treatment of microalbuminuria appears highly cost-beneficial and substantially increases life expectancy. The development of microalbuminuria, for which all diabetic patients aged 12 to 70 years should be screened, should alert the physician to set in motion a program of assessment, monitoring, and correction of all risk factors for renal and cardiovascular disease.
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PMID:Prognostic significance of microalbuminuria. 781 38

An increase in glomerular filtration rate (hyperfiltration) may be an important early event in the initiation of diabetic nephropathy but the prevalence of hyperfiltration appears to vary between different populations with type 2 diabetes. We have measured glomerular filtration rate using 51Cr EDTA clearance in 15 young Polynesians (mean age 32 years), 1-30 months after the initial diagnosis of type 2 diabetes and 15 control Polynesian subjects of comparable age and sex distribution. The mean glomerular filtration rate in the diabetic subjects (216 ml/min) was 57% greater than that of the controls (137.5 ml/min, P < 0.0001). About one-third of their excess in glomerular filtration rate could be accounted for by the marked obesity of the diabetic subjects, but even after correcting for body size the diabetic subjects still had a significantly higher mean glomerular filtration rate than controls (165.6 vs. 119.6 ml/min per 1.73 m2, P < 0.001); 73% of the diabetic subjects had hyperfiltration (> 140 ml/min per 1.73 m2). The diabetic subjects were normotensive but nonetheless had increased rates of albumin excretion (median 61 versus 9 mg/day, P < 0.001). We conclude that hyperfiltration is common in young Polynesians with recently diagnosed type 2 diabetes. Prospective studies are needed to determine whether this early abnormality of renal function heralds the later development of overt nephropathy.
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PMID:Glomerular hyperfiltration in young Polynesians with type 2 diabetes. 785 Dec 69

There have been few reports of follow-up studies on mortality and causes of death from diabetics in Japan. One group of patients with non-insulin-dependent diabetes (NIDDM) was followed up in Osaka and the other group in Tokyo. Results from both studies were almost the same in which diabetic nephropathy and coronary heart disease were important as the causes of death. Because of a small number of patients with insulin-dependent diabetes (IDDM) follow-up studies are difficult in Japan, and only one study was reported from the Diabetes Epidemiology Research International (DERI) Mortality Study Group. Although a very large mortality of IDDM in Japan was reported in this study, this is now improving rapidly.
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PMID:Mortality and causes of death in follow-up diabetic population in Japan. 785 23

The characteristic features of OLETF rats are: (1) late onset of hyperglycemia (after 18 weeks of age); (2) a chronic course of disease; (3) mild obesity; (4) clinical onset of diabetes mellitus (DM) mostly in males; (5) hereditary trait: (a) multiple recessive genes are involved in the induction of DM; (b) rat MHC, RT1 has no diabetogenic effect; (c) control strain, LETO appears to share some of diabetogenic genes with OLETF rats; (d) female OLETF rats also carry diabetogenic genes; and (e) one of the diabetogenic genes, designated as odb-1, is transmitted linked with the X-chromosome of OLETF rats, however testosterone is an important factor involved in developing diabetes; (6) the changes of pancreatic islets can be classified into three stages: (1) an early stage (at less than 9 weeks of age) mild lymphocyte infiltration; (2) a hyperplastic stage (10-40 weeks of age); hyperplastic change and fibrosis in or around islets; (3) a final stage (at more than 40 weeks of age) showing atrophy of islets; (7) diabetic nephropathy; (a) diffuse glomerulosclerosis; (b) nodular lesion (thickening of basement membranes, mesangial proliferation, fibrin cap). These clinical and pathologic features of disease in OLETF rats resemble those of human NIDDM.
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PMID:OLETF (Otsuka Long-Evans Tokushima Fatty) rat: a new NIDDM rat strain. 785 27


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