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)

The value of high polyunsaturated fatty acid (PUFA) diets in preventing diabetic nephropathy in rats was studied. Diabetes was induced by intravenous injection of streptozotocin (SZ), 65 mg/kg. Rats were divided in four groups fed diets containing 11% fat for 38 weeks. Dietary fat derived from four sources: beef tallow (BT; rich in saturated fatty acids), evening primrose oil (EPO; rich in gamma linolenic [GLA] and linoleic acids [LA]), safflower oil (SO; rich in LA), and fish oil (FO; rich in eicosapentaenoic [EPA] and docosahexaenoic [DHA] acids). Ultralente insulin was administered every other day to maintain the blood glucose levels between 11.1 and 22.2 mmol/L (200 and 400 mg/dL). The diets prepared with EPO and SO had a clear beneficial effect on proteinuria, glomerular sclerosis, and tubular abnormalities, as compared with BT. Both diets also increased the ratio of renal cortical production of 6-keto-PGF1 alpha to thromboxane B2 (TXB2), the stable metabolites of PGI2 and TXA2, respectively. They did not induce significant changes in plasma lipid composition. The FO diet did not have an effect on renal disease, but decreased plasma lipids and inhibited eicosanoid synthesis by platelets and kidney cortex. FO feeding was associated with a lowered 6-keto-PGF1 alpha/TXB2 ratio. It is concluded that high LA diets are protective in this model of diabetic nephropathy. The effect may be secondary to modifications of the eicosanoid balance. Diets containing FO have a beneficial effect on plasma lipids in this model.
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PMID:High linoleic acid diets ameliorate diabetic nephropathy in rats. 239 16

Glomerular diseases other than diabetic glomerulosclerosis (DGS) occurring in diabetic patients may pose a diagnostic challenge to both clinicians and pathologists. We studied 15 cases of membranous glomerulonephritis (MG) in patients with diabetes mellitus focusing on the morphologic changes of the kidney. Light microscopic observation revealed nodular and/or diffuse DGS in 12 cases and no DGS in three. Periodic acid-silver methenamine stain showed spikes or chain-like structures in the glomerular capillary wall in 13 cases, indicating the presence of MG. Ultrastructurally, MG was classified into Stage I (N = 2), II (N = 8), III (N = 4), or IV (N = 1). Six out of nine cases with Stages I and II MG showed a thickened lamina densa of the glomerular basement membrane (GBM), suggesting diabetic influence on the GBM. Moreover, MG in some of the cases suggested atypical ultrastructural features including (a) the presence of large immune type deposits separated by tall spikes (N = 4), (b) high electron density of deposits in spite of their intramembranous location (N = 4), and (c) the presence of immune type deposits of mesangial (N = 3) and subendothelial (N = 2) locations. It is postulated that these atypical features are caused by altered turnover of the GBM, impaired glomerular clearance of immune complexes, changes of the glomerular capillary wall as the result of hemodynamic alterations, and/or nonenzymatic glycosylation in diabetic milieu.
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PMID:Membranous glomerulonephritis in diabetic patients: a study of 15 cases and review of the literature. 240 36

To determine the specificity of the urine excretion of albumin as a measure of glomerular permeability in early insulin-dependent diabetic nephropathy, the effect of variable glomerular filtration and urine flow rates on albumin, beta 2-microglobulin excretion, and the fractional renal clearance of neutral dextran (Stokes Einstein Radius 24-46 A) was examined. Five insulin-dependent diabetic subjects with normal glomerular permeability (albumin excretion less than 30 micrograms/min) and one with elevated albumin excretion (195 micrograms/min) were studied pre and post strict glucose control with constant subcutaneous insulin infusion for 7 days. The albumin excretion in the 5 subjects never exceeded 30 micrograms/min during wide variations in glomerular filtration and urine flow rates. A positive correlation between beta 2-microglobulin excretion and urine flow (r = 0.81), and glomerular filtration (r = 0.77) rates was observed. In contrast, albumin excretion showed no correlation, indicating different factors affect the excretion rate of albumin and beta 2-microglobulin. Therefore, elevated albumin excretion (greater than 30 micrograms/min) in insulin-dependent diabetes is due to increased glomerular permeability and not changes in glomerular filtration and urine flow rates, and the albumin/ beta 2-microglobulin ratio may not be a valid indicator of changing glomerular permeability. The fractional neutral dextran clearances remained unchanged with variation in glomerular filtration and urine flow rates. The sieving curve was identical in all subjects for neutral dextran 40 A, the size of albumin, suggesting that reduced glomerular charge selectivity may contribute to increased albuminuria in progressive diabetic glomerulosclerosis.
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PMID:Factors affecting the urinary excretion of albumin in insulin-dependent diabetes. 244 93

Sprague-Dawley rats subjected to subtotal (1 7/8) nephrectomy or streptozotocin diabetes were treated with an angiotensin converting enzyme inhibitor or a calcium channel blocker and their course compared with untreated control animals. Subtotal nephrectomy led to hypertension, proteinuria, reduced creatinine clearance, and glomerulosclerosis over 6 weeks. Enalapril treatment (5 mg/kg/day, n = 11) or felodipine (30 mg/kg/day, n = 11) reduced systolic blood pressure to a comparable degree. Plasma creatinine (mumol/l) was lower after enalapril treatment (110 +/- 8, p less than 0.05) than with felodipine treatment (153 +/- 27) or no treatment (173 +/- 19, n = 18). Proteinuria (mg/24 h) was lower with enalapril treatment (15 +/- 3, p less than 0.001) than with no treatment (85 +/- 22) and increased with felodipine (221 +/- 35). Glomerulosclerosis was reduced with enalapril but not felodipine treatment. Diabetic rats were treated with enalapril (5 mg/kg/day, n = 17), verapamil (5 mg/kg/day, n = 17), or untreated. Diabetic rats had increased creatinine clearance (ml/min) compared with nondiabetic controls (1.52 +/- 0.06 vs. 1.15 +/- 0.05, n = 11, p less than 0.01). Enalapril and verapamil treatment reduced blood pressure equally. Enalapril but not verapamil reduced the elevated creatinine clearance of diabetic rats (enalapril, 1.37 +/- 0.04 ml/min, p less than 0.01; verapamil, 1.49 +/- 0.5 ml/min). Proteinuria (mg/24 h) was lower (p less than 0.05) with enalapril treatment (36 +/- 3) but not with verapamil treatment (58 +/- 10) in comparison to that in untreated diabetes (71 +/- 18).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Disparate effects of angiotensin converting enzyme inhibitor and calcium blocker treatment on the preservation of renal structure and function following subtotal nephrectomy or streptozotocin-induced diabetes in the rat. 245 24

The biosynthesis of uridine 5'-triphosphate (UTP), uridine 5'-diphosphohexoses, and 5'-diphosphohexosamines (UDP-sugars) was studied in isolated rat glomeruli 48 h after streptozotocin-induced diabetes. Compared with control, diabetic glomeruli demonstrated an increase in the following: exogenous orotate utilization, orotate incorporation into UTP and UDP-sugars, UTP accretion rate, and UDP-sugar pool size. Since these phenomena were not associated with enhanced biosynthesis of orotate de novo, the increased glomerular UDP-sugar bioavailability in diabetes is due to enhanced utilization of exogenous orotate. Plasma concentrations of orotate and uridine were measured in control, sham operated, and unilaterally nephrectomized rats receiving 5, 20, or 60% protein diets. The concentration of pyrimidine precursors correlated directly with protein intake, with doubling at the 60% dietary protein level. In conclusion, glomerular uracil ribonucleotide biosynthesis may be modulated by the quantity of dietary protein. Because UDP-sugars are necessary for basement membrane material formation, an increase in their bioavailability may be part of the metabolic change responsible for diabetic glomerulosclerosis. Diets with high protein content could augment this metabolic alteration.
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PMID:Glomerular uracil nucleotide synthesis: effects of diabetes and protein intake. 245 73

Report on 3 cases who had been non-diabetics at the time of cadaver kidney transplantation. After that within 1-5 years diabetes mellitus developed. The patients died 13-14 years after transplantation (9-12 years of diabetes duration). Autopsy revealed typical nodular glomerulosclerosis including diffuse mesangial widening, glomerular aneurysms, exudative lesions, capsular drops, arteriolosclerosis, and in 2 cases with hyalinosis of the vas efferens; moreover, chronic transplant glomerulopathy was found in all cases. Steroid therapy seemed to be responsible for the diabetic state, in 2 cases apparently in combination with disposition.
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PMID:[De novo diabetic glomerulosclerosis in kidney transplants]. 248 8

The nodular lesion in renal glomeruli develops as a localized accentuation of mesangial volume augmentation. First described by Kimmelstiel and Wilson in 1936, it was soon accepted as the characteristic form of glomerular sclerosis in patients with long-term diabetes mellitus. It has for a long time been recognized that lesions very similar to nodular glomerulosclerosis may rarely occur in patients without diabetes. Clinical and pathological investigations of such cases have shown that glomerular nodules can also develop, 1. as a sequal to light chain deposit disease associated with plasma cell dyscrasia (e.g. myelomatosis), 2. in mesangioproliferative and membranoproliferative glomerulonephritis ("lobular" GN) and 3. in some cases of glomerular amyloid deposition. A survey is given of the characteristic light microscopy, ultrastructure and immunopathology of the glomerular nodules in these diseases. The differential diagnosis and pathogenesis is discussed.
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PMID:[Clinical pathology of the glomerulus--from phenomenon to entity. The nodular-lobular lesion]. 248 39

Investigation of the effect of allo- and xenotransplantation of pancreatic tissue cultures on the hemodynamic indices of 85 patients with diabetes mellitus using ophthalmoscopy, biomicroophthalmoscopy, integral rheography, capillaroscopy and clinical biochemical tests at varying time (from 3 mos to 4 yrs.) showed a gradual improvement of the ophthalmological picture of the fundus of the eye in 58 patients (86%) during the first 9 mos with further stabilization of a process. Lower limb improvement was noted in 18% of the patients, stabilization of a process--in 74%. The improvement of the renal clinico-biochemical indices was noted in 47-67%. Contraindications for beta = culture transplantation were diabetic glomerulosclerosis with stage III chronic renal insufficiency and retinopathy of diabetorenal type.
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PMID:[Effect of the transplantation of cultured pancreatic islet cell on the status of diabetic microangiopathy]. 250 Jun 56

A 38-year-old female was admitted to our hospital because of dyspnea. The diagnosis of total lipodystrophy was made by following findings: (1) gaunt appearance; (2) insulin-resistant diabetes mellitus; (3) hyperlipidemia; (4) fatty liver. Chest X-ray demonstrated cardiomegaly, pulmonary edema and pleural effusion. Echocardiogram was characterized by left ventricular hypertrophy with asymmetrical septal hypertrophy and left ventricular dysfunction. Renal biopsy revealed focal glomerulosclerosis. We reported a patient with total lipodystrophy combined with heart failure and renal failure, which have been rarely associated with the disease.
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PMID:Total lipodystrophy with heart failure and renal failure: report of a case. 253 Mar 77

The potential pathogenic role of angiotensin-II (AII) in early progressive diabetic and renal ablation-induced glomerulosclerosis was explored and compared in the Sprague-Dawley (SD) rat and the mongrel dog. Male SD rats were divided into control and streptozotocin-treated (65 mg/kg, iv) groups. Unilateral surgical nephrectomy (Nx) was performed in half of each group. Enalapril (E; 50 mg/liter in the drinking water) was administered to half of each subgroup. Enalapril (high E; 250 mg/liter) was given to another 13 streptozotocin rats. All diabetic rats were treated with sc NPH insulin (4 U/day), and blood glucose was 520 +/- 124 mg/dl (mean +/- SD). Microalbuminuria was measured by RIA in 24-h urine collections; wet kidney weights were compared. [125I]AII binding assays were performed on isolated glomeruli. In control rats the high affinity binding dissociation constant (Kd) was 0.59 +/- 0.15 nM (n = 26; mean +/- SD) and receptor number (Ro) was 732 +/- 195 fmol/mg glomerular protein. At 3 weeks, the diabetic glomerular AII receptor Kd was 0.38 +/- 0.07 nM (n = 6; P less than 0.02 vs. control) and Ro was 784 +/- 97 fmol/mg protein (P = NS vs. control); diabetic high E Kd was 0.39 +/- 0.06 nM (n = 6; P less than 0.02 vs. control), and Ro was 873 +/- 105 fmol/mg protein (P = NS vs. diabetes without E). By 10 weeks, a Kd of 0.49 +/- 0.12 nM (n = 32; P less than 0.01 vs. control) and a Ro of 780 +/- 174 fmol/mg protein (P = NS vs. control) were observed when all of the diabetic group data were pooled. Neither Nx nor low or high dose E altered Ro. This is evidence that intraglomerular AII levels are normal or reduced after diabetes, Nx, or both. In the diabetic group, low dose E partially prevented, and high E abolished, Nx-enhanced microalbuminuria and renal hypertrophy. In nine pancreatectomized insulin-treated mongrel dogs over a 12- to 24-month period, despite moderately poor glucose control (300 +/- 75 mg/dl) and combined unilateral Nx in five dogs (12 months), elevated microalbuminuria was not observed. [125I]AII binding to isolated normal and diabetic dog glomeruli revealed the Kd to be of low affinity (1.86 +/- 0.28 to 13.80 +/- 1.88 nM), identifying the presence of type B receptors. Hence, the SD rat and mongrel dog differ in susceptibility to glomerular AII receptor type and progressive diabetic glomerulopathy.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The role of angiotensin-II in progressive diabetic glomerulopathy in the rat. 255 33


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