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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The protective effect of phosphate binder (PB) on nephropathy was examined in spontaneously hypertensive rats with non-insulin-dependent diabetes mellitus (NIDDM) fed a high-protein diet. The rats were treated with vehicle or streptozocin neonatally. After 14 weeks, all rats were fed a high-protein diet (50% protein content), and in half of the diabetic rats the diets were supplemented with PB. At 24 weeks, the urinary excretion rate of albumin and kidney weight increased in diabetic rats, but decreased or tended to decrease in diabetic rats treated with PB. The elevation of urinary excretion rate of N-acetyl-beta-D-glucosaminidase, probably due to protein load, was also abolished with PB.
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PMID:Phosphate depletion with phosphate binder arrests the development of nephropathy in spontaneously hypertensive rats with non-insulin-dependent diabetes mellitus fed a high-protein diet. 177 37

Type 1 diabetes mellitus is associated with an increase in total exchangeable body sodium. To delineate a site of possible altered sodium handling, proximal tubular sodium reabsorption (PTRNa) was measured in 30 diabetic children, age 12.0 (range 7-16) yr, duration of diabetes 4.5 (range 0.2-12) yr, and compared with 10 non-diabetic children, age 10.0 (range 8.6-12.5) yr. PTRNa was calculated from the fractional clearance of lithium, which was determined from a single blood sample and a random untimed urine sample, taken between 0700 and 0830 h at home, fasting, before insulin therapy. PTRNa was significantly increased in the diabetic children compared with the non-diabetic children (81.6(SE 1.0) vs 74.2(2.6)%, p = 0.014). There was no relationship of PTRNa with age, duration of diabetes, metabolic control (glycosylated haemoglobin, plasma and urinary glucose, plasma lactate), or urinary protein excretion (albumin, N-acetyl-beta-D-glucosaminidase). Elevated sodium reabsorption in the proximal renal tubule may account for the high total exchangeable body sodium found in Type 1 diabetic patients.
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PMID:Increased proximal tubular reabsorption of sodium in childhood diabetes mellitus. 182 44

The excretion of urinary growth hormone was measured by a highly sensitive direct immunoradiometric assay in a cross-sectional study during puberty in 70 children with Type 1 (insulin-dependent) diabetes mellitus and 94 normal children. In normal children (n = 24) and diabetic children (n = 17) overnight urinary growth hormone excretion correlated significantly with the mean overnight plasma concentration (r = 0.70, p less than 0.001, and r = 0.70, p less than 0.001), indicating that urinary GH excretion reflects the circulating endogenous GH level. Overnight urinary growth hormone excretion increased during puberty. In normal and in diabetic children there was a peak in boys at genital stage 4 (both p less than 0.01), and in girls at breast stage 2 (both p less than 0.02). The diabetic children excreted more urinary growth hormone than the normal children at every pubertal stage. Excretion of albumin, retinol binding protein and N-acetyl-beta-D-glucosaminidase was measured in urine from 38 diabetic children. Urinary growth hormone correlated weakly with urinary albumin (r = 0.49, p less than 0.01), retinol binding protein (r = 0.42, p less than 0.01), and N-acetyl-beta-D-glucosaminidase (r = 0.43, p less than 0.01). Urinary GH excretion was not related to blood glucose control (HbA1) in boys (n = 31) or girls (n = 39). The measurement of urinary growth hormone provides an assessment of endogenous growth hormone during puberty in normal and diabetic children. However, caution must be exercised in interpreting urinary growth hormone data from diabetic patients with increased excretion of albumin and retinol binding protein.
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PMID:Urinary growth hormone excretion during puberty in type 1 (insulin-dependent) diabetes mellitus. 182 39

Urinary excretion of transferrin and albumin was studied by radioimmunoassay in 47 adult patients with Type 1 diabetes and 28 control subjects. Median (range) urinary transferrin excretion rate was significantly elevated in the diabetic group 0.58 (0.02-2663.3) micrograms min-1 compared with the control group 0.04 (0.01-0.28) micrograms min-1, p less than 0.001. Urinary transferrin:creatinine ratios (x 10(2)) were different in diabetic 47 (0.6-958.0) micrograms mmol-1 and control groups 0.7 (0.06-2.3) micrograms mmol-1, p less than 0.001). There were correlations between urinary transferrin and albumin excretion rates in diabetic (r = 0.78, p less than 0.001) and control groups (r = 0.81, p less than 0.05). Forty (85%) diabetic patients had elevated transferrin excretion rates, 18 (38.3%) had elevated albumin excretion rates. All diabetic patients with elevated albumin excretion rates had elevated transferrin excretion rates. Twenty-one (77.8%) of the patients with normal albumin excretion rates had elevated transferrin excretion rates. Urinary excretion of N-acetyl-beta-D-glucosaminidase was greater in diabetic patients than control subjects (142 vs 58 mumol h-1 l-1, p less than 0.001). There were correlation between transferrin and N-acetyl-beta-D-glucosaminidase excretion (r = 0.67, p less than 0.01) and albumin and N-acetyl-beta-D-glucosaminidase excretion (r = 0.63, p less than 0.01) in the diabetic group. Elevated urinary transferrin excretion rate may be a marker for renal dysfunction in diabetes mellitus.
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PMID:Urinary transferrin excretion in type 1 (insulin-dependent) diabetes mellitus. 183 18

Urinary excretion rates of transferrin, albumin, N-acetyl-beta-D-glucosaminidase (NAG) and alpha-1-microglobulin (A1M) were measured in type 2 (non-insulin-dependent) diabetic patients at diagnosis and after 6 and 12 weeks treatment. Initially 21 (53%) patients had elevated transferrin excretion rates. The proportion of patients with raised transferrin excretion rates fell to 30% at 6 weeks and 20% at 12 weeks with treatment of diabetes. At diagnosis 11 (28%) patients had elevated albumin excretion rates and 10 of these had elevated transferrin excretion rates. After 6 weeks treatment only six (15%) had elevated albumin excretion rates and by 12 weeks this number had fallen to four (10%). NAG and A1M levels also fell with treatment of diabetes. There were correlations between the transferrin excretion rate and albumin excretion rate (r = 0.86, P less than 0.0001), transferrin excretion rate and NAG (r = 0.46, P less than 0.0001), and transferrin excretion rate and A1M (r = 0.55, P less than 0.0001) at each visit. There were weaker correlations between the albumin excretion rate and A1M and NAG at each visit. The correlations between the transferrin excretion rate and markers of tubular function (NAG and A1M) suggest that tubular dysfunction may play a part in renal loss of transferrin in diabetes mellitus. There were no differences in transferrin excretion rates between patients with and without evidence of complications.
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PMID:Transferrinuria in type 2 diabetes: the effect of glycaemic control. 185 56

Pravastatin, a novel inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, was administered to nine hypercholesterolemic patients with diabetes mellitus to examine its effects on diabetic nephropathy. Pravastatin treatment resulted in lowering serum total cholesterol by 22.1% on the average (p less than 0.001), and led to a significant reduction in urinary excretion of albumin and beta 2-microglobulin in patients with an elevated urinary protein excretion rate at the baseline period. But glycemic control, blood pressure, urinary excretion of creatinine and that of N-acetyl-beta-D-glucosaminidase showed no significant change during the study. These results suggest that reduction of atherogenic lipids and lipoproteins with pravastatin could alleviate diabetic glomerular injury.
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PMID:Amelioration of proteinuria with pravastatin in hypercholesterolemic patients with diabetes mellitus. 212 49

In 55 patients with diabetes mellitus the significant quantitative increase in numbers of N-acetyl-beta-D-glucosaminidase-positive lymphocytes in the peripheral blood has been examined by cytochemical methods. The enzyme-positive lymphocytes of these patients were characterized by prevalence of extralysosomal localization of the enzyme and a decrease in the numbers of those cells having intact enzyme-positive lysosomes. No association between these alterations and therapy with insulin or oral hypoglycemic drug and overweight could be stated.
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PMID:N-acetyl-beta-D-glucosaminidase in lymphocytes of patients with diabetes mellitus. 241 66

The influences of glucose, the benzothiadiazide derivative diazoxide (an inhibitor of insulin release), and the potent non-glucose insulin secretagogue 3-isobutyl-1-methylxanthine (IBMX) on insulin secretion and the activities of 3 different lysosomal enzymes were studied in isolated mouse islets. We found that the increase in insulin secretion during a 4 hr incubation period in the presence of 16.7 mM glucose was accompanied by an increase in islet activities of the lysosomal enzymes acid amyloglucosidase and acid alpha-glucosidase. These alpha-1,4-glucoside splitting enzyme activities were increased by 45-55% (p less than 0.01). No influence by glucose was encountered for the activities of N-acetyl-beta-D-glucosaminidase or the non-lysosomal neutral alpha-glucosidase. Upon incubation with 0.2 mM diazoxide and glucose (16.7 mM) the glucose-induced insulin secretion was markedly suppressed and no significant increase in islet lysosomal enzyme activities was observed. On the other hand, insulin secretion induced by IBMX to the same magnitude as with 16.7 mM glucose, was accompanied by an increase in islet activity of N-acetyl-beta-D-glucosaminidase (p less than 0.05), whereas no apparent changes in acid amyloglucosidase and acid alpha-glucosidase activities could be detected. In conclusion, the determination of lysosomal enzyme activities in isolated mouse islets revealed that glucose was able to induce an increased activity of glucose producing glycogenolytic acid hydrolases under conditions when a concomitant insulin secretion occurred.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes Res 1986 Oct
PMID:Insulin secretion and lysosomal enzyme activities in isolated mouse islets. Effects of glucose, diazoxide and isobutylmethylxanthine. 243 78

In the second morning urine of 51 patients with diabetes mellitus (type I/II) albumin, N-acetyl-beta-D-glucosaminidase (NAG), alpha 1-microglobulin (alpha 1-M/U), creatinine (reference parameter) as well as serum alpha 1-microglobulin and creatine were determined. Following an international expert recommendation, three groups were formed depending on albumin excretion: group 1: albumin less than 24 mg/g creatinine (normal range) group 2: albumin greater than 24 mg/g creatinine and less than 200 mg/g creatinine (so called microalbuminuria) group 3: albumin greater than 200 mg/g creatinine (manifest proteinuria) The urinary tubular parameters NAG and alpha 1-microglobulin were above normal range in 17 and 21% respectively in group 1. For group 2 the results were abnormal in 94 and 69% and for group 3 in 100% of patients. Albuminuria correlated with NAG activity, but not with alpha 1-microglobulin excretion. These results indicate, that measuring NAG and alpha 1-microglobulin as markers for tubular dysfunction can give additional diagnostic informations about type and degree of diabetic nephropathy.
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PMID:[Urinary proteins in patients with diabetes mellitus]. 247 8

There is evidence that increased excretion of urinary enzymes and low-molecular mass proteins indicate impaired tubular function. The excretion of N-acetyl-beta-D-glucosaminidase (NAG), lysozyme, and ribonuclease in Type I diabetic patients with (n = 19) and without (n = 17) persistent proteinuria (urinary protein excretion greater than 0.5 g/day) was investigated and compared with this excretion in 30 weight- and gender-matched nondiabetic subjects without renal disease. Urinary NAG excretion was significantly higher in diabetic patients with and without persistent proteinuria (1.16 +/- 0.09 and 3.19 +/- 1.2 Umol/L creatinine, respectively) compared to controls (0.37 +/- 0.03 Umol/L creatinine p less than 0.01). In addition, the urinary excretion of lysozyme and ribonuclease was significantly increased in diabetic patients. Urinary NAG was found to correlate positively with albuminuria and proteinuria (r = 0.95 and 0.93, respectively), as well as with ribonuclease and lysozyme (r = 0.93 and 0.60; p less than 0.01) in patients with persistent proteinuria. Furthermore, NAG excretion was significantly related to the duration of diabetes (r = 0.36; p less than 0.05). No relationship existed between urinary NAG and serum creatinine, beta-2-microglobulin, and degree of metabolic control (HbA7). The lysozyme excretion, but not NAG excretion, was significantly related to hypertension in patients with clinical proteinuria. In conclusion, our results suggest a relationship between the development of tubular dysfunction and the impairment of glomerular function in diabetic nephropathy. An increased excretion of NAG and low-molecular mass proteins may indicate early nephropathy
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PMID:Further evidence for tubular dysfunction in insulin dependent diabetes. 252 61


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