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

The antihypertensive effect and side-effects during 12 months' treatment with bendroflumethiazide and propranolol have been compared in two randomly selected, equally large groups (n= 53) of previously untreated male hypertensives. Systolic BP above 170 or diastolic BP above 105 mmHg on two occasions were defined as hypertension. The same BP reduction was achieved in both groups. During the 12 months' treatment one subject on bendroflumethiazide developed diabetes mellitus and one on propranolol developed cardiac decompensation. None developed gout. Contrary to what had been presumed, glucose tolerance improved during 12 months' treatment with both agents, while there were no changes in fasting blood sugar, insulin or triglyceride concentrations. No changes were found in serum potassium or total body potassium during 12 months' bendroflumethiazide treatment, while serum potassium increased during treatment with propranolol. Uric acid increased slightly during treatment with both agents. Prolongation of the follow-up to 24 months did not change any of the findings regarding metabolic changes during treatment. The frequency of subjective side-effects decreased to the same extent during treatment with both drugs. It is concluded that bendroflumethiazide and propranolol are equally useful as antihypertensive agents and that the risk of impariment of glucose metabolism and potassium balance seems to be very slight during treatment with bendroflumethiazide in mild hypertension.
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PMID:Antihypertensive effect and side-effects of bendroflumethiazide and propranolol. 93 76

To investigate if age of patients, time on CAPD, episodes of peritonitis, or systemic illness (diabetes) may affect the permeability of the peritoneal membrane to small solutes, 51 patients (eight diabetic) 57.2 +/- 9.4 years of age undergoing long-term CAPD were enrolled in a prospective study of peritoneal clearances (PC), started in January 1982. The studies were repeated, when possible, every 6 months after peritonitis episodes. The results were divided according to osmolality of solutions and dwell time. The age of patients had no influence on results. Significantly positive correlations were found between PC (1.36%) of creatinine, uric acid, phosphate, and time on CAPD. Uric acid PC (3.86%) correlated directly with time on CAPD. The PC in diabetic and nondiabetic patients were similar. Patients who had more than three episodes of peritonitis showed PC similar to those observed in patients who had less than three episodes, despite a longer time on CAPD. The stability of PC in patients undergoing long-term peritoneal dialysis suggests that CAPD may permit effective dialysis over many years.
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PMID:Peritoneal clearances. Long-term study. 319 43

The relationships between serum uric acid, serum glucose and diabetes have been examined in a survey of 7735 middle-aged men drawn at random from general practices in 24 British towns. There was a positive relationship between serum glucose and serum uric acid concentrations up to about 8.0 mmol/l; at higher levels of glucose, serum uric acid decreased. Uric acid levels were significantly reduced in insulin-dependent diabetics and in those on oral hypoglycaemics and also in 'non-diabetics' with casual glucose levels greater than 10 mmol/l. Both uric acid and glucose concentrations were positively related to body mass index; only uric acid was positively related to alcohol intake. Men on antihypertensive treatment had raised levels of uric acid (significant) and glucose (non-significant). The positive relationship between serum uric acid and serum glucose could not be explained by associations with body mass index, alcohol intake, age, social class, gout or treatment for hypertension. It probably reflects the biochemical interaction between serum glucose and purine metabolism, with increased excretion of uric acid during hyperglycaemia and glycosuria.
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PMID:Serum uric acid, serum glucose and diabetes: relationships in a population study. 362 42

As part of a study of the epidemiology of diabetes mellitus in middle-aged Swedish men, the present paper reports the prevalence and incidence of diabetes and the prevalence of impaired glucose tolerance. Two cohorts of 50-year-old men, representative of the corresponding male population of Gothenburg, Sweden, were examined in 1963 and 1973, respectively, and then followed until 1980. In the cohort of men born in 1913 (n = 855) the diabetes prevalence (WHO criteria), based on a questionnaire and fasting blood glucose, increased from 1.5% at age 50 to 7.6% at age 67. In the cohort of men born in 1923 (n = 226) the prevalence was 3.7% at age 50 and 4.0% at age 57. The overall prevalence of diabetes and impaired glucose tolerance was 25% among men born in 1913 (age 67) and 18% among men born in 1923 (age 57). The cumulative risk of developing diabetes from age 50 to 67 was 7.8%. Variables associated with impaired glucose tolerance and newly found diabetes, when degree of obesity was considered, were systolic blood pressure and triglycerides, well known risk factors for both coronary heart disease and diabetes. Uric acid, fasting insulin and glutamic puruvic transaminase, recently discussed as possible risk factors, were also associated with impaired glucose tolerance and newly found diabetes. Thus, both impaired glucose tolerance and newly found diabetes were associated with a clustering of risk factors, not only for diabetes but also for coronary heart disease.
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PMID:Diabetes mellitus in Swedish middle-aged men. The study of men born in 1913 and 1923. 367 59

Fasting plasma cholesterol, triglycerides and uric acid were measured in 109 Melanesian residents of Port Moresby and 71 residents of a Papuan coastal village. Cholesterol and triglyceride levels were low, mean cholesterol 3 . 74 and 3 . 70 mM/l and triglycerides 0 . 64 and 0 . 59 mM/l respectively in urban and rural residents, with no relation to age or sex. Uric acid was higher in urban men (0 . 37 mM/l) than either urban women (0 . 26 mM/l) or rural men and women (0 . 25 and 0 . 24 mM/l). The levels of plasma cholesterol found in this study are similar to previous reports on rural populations in Papua New Guinea. The apparent failure of plasma lipids to increase significantly in urbanised residents of port Moresby who had a significantly higher prevalence of both diabetes mellitus and obesity is unexplained.
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PMID:Plasma cholesterol, triglyceride and uric acid in urban and rural communities in Papua New Guinea. 700 59

Uric acid metabolism was investigated in 69 insulin-treated male diabetic outpatients and in 23 healthy male subjects, because of a reported coincidence between diabetes and gout. All subjects had normal serum creatinine concentrations and none received diuretic treatments. Compared with normal, the diabetics had significantly lower mean serum uric acid concentrations (0.34 +/- 0.08 (SD) mmol/l versus 0.23 +/- 0.06 mmol/l, p less than 0.001). 17% of the diabetic patients had serum concentrations below the normal mean--2 SD. In contrast, the diabetic patients had a 42% increase in renal uric acid excretion rate (p less than 0.01), and an 83% increase in the ratio of uric acid clearance/creatinine clearance (p less than 0.001). These indices of renal uric acid excretion were both positively correlated to fasting blood glucose levels (r=0.57, p less than 0.001, and r=0.50, p less than 0.001, respectively), to the degree of glycosuria (r=0.73, p less than 0.001, and r=0.63, p less than 0.001, respectively), and to the magnitude of water diuresis (r=0.60, p less than 0.001, and r=0.39, p less than 0.01, respectively). The hypouricaemia observed in these insulin-dependent diabetic male subjects may probably be caused by the increased renal excretion of uric acid in the presence of hyperglycaemia. The study gave no evidence of increased serum uric acid concentrations in insulin-dependent diabetics. It is therefore likely that any coincidence between gout and diabetes derives from other coexisting serum uric acid raising factors.
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PMID:Renal hypouricaemia in insulin treated diabetes mellitus. 704 28

By central venous catheterization, 6 control persons, 7 patients with liver cirrhosis and 6 patients with diabetes mellitus were infused for 48 h with a 20% (w/v) mixture of glucose/xylitol (1:1). The infusion 48 h with a 20% (w/v) mixture of glucose/xylitol (1:1). The infusion rate of 0.125 g monosaccharide/kg/h could be maintained with minor deviations. There were no significant changes in blood glucose levels using this infusion regimen. Lactate levels, however, did increase constantly during the whole infusion period. In the liver group as well as in the diabetic group we could measure values between 1.5 and 3.9 mmol/l. Triglycerides increased solely in the diabetic group. Uric acid concentrations were elevated in all 3 groups. Clinically significant side effects were not observed.
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PMID:[Carbohydrate infusion in internal diseases. A comparative study in metabolically healthy, liver diseased and diabetic patients. VI. Infusions of a glucose/xylitol mixture (1:1 ratio) over a 48-hour period]. 704 70

Urokinase (u-PA) dissolves and removes fibrin deposits in the renal secretory pathways in various renal diseases. During pregnancy nephropathy creates a problem in preeclampsia and diabetes, but the underlying mechanism of glomerular damage is different. Preeclamptic nephropathy is characterized as 'glomerular endotheliosis' with hypertrophy of the intracapillary cells, and diabetic nephropathy as 'glomerulosclerosis' with hyaline deposits. The role of fibrin deposition for the etiology of renal damage in preeclampsia is controversial. Changes of the urinary secretion of u-PA may reflect the type of glomerular damage. Our hypotheses were that renal insufficiency is associated with a low u-PA activity in both conditions, and that severe disease is parallel to declining concentrations of u-PA. We compared the glomerular filtration rate, S-Creatinine and S-Urate with urinary u-PA excretion in 24 hypertensive and 20 diabetic pregnant women. In diabetic patients, a low u-PA concentrations was associated with an impaired renal function. In hypertensive pregnancy, the u-PA excretion did not reflect the severity of the hypertensive disease or renal function. No association was found between u-PA excretion and renal function post partum in any group. We conclude that renal urokinase activity plays a role for renal function in diabetic but not in hypertensive pregnancy.
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PMID:Renal function and urinary urokinase in hypertensive and diabetic pregnancies. 782 57

Most of the primates, unlike other mammals, have mutations in urate oxidase gene and cannot catabolize urate in the bodies. In addition to the genetic defects, some human subjects have various abnormalities in urate metabolism. Urate metabolism abnormalities are classified into two categories, hyperuricemia and hypouricemia. Usually, the urate pool size of an adult male is about 1,200 mg, and 700 mg urate is produced daily. The production is balanced by the excretion of urate into urine (500 mg) and intestine (200 mg). If this balance is disturbed, either hyperuricemia or hypouricemia occurs. According to the mechanisms, hyperuricemia is classified into overproduction and underexcretion, and hypouricemia into underproduction and overexcretion. Overproduction of ruate is caused by PRPP synthetase superactivity, HPRT deficiency, leukemia and alcohol ingestion. Underexcretion of urate is caused by renal insufficiency and treatment by diuretics. Underproduction of urate is caused by xanthine dehydrogenase deficiency, purine nucleoside deficiency and allopurinol treatment. Overexcretion of urine is caused by familial renal hypouricemia, Fanconi's syndrome, diabetes mellitus and treatments with benzbromarone and probenecid. All of these conditions are classified, according to other aspects, into primary and secondary, and genetic and non-genetic abnormalities.
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PMID:[Abnormalities in urate metabolism: concept and classification]. 897 99

D-tagatose, a stereoisomer of D-fructose, is a naturally occurring ketohexose proposed for use as a low-calorie bulk sweetener. Ingested D-tagatose appears to be poorly absorbed. The absorbed portion is metabolized in the liver by a pathway similar to that of D-fructose. The main purpose of this study was to determine if acute or repeated oral doses of D-tagatose would cause elevations in plasma uric acid (as is seen with fructose) in normal humans and Type 2 diabetics. In addition, effects of subchronic D-tagatose ingestion on fasting plasma phosphorus, magnesium, lipids, and glucose homeostasis were studied. Eight normal subjects and eight subjects with Type 2 diabetes participated in this two-phase study. Each group was comprised of four males and four females. In the first phase, all subjects were given separate 75 g 3-h oral glucose and D-tagatose tolerance tests. Uric acid, phosphorus, and magnesium were determined in blood samples collected from each subject at 0, 30, 60, 120, and 180 min after dose. In the 8-week phase of the study, the normals were randomly placed into two groups which received 75 g of either D-tagatose or sucrose (25 g with each meal) daily for 8 weeks. The diabetics were randomized into two groups which received either 75 g D-tagatose or no supplements of sugar daily for 8 weeks. Uric acid, phosphorus, magnesium, lipids, glycosylated hemoglobin, glucose, and insulin were determined in fasting blood plasma of all subjects at baseline (time zero) and biweekly over the 8 weeks. The 8-week test did not demonstrate an increase in fasting plasma uric acid in response to the daily intake of D-tagatose. However, a transient increase of plasma uric acid levels was observed after single doses of 75 g of D-tagatose in the tolerance test. Plasma uric acid levels were found to rise and peak at 60 min after such dosing. No clinical relevance was attributed to this treatment-related effect because excursions of plasma uric acid levels above the normal range were small and were of short duration. Consistent with earlier observations on fructose, the increase of plasma uric acid was associated with a slight decrease of plasma phosphorus and a slight increase of magnesium. The daily ingestion of D-tagatose for 8 weeks had no effect on fasting plasma magnesium, phosphorus, cholesterol, triglycerides, glycosylated hemoglobin, glucose, and insulin levels. The ingestion of three 25-g doses per day for a period of 8 weeks resulted in varying amounts of flatulence in seven of the eight subjects, and some degree of diarrhea in six subjects. D-tagatose holds promise as a sweetener with no adverse clinical effects observed in these studies.
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PMID:Effects of acute and repeated oral doses of D-tagatose on plasma uric acid in normal and diabetic humans. 1034 Nov 62


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