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

Administration of a high-protein diet providing 7-7.8 g of tryptophan per kg of the ration to rats with streptozotocin and alloxan diabetes mellitus resulted in development of a trend to increased liver content of nicotinamide coenzymes and in increased 1-methylnicotinamide excretion with the urine in both groups of animals, this reflecting increased niacin synthesis from tryptophan. Sugar-reducing effect of high-dose nicotinamide was not potentiated by increase of protein share in the ration. These results permitted the authors to suggest that intensification of endogenous niacin synthesis from tryptophan contained in the ration may be one of the mechanisms of a protective effect of high-protein diets in diabetes.
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PMID:[Body niacin status in experimental diabetes mellitus; effect of protein level in the ration]. 816 15

Dietary intake was assessed, using a 3-day recorded food diary, in 122 patients with insulin-dependent diabetes. Subjects were selected randomly from patients attending a diabetic clinic and stratified for age, sex, and duration of diabetes. The findings were compared to the dietary recommendations of the European Association for the Study of Diabetes (EASD) and to the findings in a recent Irish National Nutrition Survey. The average daily protein intake among diabetic patients was 18% of the total calories, significantly higher than recommended by EASD and significantly higher than in the age-matched general population. Dietary fat intake was on average 37% of total calorie intake, again significantly higher than recommended and greater than in the general population among older patients. Saturated fat intake was higher than recommended and polyunsaturated fat intake was low. The average carbohydrate intake was 42% of total calories, significantly lower than recommended and similar to that in the general population. Sugar intake was lower and starch intake was higher among patients than in the general population, however. Fibre intake was also lower than recommended, but was higher than in the general population. We conclude that the present dietary targets for diabetic patients are not being fully achieved.
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PMID:Are the nutritional recommendations for insulin-dependent diabetic patients being achieved? 818 Dec 58

Sugar-3-phosphates are related to aspects of diabetes which depend on protein glycosylation events. Sorbitol-3-phosphate and fructose-3-phosphate occur in normal and diabetic individuals, and glucose-3-phosphate is a potential intermediate in their biosynthesis. Almost nothing is known about enzyme pathways for their metabolic turnover. We have found that part of the phosphohydrolytic activity on glucose-3-phosphate in rat liver supernatants corresponds to a specific, Mg(2+)-dependent, glucose-3-phosphatase much less or not active on other phosphate esters, including glucose-1-phosphate, glucose-6-phosphate, fructose-1-phosphate, fructose-6-phosphate and p-nitrophenyl-phosphate. This finding opens a route to a better understanding of the metabolism and role of sugar-3-phosphates.
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PMID:Detection of specific glucose-3-phosphatase activity in rat liver. 831 79

Sugar alcohols have been reported to accumulate in retinal pigment epithelium (RPE) of diabetic animals. This finding has raised interest in the role of RPE in diabetes-associated retinal changes such as cystoid macular edema. To confirm the presence of aldose reductase in this tissue, the NADPH-dependent enzyme was purified to an apparent homogeneity from cultured human RPE cells, characterized, and its biochemical properties investigated. The induction of aldose reductase by hypertonic stress was also examined. The purification of aldose reductase was performed by a series of chromatographic steps which include gel filtration, affinity chromatography and chromatofocusing. Final purity achieved was monitored by SDS-polyacrylamide gel electrophoresis (SDS-PAGE). The kinetic properties and susceptibility to inhibition of the purified aldose reductase were essentially identical to aldose reductase purified from human placenta and kidney. In addition to aldose reductase, chromatofocusing demonstrated the presence of aldehyde reductase, another NADPH-dependent reductase. However, the amounts of aldehyde reductase present were much smaller than those of aldose reductase and the levels of aldehyde reductase appeared too small to contribute to the polyol production in the RPE cells. Culture of RPE cells in hypertonic medium containing 150 mM sodium chloride (600 mosmol total) increased both reductase activity, monitored with DL-glyceraldehyde as substrate, and immunoblot staining for aldose reductase. Chromatofocusing of RPE cells cultured in hypertonic media resulted in a prominent increase in the peak corresponding to aldose reductase compared to the peak height of cells grown in control medium. No increase in aldehyde reductase from RPE cells cultured in hypertonic medium was observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Aldose reductase in human retinal pigment epithelial cells. 840 90

To investigate the pathogenesis of diabetic neuropathy in non-insulin-dependent diabetes mellitus, Otsuka Long-Evans Tokushima Fatty rats, an animal model of non-insulin-dependent diabetes mellitus, and non-diabetic Long-Evans Tokushima Otsuka rats were fed with or without sucrose and/or cilostazol, an anticoagulant, for 8 weeks. Sucrose-fed diabetic rats showed a delayed motor nerve conduction velocity, decreased R-R interval variability of electrocardiogram, reduced sciatic nerve blood flow, increased platelet aggregability and a decreased erythrocyte 2,3-diphosphoglycerate concentration compared with non-sucrose-fed diabetic rats and non-diabetic rats. These abnormalities were significantly prevented by treatment with cilostazol without changes in the nerve tissue levels of polyols. These findings indicate that sucrose-fed Otsuka Long-Evans Tokushima Fatty rats may be a useful animal model of neuropathy in non-insulin-dependent diabetes mellitus, and that cilostazol may prevent the development of diabetic neuropathy by modifying vascular factors.
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PMID:Nerve function and blood flow in Otsuka Long-Evans Tokushima Fatty rats with sucrose feeding: effect of an anticoagulant. 891 16

Recent reports suggest that excess amounts of sugar alcohol are linked to leukocyte dysfunctions associated with diabetes. As the polyol pathway has not been firmly established in leukocytes, we have investigated NADPH-dependent reductases and sugar alcohol formation in dog leukocytes. NADPH-dependent reductase activity was observed with DL-glyceraldehyde as substrate in both mononuclear and polymorphonuclear leukocytes isolated from dog. By chromatofocusing, this activity corresponded primarily to aldehyde reductase rather than aldose reductase. The enzymatic conversion of glucose to the sugar alcohol sorbitol in leukocytes was confirmed in vitro by 19F nuclear magnetic resonance (NMR) spectroscopy using 3-deoxy-3-fluoro-D-glucose as substrate. The NMR spectrum obtained after incubation with 10 Mm 3-deoxy-3-fluoro-D-glucose at 37 degrees C for 24 h displayed newly formed 3-deoxy-3-fluoro-D-sorbitol and 3-deoxy-3-fluoro-D-fructose peaks with both mononuclear and polymorphonuclear leukocytes. Sugar alcohol production in leukocytes from galactose-fed dogs was also observed in vivo. Galactitol accumulation was consistently observed by gas chromatography to occur in mononuclear cells while only trace amounts of galactitol were observed in polymorphonuclear leukocytes. Activation of NADPH oxidase activity in neutrophils isolated from galactose-fed dogs by zymosan was also significantly reduced compared to that of nongalactosemic control dogs. These results indicate that glucose is converted to fructose through sorbitol in both mononuclear and polymorphonuclear leukocytes despite the observations that these cells primarily contain aldehyde reductase rather than aldose reductase. In vivo, sugar alcohol accumulation in mononuclear cells is greater than in polymorphonuclear leukocytes.
J Diabetes Complications
PMID:Polyol pathway and NADPH-dependent reductases in dog leukocytes. 897 81

The aim of the present study was to evaluate the effects of three fibres (sugar-beet fibre, guar gum and inulin) incorporated in the basal diet of healthy dogs at 7 per cent of dry matter (DM). Parameters examined included stool output, water consumption, nutrient digestibility and fasting and postprandial plasma metabolites. All fibres increased wet faecal output; an increase in faecal DM output being observed with sugar-beet fibre only. Sugar-beet fibre and inulin increased daily water consumption. Sugar-beet fibre and guar gum decreased DM digestibility. The three fibres diminished organic matter and crude protein digestibility while ether extract digestibility was decreased by guar gum and inulin. Guar gum induced lower postprandial insulin, alpha-amino-nitrogen and urea plasma concentrations. Guar gum also lowered fasting cholesterolaemia. Sugar-beet fibre and inulin showed no metabolic effects. These physiological properties suggest that guar gum would be a suitable ingredient for dietary therapy of chronic diseases such as diabetes mellitus or hyperlipidaemia in the dog.
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PMID:The influence of sugar-beet fibre, guar gum and inulin on nutrient digestibility, water consumption and plasma metabolites in healthy Beagle dogs. 962 62

The Goto-Kakizaki (GK) rat is a spontaneously diabetic animal model of non-insulin-dependent diabetes mellitus, which is characterized by progressive loss of beta cells in the pancreatic islets with fibrosis. In the present study, we examined the effects of sucrose feeding on the islet pathology in this model. Six-week-old GK rats were fed with 30% sucrose for 6 weeks to induce severe hyperglycemia, and their condition was compared with that of nontreated rats. Age-matched normal Wistar rats were also given sucrose for the same periods and used for comparison. The sucrose-treated GK rats showed elevated blood glucose levels on oral glucose tolerance tests at 60 minutes and 120 minutes, representing 123% and 127% of values in untreated GK rats, respectively. At the end of the study, the mean beta-cell volume density in GK rats was 50% less than that in untreated Wistar rats. Sucrose feeding further reduced the volume densities of beta cells to only 50% of the levels of age-matched GK rats. Apoptotic cells were found in islet beta cells only in GK rats fed sucrose (mean 0.067%). There appeared to be more islets that immunohistochemically stained strongly positive with 8-hydroxy-deoxyguanosine as a marker of oxidative damage of DNA in GK rats fed sucrose compared with those not given sucrose. GK rats not fed sucrose showed significantly lower proliferative activity of beta cells measured by 5-bromo-2'-deoxyuridine uptake and intensified expression of Bcl-2 immunoreactivities at 6 weeks of age compared with those in age-matched Wistar rats. These two indices were reduced in both GK and Wistar rats with increasing age and were not affected by sucrose feeding in either group. The present study thus indicated that sucrose feeding promoted the apoptosis of beta cells in GK rats through increased oxidative stress without altering their proliferative activity.
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PMID:Accelerated loss of islet beta cells in sucrose-fed Goto-Kakizaki rats, a genetic model of non-insulin-dependent diabetes mellitus. 970 13

Several recent studies with the sorbitol dehydrogenase inhibitors 4-[4-(N,N-dimethylsulfamoyl)-piperazino]-2-methylpyrimidine, SDH-1, and its active metabolite 4-[4-(N, N-dimethylsulfamoyl)piperazino]-2-hydroxymethylpyrimidine , SDH-2, suggest that inhibition of sorbitol dehydrogenase may be beneficial in delaying the onset of diabetic complications due to their ability to ameliorate redox changes associated with polyol metabolism. To compare the relative importance of sorbitol dehydrogenase versus aldose reductase inhibition on sugar cataract formation, cataract formation was monitored in 50% galactose-fed and diabetic rats treated with/without the sorbitol dehydrogenase inhibitors SDH-1 or SDH-2 or the aldose reductase inhibitors AL 1576 or Ponalrestat. For these studies, diabetes was induced in young 50 g rats with streptozotocin while galactosemia was produced by feeding a diet containing 50% galactose. Inhibitors were administered in the diet with the diet containing 0.06% (w/w) of the sorbitol dehydrogenase inhibitors or Ponalrestat, and 0.0125% (w/w) of AL 1576. Cataract formation was monitored by hand-held slit lamp and polyol levels were measured by gas chromatography. Sugar cataract formation was accelerated in diabetic rats treated with sorbitol dehydrogenase inhibitors while no difference in cataract formation was observed in galactose-fed rats treated with/without SDH inhibitors. Cataract formation was inhibited in both diabetic and galactosemic rats by either Ponalrestat or AL 1576. These results support the concept that sugar cataract formation is initiated by the aldose reductase catalysed intracellular accumulation of polyols and that these sugar cataracts can be prevented through inhibition of aldose reductase.
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PMID:Effect of sorbitol dehydrogenase inhibition on sugar cataract formation in galactose-fed and diabetic rats. 973 86

Authors reviews--upon literature data--the metabolism of carbohydrates, with special regard to lipogenesis, which is of less importance and has no role in obesity. Out of the plasma lipids, in the case of extreme sugar consumption, only the level of triglicerides shows increase. Sugar is one but not the only factor caries. Sugar promotes the learning and remembering function of the brain and possibly, affects behaviour, too. Oligosaccharides may contribute to the favourable changes in the intestinal microflora. Carbohydrates and within them, sugars, play no unfavourable role in the development of diabetes mellitus, obesity, cardiovascular disease, when nutrition is well balanced.
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PMID:[Physiological role of dietary carbohydrates in diet of hungarian population. Epidemiological study]. 982 67


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