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

Guar gum, a dietary fiber known to improve glucose tolerance, was fed to rats with established diabetes to determine its effect on renal enlargement and microalbuminuria. Diabetic rats were fed a modified AIN-76A (basal) diet for 4 wk, at which time half the rats continued to receive the same basal diet (DB-BA group) and half were switched to a 5% guar gum diet (DB-GG group). Nondiabetic rats fed the basal diet served as controls (NRL group). After 8 additional weeks the animals were killed. Glycated hemoglobin, a measure of long-term blood glucose control, was 14.4% in the DB-BA group and 12.4% in the DB-GG group, a statistically significant difference (P < 0.05). Kidney weight of the DB-BA group (3.51 g) was significantly greater than that of the DB-GG group (2.76 g) (P < 0.05). Eight weeks after induction of diabetes, 24-h urinary albumin excretion was highest in the DB-BA group and lowest in the NRL group; excretion in the DB-GG group (4 wk of guar feeding) was intermediate. However, by 12 wk no differences in albumin excretion among the groups were apparent. These results suggest that guar gum may be useful for slowing the progression of diabetic nephropathy and that guar gum deserves further study in this regard.
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PMID:Dietary guar gum halts further renal enlargement in rats with established diabetes. 145 24

Ascorbic acid (AA), dehydroascorbic acid (DHAA), and vitamin E were measured in tissues and plasma of 30 control and 30 spontaneously diabetic BioBreeding rats (BBdp) during development and before the onset of diabetes. At weaning, rats were fed an AIN-76 semisynthetic diet for 30, 64, or 113 days, after which plasma and tissues from 10 rats of each group were collected and analysed for AA, DHAA, and vitamin E. AA and DHAA levels were significantly increased in plasma and spleen of the diabetes-prone rats compared with those of the control group at 30 and 64 days, but the difference disappeared by 113 days. No differences were observed in liver, adrenals, thymus, and pancreas at any of the time periods. However, lower levels of vitamin E were observed in adrenal gland, thymus, and pancreas of the diabetes-prone rats. It is concluded that BBdp rats have an altered metabolism of AA, DHAA, and vitamin E, before the onset of diabetes. These changes could be due to genetic and physiological factors operating during development of this rat strain.
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PMID:Vitamin C and vitamin E status in the spontaneously diabetic BB rat before the onset of diabetes. 198 74

The present study was designed to examine further the impact of individual plant protein sources found in a diabetogenic, cereal-based, rodent laboratory diet, NIH-07 [open formula, nonpurified rat and mouse diet (positive control)], on the development of diabetes. Diabetes-prone BB rats that were pan-T(OX19+)-lymphopenic were fed a low diabetogenic diet during gestation and lactation. Progeny of these rats were fed a normal or autoclaved NIH-07 diet, or one of eight other diets based on the AIN-76A formulation, with modified protein sources as follows: hydrolyzed casein (HC), soybean meal, HC+ trypsin inhibitor (TI) in water (2 mg/mL, wheat germ, alfalfa seeds, Brewer's yeast, red lentils and a plant protein mixture. Feeding soybean meal increased the incidence of diabetes compared with the negative control, HC diet (47% vs. 12% incidence, P = 0.02). Wheat germ, alfalfa seeds and plant protein mixture resulted in an intermediate incidence of diabetes of 33%; the incidence was lower for Brewer's yeast and lentils (20% and 13%). Autoclaving (121 degrees C, 10 min) the NIH-07 diet or the presence of TI in drinking water had a minimal effect on diabetes frequency, suggesting heat-labile plant toxicants were not directly involved. Thus, certain dietary plant protein sources or associated agents may influence the development of spontaneous diabetes in the BB rat.
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PMID:Dietary plant materials and development of diabetes in the BB rat. 203 75

Nonobese diabetic/Lt mice exhibit a diabetes incidence greater than 70% in females at 30 wk of age. In studies designed to see whether increased dietary carbohydrate, fat, or protein influenced the severity or age at onset of the syndrome, we fed semipurified AIN-76 diet adulterated with increased amounts of these ingredients. Surprisingly, all AIN-76-based diets greatly reduced the expected incidence of diabetes at 30 wk. In addition, a hypoallergenic infant formula, Pregestimil, containing casein hydrolysate in place of protein, completely prevented diabetes up to 1 yr of age. To assess how dietary components might modulate the diabetes incidence, we adulterated standard AIN-76 diet with skim milk, gluten, brewer's yeast, or a natural-ingredient rodent open-formula mouse diet (Old Guilford 96 [OG96]. No increase in diabetes incidence was seen with skim milk (10%) or wheat gluten (10%), whereas brewer's yeast (10%) and OG96 (25%) added to AIN-76 increased the incidence compared to mice fed OG96 only. The diabetogenic factor or factors in OG96 could be extracted by chloroform plus methanol (2:1), leaving little activity in the residue. We conclude that diet is a critical factor in diabetes development and that unknown chloroform-methanol-soluble substances in natural-ingredient chow not found in semipurified diets can enhance the development of diabetes in genetically susceptible mice.
Diabetes 1990 Apr
PMID:Effect of diet on incidence of diabetes in nonobese diabetic mice. 231 46

Dimethyl sulfoxide (DMSO), a hydroxyl radical scavenger, is known as an immunosuppressive agent and can reduce autoantibody levels in experimental autoimmune diseases. Because classic diabetogens damage the DNA and membrane of the beta-cell by the generation of free radicals, the purpose of these investigations was to determine whether the intake of DMSO or its derivatives methylsulfonylmethane (MSM) and dimethylsulfide (DMS) could prevent the expression of autoimmune diabetes in the spontaneously diabetic NOD mouse. DMSO (2.5%), MSM (2.5%), and DMS (0.25%) were added to the drinking water of female NOD mice immediately after weaning. Control animals were maintained on regular drinking water. The presence of overt diabetes was monitored from the age of 2 mo by weekly urinary glucose testing until the animals either became overtly glucosuric or were greater than 240 days of age. In contrast to what we expected, DMSO (2.5%) markedly increased the rate at which the animals expressed overt diabetes (P less than .0004, log-rank test). MSM had no effect, whereas DMS reduced the incidence and rate of diabetes onset. When DMSO (2.5%) was administered to male NOD mice and control strains of mice (BALB/c and ICR), the control group did not develop glucosuria or insipidus, whereas DMSO increased the incidence of diabetes in the male NOD mice from 21 to 79%. In contrast, when DMSO was fed to female NOD mice on a purified AIN-76 diet, diabetes onset was reduced to 36%. We conclude that DMSO accelerates the uptake of dietary diabetogens into the beta-cell of genetically susceptible animals (NOD mice). The protective effect of the purified diet in such animals may be due to a lack of putative diabetogens in purified diet, or alternatively, the diet itself contains factor(s) that protect the beta-cell from autoimmune attack and/or destruction.
Diabetes 1989 Feb
PMID:Dimethyl sulfoxide modulation of diabetes onset in NOD mice. 291 23

Diabetes-prone BB Wistar rats were fed a modified AIN-76 diet providing the following amounts of iodine for 10 wk: 0.2 mg/kg diet (recommended amount); 1.0 mg/kg; 2.0 mg/kg; or 3.0 mg/kg. The thyroids were examined for gross and microscopic changes and sera were assayed for antibodies to triiodothyronine (T3), thyroxine (T4), and thyroglobulin (Tg). The body weights and food consumption of the rats fed 0.2 mg of iodine/kg were significantly lower than those of the animals fed higher amounts. Urinary iodine excretion reflected dietary intakes. The thyroids from animals fed 2.0 and 3.0 mg/kg were significantly (P less than 0.01) larger than those from animals fed 0.2 mg/kg. One rat fed 0.2 mg/kg and 2 rats in each group fed 2.0 and 3.0 mg/kg had extensive lymphocytic thyroiditis. Three rats fed 1.0 mg/kg, 6 fed 2.0 mg/kg and 6 fed 3.0 mg/kg had enlarged thyroids. Two rats fed 0.2 mg/kg, 2 fed 2.0 mg/kg and 6 fed 3.0 mg/kg had detectable Tg antibodies. These data suggest that high iodine intakes increase Tg antibodies, which may be associated with an increase in autoimmune thyroiditis in these animals.
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PMID:Effect of dietary iodine on autoimmune thyroiditis in the BB Wistar rats. 292 47

Environmental agents have been implicated in the pathogenesis of insulin dependent diabetes (IDD). These studies were designed to learn if dietary protein influences the development of IDD in the BB rat. Specifically, analysis involved the effects of substituting a modified, semi-synthetic diet (AIN-76) containing soy protein as the sole protein source for the standard chow containing a mixture of animal and non-animal protein. IDD was less frequent (73% vs. 38%, P less than or equal to 0.01), and the onset of diabetes was retarded (110 +/- 11.0 vs. 92 +/- 15.5 days, P less than or equal to 0.01) in rats fed the study diet versus standard chow, respectively. The frequency of thyroid collodal autoantibodies was also significantly decreased in rats fed the study diet (56% vs. 23%, P less than or equal to 0.04), whereas frequencies of smooth muscle and gastric parietal cell autoantibodies were less frequent, but not significantly so. Lymphocyte counts and subsets were unaffected. In non-diabetic rats at greater than 180 days of age, insulitis was less severe in the experimental group. These findings suggested that dietary protein may influence the development of IDD in the BB rat.
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PMID:Dietary protein restriction reduces the frequency and delays the onset of insulin dependent diabetes in BB rats. 315 50

Weanling diabetes-prone BB rats were fed AIN-76 diets containing high (HE, 1 g/kg diet), basal (NE, 0.2 g/kg) or low (LE, trace) vitamin E and were killed at 21, 42 or 60 days of age. Plasma and tissues (adrenals, pancreas, spleen, thymus, liver, brown and white adipose tissue, muscle and testes) were analysed for vitamin E. Vitamin E levels reflected the level in the diet and no diabetic animals were detected at these times. In a second experiment, a total of 90 diabetes-prone BB rats were kept on diets LE and HE for 6 months or until they became diabetic. 11/45 on LE and 5/45 on HE became diabetic. Again, plasma and tissue levels of vitamin E reflected the levels in the diet with the exception of the thymus of diabetic rats fed the high vitamin E diet. Thymus vitamin E levels (microgram/g tissue) were 1.8 and 1.2 in LE-fed diabetics and asymptomatic rats, respectively; and 22.7 and 49.5 in HE-fed diabetics and asymptomatic rats, respectively. The last 2 values were significantly different (p less than 0.005). There were no other differences in plasma or tissue levels of vitamin E in these groups of animals. These findings suggest that high dietary vitamin E may decrease the incidence of diabetes in animals which are able to accumulate sufficient amounts of the vitamin in the thymus. Since the thymus plays a key role in the maturation of T cell populations, which appear to be altered in this disease, it seems possible that the protective effect may be exerted at this level.
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PMID:Effect of dietary vitamin E on the vitamin E status in the BB rat during development and after the onset of diabetes. 352 49

The acute diabetic syndrome in the BB Wistar rat resembles human type 1 (insulin-dependent) diabetes, including a possible association with T cell-mediated, (auto)immune processes. In most previous studies 'normoglycemic' littermates of diabetic BB rats have been used as controls and little attention has been paid to the role of diet. It now appears that asymptomatic/diabetes-prone littermates of diabetics have immune system defects as well as metabolic abnormalities. Since there are also indicators that the disease process starts before animals become symptomatic, we looked for prospective metabolic changes in prediabetic, asymptomatic/diabetes-prone and control (diabetes-free) BB rats following intervention in the immune system while maintaining the animals on a defined diet (AIN-76). The results reported here confirm and extend the finding of Like et al. (1982) that neonatal thymectomy reduces the frequency of the syndrome and emphasize the role of diet in modifying its expression. In contrast to previous reports of hyperglucagonemia only after onset of diabetes, asymptomatic/diabetes-prone animals had periodic increases of plasma glucagon values up to 3-fold those of diabetes-free controls; prediabetics displayed a similar pattern. Asymptomatic/diabetes-prone rats also tended to have slightly higher blood cholesterol levels. The low incidence and delayed onset of the syndrome in rats fed a modified AIN-76 diet (27%, 127 +/- 21 days) compared to the previous chow-fed generation (60%, 93 +/- 18 days) and chow-fed littermates (38%, 87 +/- 16 days) suggested that diet can modify expression of the syndrome.
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PMID:Time course of serum glucoregulatory variables and lipids following neonatal thymectomy of diabetes-prone and control BB Wistar rats fed a defined diet. 638 88

We determined whether an oral administration of the synthetic antioxidant, tert-butylhydroquinone (TBHQ), or the naturally occurring lipoxygenase inhibitor, curcumin, to rats would provide protection against the diabetogenic effect of streptozotocin (STZ). Male Sprague-Dawley rats were fed on an AIN-76-based purified diet containing 0.0028% TBHQ or on the purified diet with a daily intragastric administration of curcumin (200 mg/kg of body weight) for one week while receiving intravenously administered STZ. The rats fed on the TBHQ-containing diet were resistant to diabetes development when compared with the rats fed on the TBHQ-free diet and had a higher body weight gain and lower serum glucose concentration. Glucose-stimulated insulin secretion from the pancreatic islet in the rats that had received TBHQ was higher than that in the control rats. The rats receiving curcumin showed no beneficial effect on these diabetic symptoms. These findings provide direct evidence for the suggestion that dietary supplementation of an antioxidant may exert a preventive effect on the diabetogenic action of free-radical producers.
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PMID:Protection against the diabetogenic effect of feeding tert-butylhydroquinone to rats prior to the administration of streptozotocin. 1092 84


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