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

Chemically induced diabetes in the rat is associated with a number of functional abnormalities in the intestinal tract. The transport of glucose, amino acids and fatty acids are increased, whereas that of calcium and magnesium is decreased. Previous studies in calcium transport utilized in vivo perfusion and in vitro everted gut sac techniques. The present studies determined calcium uptake by the brush border membranes of controls, diabetic and diabetic rats treated with insulin or 1,25(OH)2 Vitamin D3. Calcium uptake with time was markedly decreased in diabetic rats compared to controls. Calcium uptake at 30 minutes was 4.4 +/- 0.8 and 28 +/- 0.9 nmoles/mg protein in control and diabetic rats, respectively (p less than 0.001). Kinetics of calcium uptake at 5 seconds showed a Vmax of 2 +/- 0.02 and 2.5 +/- 0.1 nmoles/mg protein (p less than 0.05) and a Km of 0.6 +/- 0.1 and 0.54 +/- 0.1 mM in diabetic and controls, respectively. Calcium uptake at 30 minutes showed a Vmax of 15.4 +/- 1.2 and 144.8 +/- 12 nmoles/mg protein (p less than 0.001) and Km values of 0.6 +/- 0.09 and 0.5 +/- 0.08 mM in diabetics and controls, respectively. 1,25(OH)2 Vitamin D3 treatment increased Vmax to 42.8 +/- 6 nmoles/mg protein/30 minutes, whereas insulin treatment increased the Vmax to 71 +/- 8 nmoles/mg protein/30 minutes. The results suggest that calcium uptake by brush border membranes is markedly decreased in diabetic brush border membranes compared to controls. 1,25(OH)2 Vitamin D3 and insulin partially corrected calcium uptake by diabetic brush border membranes.
Diabetes Res 1991 May
PMID:Calcium uptake by jejunal brush border membrane of the diabetic rat. 181 79

The gut may be a site of early diabetic neuropathy in humans and rats. The latter may provide appropriate models of these conditions. Therefore, cholinergic function was examined in two gut smooth muscle preparations from control, 30-day, and 6-month streptozotocin-diabetic and similarly diabetic rats that had received continuous treatment with an aldose reductase inhibitor, ponalrestat. Responses of terminal ileum longitudinal muscle to transmural nerve stimulation were depressed in preparations from untreated 30-day diabetic animals. Responses to exogenous acetylcholine were also depressed, by at least the same extent, in preparations from both 30-day and 6-month diabetic groups. Ponalrestat treatment prevented both changes in the 30-day study but did not prevent a depression of responses to acetylcholine in the 6-month study. Neither diabetes nor ponalrestat affected responses of esophageal muscularis mucosa to electrical stimulation or to exogenous acetylcholine. These observations suggest a change in the smooth muscle and/or noncholinergic innervation rather than in the cholinergic nerves of the ileal preparation. Cholinergic function in the ileum did not, therefore, seem to be an appropriate model of diabetic neuropathy.
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PMID:Effects of diabetes on cholinergic transmission in two rat gut preparations. 189 95

Twenty patients with gastrointestinal mucormycosis are reviewed. This often fatal opportunistic fungal infection was diagnosed histologically, and was categorized as colonization (five patients), infiltration (seven patients), or vascular invasion (eight patients). There were no fatalities from colonization. In 10 patients, mucormycosis complicated peptic ulcer disease. Seven of these patients had infiltrative or invasive disease. The presentation and operative findings mimicked malignancy in five of these seven patients, and six had successful surgical intervention. The other patient was cured by medical therapy alone. Ten patients had infection associated with other gastrointestinal diseases: post-traumatic peritonitis (four patients), transmural amoebiasis (two patients), tuberculosis (one patient), gastroenteritis (one patient), gastric carcinoma (one patient) and diabetes (one patient). Eight patients had significant infection and only one survived. In this series, mucormycosis had a less aggressive course when complicating peptic ulcer than when it occurred in association with other gut diseases.
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PMID:Gastrointestinal mucormycosis. 191 15

The gastrointestinal tract is frequently involved by diabetes, especially when automatic neuropathy is present. Hollow viscera motor activity is especially effected; in particular, gastric and small bowel function may be severely impaired, due to gastroparesis and dysmotility, although motility of the entire gut may be abnormal. The present review focus on the various aspects of abnormal motility of single digestive viscera in diabetic patients.
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PMID:Diabetes and gastrointestinal motor activity. 192 90

Mitochondrial DNA (mtDNA) deletion is associated with a variety of clinical entities. In addition to progressive external ophthalmoplegia and Kearns-Sayre syndrome, mtDNA deletions have been demonstrated in Pearson's syndrome. We report an mtDNA deletion in an infant with a variant of Pearson's syndrome. Not only does she have congenital anemia, severe tubulopathy, and exocrine pancreas insufficiency, but she also has diabetes and cerebral atrophy. However, there are no signs of gut or liver involvement. Bone marrow improved while new tissues were involved, thus showing variability in progression of the disease. Decreased respiratory chain enzyme activities were demonstrated in muscle, and an mtDNA deletion was demonstrated in muscle, kidney, leukocytes, and fibroblasts.
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PMID:Congenital hypoplastic anemia, diabetes, and severe renal tubular dysfunction associated with a mitochondrial DNA deletion. 195 15

1. The effect of alpha 2-adrenoceptor agonists on gastrointestinal motility was assessed in normoglycaemic and streptozotocin-diabetic mice. 2. The alpha 2-adrenoceptor agonists used were: clonidine (0.1, 0.3 and 1 mg kg-1, azepexole (10, 20 and 40 mg kg-1), tizanidine (1, 3 and 10 mg kg-1) and ST-91 (10, 20 and 30 mg kg-1). 3. Acute hyperglycaemia was induced by D-(+)-glucose (5 g kg-1) and chronic hyperglycaemia by streptozotocin (200 mg kg-1) injection. 4. The gut motility was quantitated using the charcoal meal test. 5. The results indicate that in normoglycaemic and acutely hyperglycaemic mice, all of the alpha 2-adrenoceptor agonists used produced significant inhibition of meal transit. 6. However, in streptozotocin-diabetic mice, the anti-transit effect of alpha 2-adrenoceptor agonists was attenuated. 7. Since streptozotocin-induced diabetes but not acute hyperglycaemia was associated with the attenuation of anti-transit effect, elevated blood sugar is not the mechanism for the observed effect. 8. As with groups treated with clonidine, azepexole or tizanidine, the anti-transit effect of a peripherally acting alpha 2-adrenoceptor agonist, ST-91, was attenuated in streptozotocin-diabetic mice. This suggests the involvement of peripheral mechanism(s) in attenuating the anti-transit effect of alpha 2-adrenoceptor agonists. 9. These results identify the need for critical evaluation of the role and efficacy of alpha 2-adrenoceptor agonists in the therapeutic management of diabetic diarrhoea.
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PMID:Streptozotocin-diabetes attenuates alpha 2-adrenoceptor agonist-induced delay in small intestinal transit in mice. 197 57

Human growth hormone (hGH) and prednisone cause insulin resistance and glucose intolerance. However, it is unknown whether hGH and prednisone antagonize insulin action on protein, fat, and carbohydrate metabolism by a common or independent mechanism. Therefore, protein, fat, and carbohydrate metabolism was assessed simultaneously in four groups of eight subjects each after 7 days of placebo, recombinant DNA hGH (rhGH; 0.1 mg.kg-1.day-1), prednisone (0.8 mg.kg-1.day-1), or rhGH and prednisone administration after an 18-h fast and during gut infusion of glucose and amino acids (fed state). Fasting plasma glucose concentrations were similar during placebo and rhGH but elevated (P less than 0.001) during combined treatment, whereas plasma insulin concentrations were higher (237 +/- 57 pmol/ml, P less than 0.001) during combined than during placebo, rhGH, or prednisone treatment (34, 52, and 91 pM, respectively). In the fed state, plasma glucose concentrations were elevated only during combined treatment (11.3 +/- 2.1 mM, P less than 0.001). Plasma insulin concentrations were elevated during therapy with prednisone alone and rhGH alone (667 +/- 72 and 564 +/- 65 pmol/ml, respectively, P less than 0.001) compared with placebo (226 +/- 44 pmol/ml) but lower than with the combined rhGH and prednisone treatment (1249 +/- 54 pmol/ml, P less than 0.01). Protein oxidation [( 14C]leucine) increased (P less than 0.001) with prednisone therapy, decreased (P less than 0.001) with rhGH treatment, and was normal during the combined treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1991 Jan
PMID:Differential effects of prednisone and growth hormone on fuel metabolism and insulin antagonism in humans. 201 69

To establish whether secretion of proglucagon-derived peptides (PGDPs) by the intestinal L cell is nutrient- and/or location-dependent, 0.9% saline, 200 mM glucose, or emulsified fats were administered into the ileal or duodenal lumen of normal rats. Fat administration, but not saline or glucose treatment, significantly increased circulating levels of the intestinal PGDPs in a time-dependent fashion, indicating a selectivity of the L cell in its response to nutrients. Interestingly, the response to duodenal fats was quantitatively and qualitatively identical to the response to ileal fats, despite 50-fold lower concentrations of PGDPs in the duodenum. These results suggest the existence of a duodenal factor that stimulates ileal PGDP secretion in response to fat ingestion. Ileal and plasma levels of gut PGDPs have been reported to be elevated in poorly controlled streptozotocin-diabetic rats. Whether the sensitivity of the L cell to luminal nutrients is altered in diabetes was, therefore, also examined. The L cell responses to luminal nutrients in diabetic rats were not significantly different from those of the normal rat, indicating a normal responsiveness of the L cell. However, independent of changes in glycemia, luminal glucose perfusion significantly decreased circulating glucagon levels in normal rats, but not in diabetics. Furthermore, luminal fat administration increased plasma glucagon levels in normal rats only. These results indicate that moderately controlled diabetes is associated with alterations in the pancreatic A cell, but not the intestinal L cell response to ingested nutrients. The results of the present study indicate that the response of the intestinal L cell to ingested food is nutrient-specific and that this specificity is not altered in diabetes. A duodenal-ileal axis is proposed to contribute to increments in circulating intestinal PGDPs in response to nutrient ingestion.
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PMID:Secretion of proglucagon-derived peptides in response to intestinal luminal nutrients. 203 83

An histochemical research on cholinergic and noradrenergic fibres of the adventitia layer and of the myenteric plexus of the terminal ileum from rats with streptozotocin-induced diabetes, after 20 weeks of evolution of the illness, was carried out to study changes in the innervation of the gut. The cholinergic nerves, revealed through their acetylcholinesterase activity, did not present alterations, but an evident reduction in number of the noradrenergic nerves and swollen intensely fluorescent varicosities, were observed, both in the perivascular and myenteric plexus of terminal ileum from diabetic animals.
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PMID:Effects of experimental diabetes in the noradrenergic and cholinergic nerves of the rat small intestine. 213 72

The basic prerequisite of treatment of diabetic osteopenias is perfect metabolic compensation of diabetes. Insulin administration is an advantage in this respect, as it enhances calcium absorption from the gut and reduces its urinary excretion. Conversely, oral antidiabetics interfere in a negative way with vitamin D metabolism and thus also calcium metabolism and mineralization of bone. The combination of calcium, small doses of vitamin D, NaF and exercise used in the treatment of diabetic osteoporoses leads in general to a significant rise of the calcium serum level, an insignificant rise of the phosphorus level and it reduces alkaline phosphatase activity. A certain disadvantage is the elevated urinary calcium excretion. The main drug in diabetic osteomalacia are usually large doses of vitamin D. The rise of the serum calcium level improves the metabolic compensation of diabetes in a linear fashion. Thiazide diuretics used to reduce excessive calciuria cause slight deterioration of the glucose tolerance but the compensation does not cause major difficulties.
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PMID:[Diabetic osteopathies. 6. Treatment and its pitfalls]. 213 68


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