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

In the years 1980-1983 M. xenopi was isolated from the sputum of 37 persons, 30 of them living in the agglomeration of the regional town in the region of Northern Bohemia with 1,175,000 inhabitants. Only 7 of these 30 had manifestation of pulmonary disease. M. xenopi was found repeatedly in the sputum in 5 patients out of 7 affected and in 2 out of 23 persons who showed no signs of a disease. The prevalence was in males between the age of 52-67 years. All of them suffered from other diseases, as chronic bronchitis, TB healed after lobectomy, lung cancer, fibrotic lung lesions, diabetes mellitus, gastric ulcer healed by resection, chronic alcoholism. Investigations were made for detection of the source of infection. Bacteriological examinations of cold and warm tap water in flats of 9 persons with M. xenopi in their sputa were carried out, as well as cold and warm tap water from flats of 2 healthy persons. M. xenopi was found in tap water of 5 persons with M. xenopi in their sputum and in one of the two healthy persons. In the water of one household we found M. kansasii. We came to the conclusion, that transmission carried out in susceptible persons is most probably due to aerosol during washing and showering with water, containing these mycobacteria.
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PMID:Water-borne Mycobacterium xenopi--a possible cause of pulmonary mycobacteriosis in man. 380 13

A chart review of 37 hospitalized patients with diabetes mellitus who received burn therapy showed that ten (27 percent) had preventable lower-extremity burns related to sensory loss. Most of these ten burns occurred from heat applied for self-care of diabetes, namely, from hot tap water, a hot moist compress, or a heating pad. These ten patients, compared with the other 27 diabetic burn patients, were more likely to be men younger than 45 years old, to have insulin-dependent diabetes, and to have been burned during self-treatment. These findings underscore the importance of injury-prevention educational efforts by physicians in cautioning their diabetic patients, especially those with lower-extremity sensory losses, about potential burns from heat applied to the lower extremities for self-care.
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PMID:Lower extremity burns related to sensory loss in diabetes mellitus. 380 25

Normal nondiabetic homozygous and heterozygous littermates of db/db diabetes-prone mice (seven/group) were fed a 5% solution of glucose as their sole source of liquid for 10 wk. Controls (seven/group) drank tap water, and both groups received stock diet ad libitum. Body weights, tail lengths, food and fluid consumption were recorded throughout the study, and plasma and urine glucose were measured during wk 10. The total caloric intake, including the glucose solution drunk by some of the mice, was not significantly different among the four groups. No differences in plasma or urine glucose were detected. Total-body dry weight, water and lipid were measured, and pancreata were analyzed for beta-cell polyploidy by a combination of Feulgen cytophotometry and nuclear size analysis. The percentage of polyploid beta-cells was significantly higher in the animals that drank glucose than in those that drank water and was independent of both genotype and growth indices attributable to genotype. The greater polyploidization was interpreted as reflecting premature aging of the beta-cell population. It was hypothesized that such glucose-induced premature aging in animals with a genetically restricted potential for beta-cell proliferation could contribute to the precipitation of overt diabetes.
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PMID:Excess glucose intake induces accelerated beta-cell polyploidization in normal mice: a possible deleterious effect. 388 72

In rats with deoxycorticosterone acetate (DOCA) salt hypertension, induction of diabetes with streptozotocin did not aggravate the elevation in blood pressure, but pressor and sympathetic nerve responses to electrical stimulation of the ventromedial hypothalamus were enhanced. Along with glycosuria and hyperglycemia, the other effects of streptozotocin-induced diabetes were: reduced body weight, increased fluid intake, and bradycardia. Despite enhanced responsiveness to hypothalamic stimulation, blood pressure increases produced by intravenous injections of norepinephrine, tyramine, or vasopressin were unaltered. When pressor responses were compared in diabetic rats drinking either tap water or isotonic saline solution, no appreciable differences occurred. It was considered possible that hypothalamic responsiveness was enhanced in diabetic-DOCA hypertensive rats by increases not only in sympathetic nerve firing but also in release of endogenous norepinephrine.
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PMID:Hypothalamic responsiveness in DOCA hypertensive rats augmented by streptozotocin-induced diabetes. 618 70

Goodson and Hunt showed that wound healing is impaired in streptozotocin (Sz) diabetic rats; we speculated that this impairment results from defective early inflammatory responses to wounding. Because we had shown that supplemental vitamin A stimulates the early inflammatory response to wounding in nondiabetic rats, we studied the effect of supplemental vitamin A on wound healing in rats with Sz-induced diabetes. Male Sprague-Dawley rats were fed a commercial rat chow containing twice the amount of vitamin A recommended by the NRC for healthy rats. The rats ate and drank (tap water) ad libitum. Two-thirds of the rats were injected (intravenously) with Sz 60 mg/kg body weight. All of these rats became diabetic (hyperglycemia greater than 350 mg/dl, hyperphagic, polydipsic, polyuric, glycosuric greater than 2%). Seven days later, half of the Sz-injected rats were continued on the chow (Group 2) while the other half (Group 3) were switched to the chow supplemented with 150,000 units of vitamin A/kg chow. The next day, all were wounded (7 cm skin incisions and s.c. polyvinyl alcohol sponge implants). Similarly wounded saline injected nondiabetic rats ingesting the unsupplemented chow served as controls (Group 1). The wounds of Group 2 rats healed poorly compared to Group 1 (breaking strength of skin incisions, 308 +/- 19 g vs 584 +/- 23 g, p less than 0.001; hydroxyproline of the sponge reparative tissue, 0.87 mg vs 2.40 mg/100 mg sponge p less than 0.001). Supplemental vitamin A (Group 3) did not affect the hyperglycemia, hyperphagia, polydipsia or glycosuria, but increased the breaking strengths of the incisions of the diabetic rats (468 +/- 40 g, p less than 0.001), and the sponge hydroxyproline (2.38 mg/100 mg sponge, p less than 0.001). In another experiment, in which the wounding and start of supplemental vitamin A were delayed until 28 days after streptozotocin administration (50 mg/kg body weight), similar results were obtained. Streptozotocin diabetes also caused a decrease in the cross-linking of reparative collagen as judged by the ratio of breaking strengths of skin incisions before and after formalin fixation. Supplemental vitamin A did not influence this defect. Sz also caused peripheral lymphocytopenia, adrenal hypertrophy and thymic involution which responded to the supplemental vitamin A. Based upon experimental data and theoretical considerations we conclude Sz diabetes causes two defects in wound healing: a) quantitatively (reduction in reparative collagen accumulation) and b) qualitative reduction in the degree of cross-linking of reparative wound collagen. The action of supplemental vitamin A in correcting the impaired wound healing, adrenal enlargement, thymic involution and lymphocytopenia of Sz-diabetic rats is independent of an effect on their disturbed carbohydrate metabolism.
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PMID:Impaired wound healing in streptozotocin diabetes. Prevention by supplemental vitamin A. 645 99

These studies were designed to test whether a putative gastrointestinal factor (separate from that stimulating insulin release) is involved in the enhancement of liver glycogen storage during oral glucose ingestion. To do this, we compared net hepatic glucose uptake in conscious dogs, following oral glucose administration, with hepatic uptake during intraportal glucose infusion. The rate of intraportal glucose infusion was calculated to match the time course of gut glucose absorption in the oral administration experiments. In control studies, intragastric instillation of tap water [90 +/- 2.4 (SE) in four dogs had no effect on basal rates of gastrointestinal (GI) glucose uptake (16 +/- 1 mg/min) oe hepatic glucose production (97 +/- 3 mq/min). Net basal GI lactate production was equal to GI glucose utilization (P greater than 0.1); glycolytic conversion of glucose to lactate accounted for all basal GI glucose utilization. In oral experiments, gastric instillation of 1.2 g/kg glucose (N = 8) caused GI glucose absorption to increase within 5 min (P less than 0.01). Net glucose absorption from the gut was maximal (355 1.55 mg/min) at 60 min, and was complete at 165-240 min (mean = 186 min). During absorption, liver switched from production to net uptake by 30 min (P less than 0.01); production was resumed by 3 h. Total glucose taken up by liver was 7.19 +/- 1.8 g (23% oral load). No net metabolism of the instilled glucose to lactate occurred during absorption; GI lactate production was the same during absorption (13.0 +/- 5.0 mg/min) as before glucose instillation (11.2 +/- 2.0 mg/min; P greater than 0.45). In intraportal experiments, intraportal glucose infusion (total = 1.09 g/kg) induced liver to take up glucose by 15 min (P less than 0.01); total hepatic uptake (4.6 +/- 1.5 g) was not significantly different from the oral experiments (P greater than 0.15). Also, nonsplanchnic glucose uptake was the same in the oral (25.1 +/- 2.2) and intraportal (25.2 +/- 1.4) studies. The lack of difference between hepatic and extrahepatic fates of administered glucose with oral and intraportal administration indicates that no putative gut factor need be invoked to explain hepatic glycogen deposition during oral glucose, and it seems probable that no such factor exists in the dog.
Diabetes 1982 Jan
PMID:Intraportal glucose infusion matched to oral glucose absorption. Lack of evidence for "gut factor" involvement in hepatic glucose storage. 715 23

Ingestion of a high-protein diet or intravenous administration of amino acids is associated with an increase in glomerular filtration rate (GFR). It can also lead to renal hypertrophy, and, if sustained, may cause glomerular sclerosis. L-Arginine administration ameliorates the progression of renal disease in rats with subtotal nephrectomy and prevents the increase in GFR observed in rats with experimental diabetes. The present study examines the potential effect(s) of L-arginine administration (1%) in the drinking water on the renal hypertrophy that occurs in rats fed a high-protein diet for 1 month. Four groups of female Sprague-Dawley rats, six in each group, were studied (95 +/- 1 g). Groups 1 and 2 were fed a low-protein diet (12% casein, 0.504% L-arginine); Group 1 was given tap water, whereas Group 2 was given tap water supplemented with L-arginine. Groups 3 and 4 were fed a high-protein diet (40% casein, 1.68% L-arginine); Group 3 was given tap water, whereas Group 4 was given tap water supplemented with L-arginine. The rats had free access to food and water during the study period. The kidney weight and the kidney to body weight ratio of rats of Group 3 were significantly greater than in the other groups of rats. Renal hypertrophy was prevented in the rats of Group 4. The excretion of orotic acid in the urine, an index of L-arginine deficiency, was significantly greater in rats of Group 3 than in rats of Group 4. Thus, the renal hypertrophy that occurs in rats fed a high-protein diet was decreased in rats given L-arginine supplementation in the drinking water. This effect was associated with less excretion of orotic acid in the urine in rats given L-arginine. A relative deficiency of L-arginine may occur during high-protein feeding that may shunt nitrogen metabolism from the urea cycle to the orotic acid pathway.
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PMID:Dietary supplementation of L-arginine ameliorates renal hypertrophy in rats fed a high-protein diet. 820 40

The effect(s) of L-arginine administration on the renal function of rats with untreated diabetes mellitus was examined. Rats received streptozotocin (N = 11) or vehicle (N = 12): Group 1 (normal rats, N = 6) drank tap water; Group 2 (normal rats, N = 6) drank tap water containing 1% L-arginine; Group 3 (diabetic rats, N = 5) drank tap water; and Group 4 (diabetic rats, N = 6) drank tap water with 1% L-arginine. Rats were fed a standard rat chow diet (22.8% protein, 142% L-arginine) with free access to food and water for 14 wk. Diabetic rats gained less weight, had significantly lower plasma levels of albumin and L-arginine, and had greater values for 24-h urine volumes and urine excretion of glucose, protein, urea, creatinine, nitrate, and nitrite than control rats. Diabetic rats given L-arginine (Group 4) had significantly lower protein and cGMP excretion in the urine than did rats of Group 3. The administration of L-arginine did not affect the plasma levels of glucose or L-arginine in Groups 2 or 4 compared with those of their respective controls. Group 3 had significantly higher values for GFR than did the other three groups of rats, but values for effective RPF, mean arterial pressure, hematocrit, and renal vascular resistance were not significantly different between Groups 3 and 4. There was no significant difference in glomerular morphology among the four groups of rats as determined by light microscopy, and both groups of diabetic rats exhibited the Armanni-Ebstein lesion in their tubules.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:L-arginine administration prevents glomerular hyperfiltration and decreases proteinuria in diabetic rats. 828 12

Chronic hyperglycemia causes near-total disappearance of glucose-induced insulin secretion. The etiology has been suggested to be a nonsustainable stimulation of insulin release that causes beta-cells to become unresponsive to glucose through an undefined mechanism. We used an inhibitor of insulin secretion, diazoxide, to test this hypothesis in 90% pancreatectomized (Px) rats. Px rats were given 5 days of diazoxide (30 mg/kg orally twice a day) or tap water starting on postoperative day 8, 15, or 22. In vitro pancreas perfusions were conducted 36 h posttreatment (2, 3, or 4 weeks after surgery) using a protocol of 15 min of 16.7 mM glucose followed by 15 min of 16.7 mM glucose plus 10 mM arginine. In 2-week Px rats, insulin responses to 16.7 mM glucose and to glucose/arginine were both appropriate for the reduced beta-cell mass, i.e., no defect in beta-cell glucose responsiveness had yet occurred. Diazoxide had no affect on insulin release at this time. Between 2 and 3 weeks after pancreatectomy, insulin output to 16.7 mM glucose fell 75%, and that to glucose/arginine fell 50%. Diazoxide given at this time partially blocked the fall in glucose-induced insulin secretion and totally prevented that with arginine. The increased insulin secretion caused by diazoxide was accompanied by 1) lower nonfasting plasma glucose values, 2) improved glucose tolerance after oral glucose load, and 3) a 50% increase in pancreatic insulin content. Our results support the concept that excessive insulin secretion is a major cause of the hyperglycemia-induced loss of beta-cell glucose responsiveness. A leading candidate for the mechanism of this effect is depleted pancreatic insulin stores. Overstimulation of insulin secretion provides a new target for pharmacological therapy aimed at reducing glucose intolerance in non-insulin-dependent diabetes mellitus.
Diabetes 1994 Feb
PMID:Diazoxide causes recovery of beta-cell glucose responsiveness in 90% pancreatectomized diabetic rats. 828 40

To ensure an acceptable quality of life for Type 2 diabetic patients, the food recommendations have to be as liberal and individualized as possible. Unfortunately, disagreements exists about the consumption of different types of wine. Diabetic patients are advised by some to restrain their wine intake and to use dry wine containing little carbohydrate, while others are more liberal. The purpose of this study was to evaluate the effects of dry and sweet wine on the glycaemic control in Type 2 diabetes. Twelve diabetic patients consumed a light meal with either 300 ml tap water 300 ml dry white wine, 300 ml sweet white wine with ethanol added or 300 ml dry white wine with glucose added. Similar glucose, insulin, and triglyceride responses were obtained in all four situations. There was a greater suppression of the free fatty acid levels in the three situations with wine as compared with water (p < 0.001). This effect may be caused by an attenuation of the free fatty acid mobilization and esterification of free fatty acids to triglycerides induced by alcohol. Our results indicate that patients with well-controlled Type 2 diabetes can drink moderate amounts of wine with meals without risking acute deterioration of glycaemic control. Whether the wine is dry or sweet has no impact on the glycaemic control.
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PMID:Wine for type 2 diabetic patients? 785 Oct 78


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