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

A physiological investigation on an outbreak of diuresis syndrome in commercial broiler breeder hens was carried out. Daily water consumption increased 4-fold and daily manure wet weight increased two-fold in affected hens. 2. The syndrome did not have a genetic basis. It was associated with kidney dysfunction which, once acquired, was not alleviated by changing the diet, the drinking water, or the environment. Diuresis ceased when water intake was restricted and returned when water was again made freely available. 3. The syndrome was not caused by nephrogenic diabetes insipidus or diabetes mellitus. Key changes in kidney function associated with diuresis included: increased urine flow, decreased urine osmolality, reduced glomerular filtration rates, increased fraction of the glomerular filtration rate excreted as urine and decreased urinary hydrogen ion concentrations. 4. Preliminary histopathological findings and the physiological patterns of kidney dysfunction indicated that the diuresis syndrome was associated with permanent kidney damage, probably caused by the Arkansas strain of infectious bronchitis virus.
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PMID:Physiological evaluation of diuresis in commercial broiler breeders. 276 79

Proton-Induced X-Ray Emission (PIXE) analysis of blood samples from diabetic pregnant women was carried out. Elements S, Ca, P, K, Cl, Fe, Zn, Cu, Rb and Br were detected in red blood cells, while S, Ca, P, K, Cl, Fe, Zn, Cu, Ni, Br in the plasma. The concentrations of P, S, Ni, Cu were found to be higher, while those of K, Fe, and Zn were lower in diabetic plasma than in controls. Significantly higher concentrations were measured for P, S, Cl, Fe, Zn and Rb in diabetic erythrocytes compared to normals. Statistical evaluation of the results also indicated significant alteration in the changes of concentrations throughout the pregnancy. Diabetes also resulted in changes in most of the correlations observed in normal pregnancy between the concentrations of elements.
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PMID:Determination of trace and bulk elements in plasma and erythrocytes of diabetic pregnant women by PIXE method. 288 Jul 59

The reduction of oxygen by the ene-diol tautomer of simple monosaccharides produces hydrogen peroxide and alpha-oxoaldehydes. This process, termed monosaccharide autoxidation, occurs at physiological pH and temperature and may contribute to the development of several pathological processes. Enolization of the monosaccharide to an ene-diol tautomer is a prerequisite for the reaction of the monosaccharides with oxygen. The reaction kinetics suggest a two step process: the enolization of the monosaccharide to the ene-diol followed by the reaction of the ene-diol with oxygen. Free-radical reactive intermediates are formed by the reaction of the ene-diol with oxygen: superoxide, semidione, and 1-hydroxyalkyl radicals are formed under physiological conditions (hydroxyl radicals are also detected at high pH). The autoxidation of monosaccharides stimulates the oxidation of oxyhemoglobin in erythrocytes, producing methemoglobin and hydrogen peroxide, and the oxidation of reduced pyridine nucleotides NAD(P)H to the oxidized congener NAD(P)+ and enzymatically inactive nucleotide. This stimulates oxidative metabolism (via the hexose monophosphate shunt) and alpha-oxoaldehyde metabolism (via the glyoxalase system) in erythrocytes in vitro. The oxidative challenge is relatively mild even with very high concentrations (50 mM) of monosaccharide. However, crosslinking of membrane proteins by alpha-oxoaldehydes is enhanced; this effect may exacerbate ageing and decrease the lifetime of erythrocytes in circulation. In vivo, the autoxidation of monosaccharides is expected to be a chronic oxidative process occurring in biological tissue which utilises simple monosaccharides, e.g., in glycolysis and gluconeogenesis. Monosaccharide autoxidation is suggested to be a determinant in the control of cellular mitosis and ageing, providing physiological substrates for the glyoxalase system, and may contribute to the chronic disease processes associated with diabetes mellitus and the smoking of tobacco.
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PMID:Monosaccharide autoxidation in health and disease. 300 96

We report a 31-yr-old nondiabetic male patient with acanthosis nigricans whose hyperinsulinemia and insulin resistance could not be explained by anti-receptor antibodies or by an intrinsic defect of insulin binding to his cells. An acid-alcohol extract of the patient's serum contained a factor that inhibited insulin-stimulated glucose transport in rat adipocytes. Low levels of the factor could be detected in 9 of 13 unselected patients with non-insulin-dependent diabetes. The factor was heat stable and resistant to treatment with acid, base, and various lytic enzymes. It eluted from a Bio-Gel P-2 column with an apparent molecular weight of 300. The factor also inhibited stimulation of glucose transport in adipocytes by the insulin mimickers hydrogen peroxide and sodium vanadate. In vitro incubation of rat soleus muscles in the presence of the factor resulted in inhibition of insulin-stimulated glucose transport. The factor enhanced 125I-labeled insulin binding in both adipocytes and muscle. A preparation of insulin receptors obtained from muscles incubated with serum factor showed increased binding of 125I-insulin to the alpha-subunit of the insulin receptor. Autophosphorylation of the beta-subunit and phosphorylation of exogenous substrate were increased in the receptor preparation obtained from muscles that had been incubated with serum factor. However, the increase in kinase activity was approximately the same as the increase in binding activity. No difference in kinase activity was observed when assayed under conditions in which 125I-insulin binding activity had been equalized.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1988 Sep
PMID:Inhibition of insulin-stimulated glucose transport by factor extracted from serum of insulin-resistant patient. 304 87

Postprandial hyperglycemia in diabetic patients can be modified by delaying the digestion and/or absorption of dietary carbohydrates. We have studied an orally active alpha-glucosidase inhibitor, Bay 1099, in normal volunteers to determine whether these inhibitors can decrease postprandial rises in serum glucose without causing gastrointestinal symptoms or significant fecal caloric wastage. Six subjects were given 25, 50, or 100 mg of Bay 1099 or placebo before meals for 1 week, each with a 1-week washout period. Fasting and postprandial concentrations of glucose, insulin, glucagon, enteroglucagon, and gastrointestinal inhibitory peptide (GIP) were measured after the first and last dose of Bay 1099, and the fecal excretions of protein, fat, fiber, and total calories were measured on the last three days of each diet. The passage of unabsorbed carbohydrate into the colon was determined by breath hydrogen analysis three times during each study week. Increasing doses of Bay 1099 were found to decrease the postprandial rise in serum glucose concentration, delay the time to peak insulin concentration, and decrease the output of GIP after the meal. No adaptation was apparent after 1 week of therapy. A dose of inhibitor (50 mg tid), which greatly improves postprandial glucose and hormone output in diabetes, was associated with minimal symptoms and no excess fecal caloric losses. Thus, glucosidase inhibitors such as Bay 1099 may be useful in the management of patients with carbohydrate intolerance.
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PMID:Intestinal and metabolic responses to an alpha-glucosidase inhibitor in normal volunteers. 305 29

1. Somatostatin analogues, such as SMS 201-995 (sandostatin), have been suggested as treatment for a variety of disease states including acromegaly, secretory gastrointestinal tumours and diabetes mellitus. 2. Somatostatin-14 has actions to prolong gastro-intestinal transit time and inhibit intestinal absorption, and we have therefore studied the effects of SMS 201-995 on these processes. Five male subjects received a test meal having been given either saline or 50 micrograms of SMS 201-995 subcutaneously 30 min before ingestion. 3. SMS 201-995 caused a delay in mouth-to-caecum transit time for lactulose assessed by breath hydrogen analysis (316 +/- 17 vs 192 +/- 14 min, mean +/- SEM, P less than 0.01), a delay (234 vs 120 min, P less than 0.05) in the plasma peak of the non-metabolizable glucose analogue 3-O-methylglucose and conversion of the expected postprandial rise in serum triglycerides (with saline 1.02 +/- 0.20 to 1.51 +/- 0.28 mmol/l, P less than 0.05) to a decrease below basal values (with SMS 201-995 0.97 +/- 0.80 to 0.79 +/- 0.11 mmol/l, P less than 0.05). 4. After SMS 201-995, an enhancement of the increase in blood glucose (8.2 +/- 0.7 vs 4.7 +/- 0.2 mmol/l, P less than 0.01) and inhibition and postponement of the postprandial rise in insulin (27.6 +/- 6.7 vs 9.9 +/- 2.1 m-units/l, P less than 0.05) occurred. Furthermore, a rise in non-esterified fatty acids, glycerol and 3-hydroxybutyrate, compared with the decline in concentrations of these metabolites after saline, was observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of the somatostatin analogue SMS 201-995 (sandostatin) on mouth-to-caecum transit time and absorption of fat and carbohydrates in normal man. 305 74

Phosphorus is the sixth most abundant element in the body after oxygen, hydrogen, carbon, nitrogen, and calcium. It comprises about 1% of the total body weight of humans. Eighty-five percent of it is stored in the bone in the form of hydroxyapatite crystal; 14% is in the soft tissues in the form of energy-storing bonds with nucleotides (ATP, GTP), nucleic acids in chromosomes and ribosomes, 2,3-DPG in the red blood cells, and phospholipids in the cells' membranes. Less than 1% is in the extracellular fluids. Phosphate balance is maintained by multiple systems. The gut is responsible for the absorption of two thirds of the 4-30 mg/kg/day of phosphate intake. Absorption sites are all along the gut; in humans the most active site is the jejunum. The kidney filters 90% of the plasma phosphate and reabsorbs it in the tubuli. In states of hypophosphatemia the kidney can reabsorb the filtered phosphates very efficiently, reducing the amount excreted in the urine virtually to zero. The healthy kidney can excrete high loads of phosphate and rid the body of phosphate overload. Through the vitamin D-PTH axis the endocrine system regulates the phosphate balance by influencing the kidney, gut, and bone. Other hormones, including thyroid, insulin, glucagon, glucocorticosteroid, and thyrocalcitonin, play a lesser role in regulation of phosphate metabolism. Because of the complex control of phosphate homeostasis, various clinical conditions may lead to hypophosphatemia. These include nutritional repletion, gastrointestinal malabsorption, use of phosphate binders, starvation, diabetes mellitus, and increased urinary losses due to tubular dysfunction. The clinical picture of phosphate depletion is manifested in different organs and is due mainly to the fall in intracellular levels of ATP and decreased availability of oxygen to the tissues, secondary to 2,3-DPG depletion. The various manifestations of phosphate depletion are listed in Table 2. The treatment of hypophosphatemia consists of administering enteral or parenteral phosphate salts. An important aspect of dealing with the potentially serious effects of phosphate depletion is to prevent the depletion from happening in the first place. Hyperphosphatemia can occur in renal failure, hemolysis, tumor lysis syndrome, and rhabdomyolysis. The treatment of hyperphosphatemia usually consists of fluid administration (in the absence of kidney failure). In chronic hyperphosphatemia, phosphate binders such as aluminum and magnesium salts can reduce the phosphate load. The use of these phosphate binders is limited by their potential side effects.
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PMID:Consequences of phosphate imbalance. 306 Jan 61

ICRF-187, (+)-1,2-bis(3,5-dioxopiperazine-1-yl)propane, has been shown to protect against alloxan diabetes (el-Hage et al., 1981). Since alloxan-induced pancreatic beta cell damage is thought to be mediated through the generation of highly reactive oxygen radicals by a metal catalyzed reaction involving both superoxide anion and hydrogen peroxide, in the present study the protective activity of ICRF-187 was compared with that of free radical scavengers, microsomal enzyme inhibitors and chelating agents. The free radical scavengers DMSO, vitamin E and WR2721 markedly reduced alloxan-induced hyperglycemia. ICRF-187 was found not to interact with superoxide anions, and there is no evidence to indicate that any of the known biological effects of ICRF-187 are mediated through free radical scavenging activity. SKF-525 and cimetidine, known inhibitors of drug metabolizing enzymes, also protected against the diabetogenic action of alloxan. Since it was found that ICRF-187 did not alter hexobarbital sleeping time, this compound must protect by a mechanism other than microsomal enzyme inhibition. Since the chelating agents EDTA and DETAPAC were found to protect against alloxan diabetes, ICRF-187 or its hydrolytic products, which are structurally similar to EDTA, could function as chelating agents. Transitional metals such as iron, zinc and copper were found to bind preferentially to a hydrolysis product of ICRF-187. Chelation of iron by ICRF-187 or its hydrolytic products could decrease in vivo formation of reactive oxygen radicals and provide a means for protecting against chronic anthracycline cardiotoxicity and alloxan diabetes.
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PMID:Mechanism of the protective activity of ICRF-187 against alloxan-induced diabetes in mice. 309 Jun 62

Previous studies from our laboratory have demonstrated the presence of complex alterations in the activities of antioxidant enzymes in various tissues of rats with streptozotocin (STZ)-induced diabetes. In the present investigation, it is shown that rats made diabetic with alloxan (ALX), an agent differing from STZ both chemically and in its mechanism of diabetogenesis, show virtually identical tissue antioxidant enzyme changes which, as is the case with STZ, are preventable by insulin treatment. The finding that the patterns of antioxidant enzyme alterations in chemically-induced diabetes are independent of the diabetogenic agent used and the presence of similar abnormalities in tissues of spontaneously diabetic (BB) Wistar rats (particularly when diabetic control is less than optimal) suggest that the changes observed are a characteristic feature of the uncontrolled diabetic state and that these may be responsible for (or predispose to) the development of secondary complications in clinical diabetes. Comparative studies involving red cells of diabetic rats and human diabetics revealed a number of common changes, namely an increase in glutathione reductase activity, a decreased susceptibility to oxidative glutathione depletion (which was related to the presence of hyperglycemia) and an increased production of malondialdehyde (an indirect index of lipid peroxidation) in response to in vitro challenge with hydrogen peroxide. In the diabetic patients, the extent of this increase in susceptibility of red cell lipids to oxidation paralleled the severity of diabetic complications. Our results suggest that increased (or uncontrolled) oxidative activity may play an important role in the pathogenesis of complications associated with the chronic diabetic state.
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PMID:Antioxidant enzyme alterations in experimental and clinical diabetes. 323 Dec 24

The present study aimed at investigating the metabolic effects and tolerance of two desoxynojirimycin derivatives with alpha-glucosidase inhibitory properties (BAY m 1099 and BAY o 1248). The study was performed in a double-blind cross-over manner on 7 insulin-treated outpatient diabetics (6 males, 1 female; mean age 43 +/- 14 years; mean duration of diabetes 5.8 +/- 4.2 years; all within +/- 10% of their ideal body weight). The usual diet containing 24.5 +/- 8 g dietary fibers and 52 +/- 22 g simple sugars was maintained throughout the study. After a 7-day run-in period, 4 consecutive periods of 7 days were considered for each patient. The patients were randomly allocated for 1 week to BAY o 1248 (20 mg with breakfast) or Bay m 1099 (50 mg with breakfast and dinner). After a 7-day wash-out period the patients underwent the alternate treatment. At the end of each period, the patients were admitted to the Metabolic Ward for detailed metabolic and hormonal investigations. No significant changes were observed in the daily insulin requirements (45 +/- 15 U/day). HbA1c did not change significantly. Residual insulin secretion was low (plasma C-peptide: 0.077 +/- 0.09 and 0.154 +/- 0.15 pmol/ml during fasting and 2 hours post-breakfast, respectively); it was not modified by the treatments. Increments in blood glucose were significantly lower after breakfast with both drugs. No differences were observed in plasma free insulin. A marked increase in breath hydrogen was observed after lunch with BAY o 1248 only. Clinical and biological tolerance was excellent for both compounds.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Assessment of the clinical efficacy and tolerance of two new alpha-glucosidase inhibitors in insulin-treated diabetics. 331 59


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