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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of islet surface antibodies (ICSA) on in vitro insulin release was studied. Isolated rat islets were incubated in the presence of immunoglobulin preparations from patients with insulin-dependent and non-insulin-dependent diabetes mellitus (IDDM, NIDDM) and healthy subjects, and stimulated with D-glucose, L-arginine or tolbutamide. After incubation, the amount of insulin release from the rat islets was determined. The immunoglobulin preparations from 5 newly diagnosed IDDM patients who were positive for ICSA, and from 5 age-matched healthy subjects were examined. Even in the absence of complement or lymphocytes, immunoglobulin fractions positive for ICSA significantly inhibited low and high concentrations of glucose-stimulated insulin release compared with normal control (P less than 0.02), but had little influence on insulin release after stimulation with tolbutamide. Arginine-stimulated insulin release was almost the same in ICSA-positive immunoglobulin fractions and the control. Immunoglobulin fractions negative for ICSA either from four patients with recently diagnosed IDDM or from four newly diagnosed NIDDM patients had only negligible effect on insulin release after stimulation with glucose. These results suggest that ICSA in IDDM patients, even in the absence of complement or lymphocytes, may preferentially interfere with the mechanisms of glucose-stimulated insulin release in the pancreatic B cells.
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PMID:Islet cell surface antibodies preferentially inhibit glucose-stimulated insulin release in vitro. 219 Jul 82

In patients with diabetes mellitus nonenzymatic glycosylation of hemo-globin is a result of increased blood glucose concentrations. In analogy glycosylated hemo-globin fractions were determined in 23 patients with hereditary fructose intolerance (HFI) and 8 patients with galactosemia (G) by means of hemoglobin chromatography on a column packed with Bio-Rex 70 resin. The concentrations were compared to those of 14 control patients and 43 patients with type 1 diabetes mellitus. Compared to controls, in HFI- and G-patients HbAlab was significantly increased. In contrast diabetic patients presented with a marked and significant increase of the HbAlc fraction. When purified hemoglobin was incubated with different monosaccharides respectively monosaccharide phosphates, an increase of HbAlab resulted mainly after galactose and fructose-1-phosphate. The determination of HbAlab in patients with HFI and G is considered a possible means of metabolic control.
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PMID:Increased concentrations of HbAlab in hereditary fructose intolerance and galactosemia. 358 91

The usual treatment of diabetic patients during surgery with general anesthesia owes little to logic, common sense, or knowledge of requirements, and mortality and morbidity remain high in many centers. In the nondiabetic patient, surgery is accompanied by a rise in secretion of catabolic hormones, insulin-resistance and loss of protein. Therapy of the diabetic patient should be designed to account for these changes and to avoid hypoglycemia, hyperglycemia, and hyperketonemia. It is suggested that for major operations for well-controlled non-insulin-dependent diabetic (NIDDM) persons and for all minor and major operations for insulin-dependent diabetic (IDDM) persons and poorly controlled NIDDM, a combined insulin (3.2 U/h), glucose (10 g 10% dextrose/h), and potassium infusion should be used until oral feeding recommences. The insulin dose should be modified periodically according to bedside glucose monitoring. Fluids should be used as in nondiabetic patients, except that lactate-containing solutions should be avoided. Insulin requirements will be increased (1) by infection, (2) in patients with hepatic disease, (3) in obese patients, (4) in steroid-treated patients, and (5) during cardiovascular surgery. A diabetes-care team should preferably be responsible for the care of the diabetic pre-, per-, and postoperatively.
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PMID:Insulin delivery during surgery in the diabetic patient. 676 22

One proposed role of glomerular mesangial cells is the regulation of glomerular blood flow by contraction. Alterations in the contractile activity of mesangial cells could lead to alterations in glomerular hemodynamics and then to glomerular injury. In this study, the effects of glucose and insulin on the contractile response of cloned homogeneous cultures of rat glomerular mesangial cells to angiotensin II were examined. Cells were cultured in normal-glucose medium (D-glucose at 200 mg/dl) and normal-glucose medium with added insulin (4 microgram/ml). To mimic the diabetic state, cells were cultured in high-glucose medium (D-glucose at 550 mg/dl) and high-glucose medium with added insulin. The media contained 20% fetal calf serum. Cells were grown for at least 1 wk in medium prior to contraction experiments. All clones of mesangial cells grown in the presence of additional insulin, in either normal- or high-glucose media, underwent contraction when treated with angiotensin II (0.001-10 microM). Seventy-five percent of the cells contracted. Not one contracted cell was seen in cultures grown without insulin in the medium, even when exposed to 10 microM angiotensin II. From these data, it appears that insulin may be required for the contractile response of mesangial cells to angiotensin II. Loss of contractile activity by mesangial cells in low- or no-insulin conditions (e.g., juvenile diabetes mellitus) could lead to a marked increase in glomerular blood flow, ultimately resulting in glomerulosclerosis.
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PMID:Insulin requirement for contraction of cultured rat glomerular mesangial cells in response to angiotensin II: possible role for insulin in modulating glomerular hemodynamics. 705 Oct 7

Gas chromatography/mass fragmentography was applied to measure sugars in the plasma of patients with diabetes mellitus (DM). The isotope-dilution technique was used in the calculation of 1,5-anhydro-D-glucitol (1,5-AG), whereas reductive deuterization of the samples and regression analysis of the reduction products were used to calculate the concentrations of mannose, fructose and mannitol. The concentrations of mannose and glucose were closely and positively correlated both in insulin-dependent (IDDM; r = 0.74, P = 0.001) and non-insulin-dependent (NIDDM; r = 0.89, P = 0.001) DM. The close correlation was also encountered in serial samples taken from patients with widely fluctuating plasma glucose concentrations. The mannose/glucose ratio was increased in NIDDM (P = 0.007). The concentration of 1,5-AG was decreased in both types of DM, but more markedly in IDDM. The concentration was negatively correlated with glucose concentration (r = 0.071, P = 0.02) and HbAtc (r = 0.84, P = 0.001) in NIDDM. It was postulated that both mannose and glucose, by competing with 1,5-AG of renal tubular sugar carrier sites, contribute to the high urinary excretion of 1,5-anhydroglucitol leading to depletion of the sugar in the diabetic organism. The high concentrations of circulating mannose suggested further that the contribution of mannose to the adverse effects of hyperglycaemia should be examined. The study demonstrated that parallel use of the isotope-dilution and reductive deuterization techniques is quite useful in the analysis of monosaccharides in biological fluids.
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PMID:Mannose, mannitol, fructose and 1,5-anhydroglucitol concentrations measured by gas chromatography/mass spectrometry in blood plasma of diabetic patients. 881 53

This study reports the first-phase insulin response (FPIR) calculated on a wide pediatric population. 138 non-obese, ICA- and GAD65 antibody-negative subjects, without family history of IDDM, were tested in 21 Italian Pediatric Diabetic Centers, according to a standardized protocol. After an overnight fast, 0.5 g/kg body weight of 25% dextrose (maximum 35 g) was infused over 2.5-3 minutes. Blood samples were taken at -10, 1, 3, 5 and 10 minutes after dextrose infusion for determination of insulin levels by radioimmunoassay. A significant positive relationship was observed between FPIR and pubertal stage groups (p = 0.0043), suggesting a progressive rise of FPIR throughout puberty. These results have to be taken into consideration in evaluating early abnormalities of carbohydrate metabolism in pubertal subjects. According to Tanner's stage the first percentile was 53 microU/ml for stage I, 53.6 microU/ml for stages II-III and 76.6 microU/ml for stages IV-V.
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PMID:Normal values of first-phase insulin response to intravenous glucose in healthy Italian children and adolescents. The Prediabetes Study Group of the Italian Society for Pediatric Endocrinology and Diabetology (SIEDP). 888 38

To search if biological effects of GLP-I on glucose metabolism in extrapancreatic tissue are present in diabetic states, we have studied the action of GLP-I and insulin on glycogen-enzyme activity, glycogen synthesis, and glucose metabolism in isolated hepatocytes and soleus muscle from adult streptozotocin (STZ)- and neonatal STZ-treated diabetic rats. This work confirms the previously reported insulin-like effects of GLP-I on glucose metabolism in both muscle and liver tissue from normal rats (control). The present study extends those observations to the muscle and liver tissue of diabetic animals. In both muscle and liver tissue, the metabolism of D-glucose, in the absence of added peptides, was more severely affected in adult STZ (IDDM model) than in neonatal STZ (nSTZ; NIDDM model) rats, and the magnitude of hormonal effect on metabolic variables was lower in diabetic rats than in control rats, as a rule. Nevertheless, in liver and muscle tissue of diabetic rats, GLP-I was able to increase glycogen synthase activity, augment the net rate of D-[U-14C]glucose incorporation into glycogen, and increase D-[5-3H]glucose utilization, D-[U-14C]glucose oxidation, and lactate production. In conclusion, GLP-I exerts insulin-like effects on D-glucose metabolism in both muscle and liver tissue in IDDM or NIDDM animal models, and present observations reinforce the view that GLP-I may represent a most promising tool in the treatment of diabetic patients.
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PMID:Preserved GLP-I effects on glycogen synthase a activity and glucose metabolism in isolated hepatocytes and skeletal muscle from diabetic rats. 923 49

Clinical observations indicate that diabetes leads to micro- and macroangiopathy involving endothelial dysfunction. Because recent studies indicate an antiangiopathic effect of celiprolol, but not of metoprolol, in type 1 diabetes, we investigated the direct influence of exposure to high D-glucose concentrations on endothelial cells and the possible effects of both beta-blockers. Nine different chronic treatments were carried out on cultured porcine aortic endothelial cells: 1) 5 mmol/l D-glucose ("normoglycemic" cells), 2) 5 mmol/l D-glucose plus 15 mmol/l L-glucose (osmotic control), 3) 5 mmol/l D-glucose plus 0.5 micromol/l celiprolol, 4) 5 mmol/l D-glucose plus 0.05 micromol/l metoprolol, 5) 5 mmol/l D-glucose plus 0.5 micromol/l celiprolol plus 5 micromol/l propranolol, 6) 20 mmol/l D-glucose ("hyperglycemic" cells), 7) 20 mmol/l D-glucose plus 0.5 micromol/l celiprolol, 8) 20 mmol/l D-glucose plus 0.05 micromol/l metoprolol, and 9) 20 mmol/l D-glucose plus 0.5 micromol/l celiprolol plus 5 micromol/l propranolol. Using the Fura-2 technique, application of either 1 nmol/l bradykinin or 1 micromol/l ATP to the normoglycemic endothelial cells led to a significant increase in intracellular calcium, whereas the hyperglycemic cells showed significantly less reactivity to both agents. Exposure of endothelial cells to L-glucose did not show any difference to normoglycemic controls. Coadministration of 20 mmol/l glucose and celiprolol demonstrated that the alteration of the calcium signal induced by high D-glucose concentrations could be significantly antagonized with celiprolol. In contrast, coincubation with metoprolol failed to normalize the calcium signal. This effect of celiprolol was completely abolished in the presence of propranolol. In normoglycemic cells, none of the beta-blockers influenced the intracellular calcium response to bradykinin or ATP. These results indicate that chronic treatment with high D-glucose concentrations leads to an impairment of calcium signaling, which might be ameliorated by celiprolol.
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PMID:Influence of chronic exposure to high concentrations of D-glucose and long-term beta-blocker treatment on intracellular calcium concentrations of porcine aortic endothelial cells. 951 47

The usefulness of a galactose specific lectin from P. tithymaloides was examined to study the hemagglutination pattern in 193 patients with diabetes mellitus out of which 34 cases were of insulin dependent. A control of 72 normal subjects was also included. The hemagglutination titre against a partially purified lectin from P. tithymaloides of control group ranged from 9.1 to 170 units per mg protein with a mean value of 54 units per mg protein. Significantly low titre was observed in the cases with insulin dependent diabetes mellitus, while non-insulin dependent diabetes mellitus cases did not show any significant change. Further significant reduction in the titre in insulin dependent diabetes mellitus group was shown to occur along with the increased duration of the diabetic condition, reflecting measurable erythrocyte surface alterations.
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PMID:Hemagglutination pattern of galactose specific lectin from Pedilanthus tithymaloides in diabetes mellitus. 971 58

Insulin and exercise have been shown to activate glucose transport at least in part via different signaling pathways. However, it is unknown whether insulin resistance is associated with a defect in the ability of an acute bout of exercise to enhance muscle glucose uptake in vivo. We compared the abilities of insulin and isometric exercise to stimulate muscle blood flow and glucose uptake in 12 men with type 1 diabetes (age 24 +/- 1 years, BMI 23.0 +/- 0.4 kg/m(2)) and in 11 age- and weight-matched nondiabetic men (age 25 +/- 1 years, BMI 22.3 +/- 0.6 kg/m(2)) during euglycemic hyperinsulinemia (1 mU. kg(-1). min(-1) insulin infusion for 150 min). One-legged exercise was performed at an intensity of 10% of maximal isometric force for 105 min (range 45-150). Rates of muscle blood flow, oxygen consumption, and glucose uptake were quantitated simultaneously in both legs using [(15)O]water, [(15)O]oxygen, [(18)F]-2-fluoro-2-deoxy-D-glucose, and positron emission tomography. Resting rates of oxygen consumption were similar during hyperinsulinemia between the groups (2.4 +/- 0.3 vs. 2.0 +/- 0.5 ml. kg(-1) muscle. min(-1); normal subjects versus patients with type 1 diabetes, NS), and exercise increased oxygen consumption similarly in both groups (25.3 +/- 4.3 vs. 20.1 +/- 3.0 ml. kg(-1) muscle. min(-1), respectively, NS). Rates of insulin-stimulated muscle blood flow and the increments in muscle blood flow induced by exercise were also similar in normal subjects (129 +/- 14 ml. kg(-1). min(-1)) and in patients with type 1 diabetes (115 +/- 12 ml. kg(-1). min(-1)). The patients with type 1 diabetes exhibited resistance to both insulin stimulation of glucose uptake (34 +/- 6 vs. 76 +/- 9 micromol. kg(-1) muscle. min(-1), P < 0.001) and also to the exercise-induced increment in glucose uptake (82 +/- 15 vs. 162 +/- 29 micromol. kg(-1) muscle. min(-1), P < 0.05). We conclude that the ability of exercise to increase insulin-stimulated glucose uptake in vivo is blunted in patients with insulin-resistant type 1 diabetes compared with normal subjects. This could be caused by either separate or common defects in exercise- and insulin-stimulated pathways.
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PMID:Resistance to exercise-induced increase in glucose uptake during hyperinsulinemia in insulin-resistant skeletal muscle of patients with type 1 diabetes. 1137 38


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