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

A continuous extracorporeal monitoring system for blood glucose employing an electrochemical sensor is described. The sensor, about the size of a nickel, is rapid, is specific for glucose, generates its own power, and consists of two galvanic oxygen electrodes. Over one oxygen electrode is affixed a plastic matrix to which glucose oxidase is covalently bound; a blank matrix is over the other, which serves as a reference. Oxygen is consumed in the glucose-oxidase-containing matrix, decreasing the current from the underlying oxygen electrode. The current decrease is nonlinearly proportional to the glucose concentration. The sensor is clamped between small blocks of plastic fitted with inlet and outlet nipples so that blood pumped from the animal passes over the two electrodes and thence to an automated chemical analysis for comparison. Blood is collected and anticoagulant added in a double-lumen catheter. Blood is withdrawn at the rate of 1 cc. per hour. Results obtained by use of the system in rabbits are reported. The capacity of the system to continuously monitor changes in blood glucose produced by repeated glucose tolerances is shown in hypo-, normo-, and hyperglycemic animals. Some properties of the system and its calibration are discussed.
Diabetes 1976 Feb
PMID:Continuous extracorporeal monitoring of animal blood using the glucose electrode. 124 75

In this study, serum nickel levels of diabetic patients and healthy controls were determined by AAS with a graphite furnace. The serum nickel concentrations were found to be 1.15 +/- 1.89 micrograms/L in healthy controls and 0.82 +/- 0.74 microgram/L in diabetics. There was, however, no statistically significant difference between the two groups (p = 0.13). The relationship of nickel levels to diabetes type and duration, diabetic complications and treatment, sex, age, and heredity was investigated. However, again no significant differences were found, nor was there any correlation between serum nickel levels and blood sugar, HBa1c, fructosamine, sialic acid levels, and age.
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PMID:Serum nickel levels of diabetic patients and healthy controls by AAS with a graphite furnace. 128 93

G-proteins are important mediators of hormonal inhibition of insulin secretion. To characterize the pertussis toxin-sensitive substrates present in HIT cell membranes, we performed immunoblots with specific antisera and found evidence for the presence of Gi alpha 1, Gi alpha 2, Gi alpha 3, and three forms of Go alpha. We observed that pertussis toxin-sensitive substrates mediate all of the effects of SRIF, and a major portion of the effects of EPI, on insulin secretion from rat islets during static incubations. These results agree with our previously reported studies examining phasic glucose-induced insulin secretion from HIT cells. To ascertain whether inhibition of adenylate cyclase, presumably involving coupling of the catalytic subunit to Gi, may be a common mechanism for both hormones, we studied the effects of 8-bromo-cyclic AMP and found that this agent partially prevented the inhibitory effects of both hormones. We also observed that the inhibitory effects of SRIF and EPI on insulin were nonadditive, that both hormones were additive to nickel chloride during inhibition of insulin release, and that they noncompetitively inhibited glipizide-induced insulin secretion through pertussis toxin-sensitive mechanisms. Together, these results suggest that both hormones exert their effects on insulin secretion at multiple G-protein-regulated sites including adenylate cyclase and sites distal to the glipizide-binding site on the KATP channel.
Diabetes 1992 Nov
PMID:G-proteins and hormonal inhibition of insulin secretion from HIT-T15 cells and isolated rat islets. 138 67

The potential of nickel chloride to prevent streptozotocin-induced hyperglycemia was tested in rats in vivo. To induce diabetes, streptozotocin (100 mg/kg body weight) was injected as a single dose. Streptozotocin treatment resulted in a significant decrease in plasma insulin and ceruloplasmin, and pancreatic Cu, protein, and Cu-Zn superoxide dismutase activity. In rats treated with nickel chloride (10 mg/kg body weight) and streptozotocin, these values were comparable with those observed in control rats. The results indicate that nickel chloride injected before streptozotocin prevented streptozotocin-induced hyperglycemia, and suggest that the protective effect was related to Cu-Zn superoxide dismutase activity, mediated by copper.
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PMID:Effect of nickel chloride on streptozotocin-induced diabetes in rats. 304 20

Phospholipase A2 activation may be a pivotal step in glucose-induced insulin secretion; however, recent studies have focused on only one by-product (arachidonic acid). To examine the possible role of the other by-product (lysophospholipids), the lysoderivatives of alkylacyl- (ether linked) or diacylphospholipids were applied to rat islets in static incubations. 1-O-alkyl-2-lyso-sn-glyceryl-3-phosphorylcholine [lyso-PAF, the precursor of platelet-activating factor (PAF)] or lysophosphatidylcholine initiated insulin release at 1.7 mM glucose. Two preparations of PAF itself (0.005-5000 ng/ml) were without effect at 1.7 or 16.7 mM glucose, but PAF was nearly equipotent to lyso-PAF at greater than or equal to 20 micrograms/ml. A precursor-product relationship was suggested because the precursors (alkylacyl- or diacylglyceryl-phosphorylcholine) of all three active metabolites were inactive. The stimulatory effect of lyso-PAF is largely independent of any toxic or lytic effect, being biphasic, reversible, unassociated with impairment of the subsequent physiologic functioning of treated islets, and inhibitable (by Ni2+, La3+, or nordihydroguaiaretic acid but not by other lipoxygenase inhibitors). It also occurred at threshold concentrations at which islet morphology and 51Cr retention were preserved. Furthermore, lyso-PAF-induced insulin secretion was markedly impaired by reduced ambient temperature (16 degrees C) or by the impermeant anion isethionate, further implying initiation of true exocytotic granule release and fission. Lyso-PAF (but not arachidonic acid) also circumvented the inhibition of glucose-induced insulin release caused by phospholipase inhibitors. Generation of endogenous lysophospholipids through exogenous application of phospholipase A2 also initiated insulin release, an effect responding to a panel of potential inhibitors identically to that induced by exogenously provided lysophospholipids. We propose that glucose activates phospholipase A2 in the pancreatic islet, leading to the generation of lysophospholipids; the latter may couple energy production to insulin release, at least in part via the promotion of Ca2+ translocation.
Diabetes 1986 Jul
PMID:Ether-linked lysophospholipids initiate insulin secretion. Lysophospholipids may mediate effects of phospholipase A2 activation on hormone release. 308 3

In search of possible interactions between plastic tubings used for insulin-pump treatment and commercial regular insulin preparations, various catheter sets made from polyvinyl chloride (PVC), polyethylene (PE), and nylon plastics were perfused at 30 degrees C in a laboratory setting for up to 72 h. The perfused insulin solutions were analyzed by high-performance liquid chromatography and atomic absorption spectroscopy. Although no plasticizer, e.g., dioctyl phthalate, or nickel or chromium ions were found in the perfusates, substantial interactions between the plastics and the insulin solutions were detected, extraction of bacteriostatic additives from the insulin solutions in particular. The PVC retained up to 88% of the bacteriostatics from the insulin preparations, whereas PE tubings retained only 10-15%. Whether the loss of preservatives during perfusion through PVC catheters predisposes to cutaneous infections during insulin-pump therapy remains to be shown.
Diabetes Care
PMID:Interaction between plastic catheter tubings and regular insulin preparations used for continuous subcutaneous insulin-infusion therapy. 329 80

Copper-zinc superoxide-dismutase (SOD-E.C. 1.15.1.1.) is present in high concentration in the beta-cells of pancreatic islets, and its specific activity correlates with maintenance of beta-cell function. In this paper the authors studied the effect of nickel chloride (s.c.) on alloxan toxicity. It was found that alloxan (100 mg x kg-1) inhibited insulin release of rats islets and thus, induced hyperglycemic response. The activity of erythrocytes and pancreatic SOD enzymes was partially inhibited upon alloxan treatment. It was found that nickel chloride (s.c. 10 mg x kg-1) produced stimulation of insulin release in rats treated by subcutaneous (s.c.) alloxan injection. The potential of NiCl2 to prevent alloxan induced diabetes was shown by the observed SOD specific activity increase in rats. In conclusion, our experiments show that nickel chloride prevented alloxan induced toxicity in rats.
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PMID:[Nickel chloride and alloxan. I. Determination of glucose, insulin and superoxide dismutase in blood and pancreas of rats]. 333 32

The Thermal Sensitivity Tester (TST) is a portable device designed to quantify the ability to discriminate small differences in temperature at the distal extremities of the hands and feet. The testing surfaces are two identical nickel-coated copper plates, which can be set and maintained over a wide range of temperature levels. The threshold for detecting the colder surface is determined using a two-alternative, forced-choice algorithm. The mean threshold in the normal population is 0.67 degree C and 1.01 degree C for the index finger and great toe, respectively. The TST is especially useful in diabetic neuropathy and for rapid screening of large populations under field conditions.
Diabetes 1986 May
PMID:Thermal sensitivity tester. Device for quantitative assessment of thermal sense in diabetic neuropathy. 395 85

Insulin antibodies measured by a radioimmune method (ABR) are significantly better inducers of hyperglycemia than are insulin antibodies measured by an immune hemolysis method (ABH) when injected intraperitoneally into mice. The ability to induce hyperglycemia by an insulin antiserum can be predicted by the titer of ABR measured. ABR interact in vitro with determinants severely perturbed on nickel-insulin, partially perturbed on proinsulin and desasparagine-desalanine insulin, and unaffected on zinc-insulin or zinc-free monocomponent insulin. ABH, on the other hand, interact in vitro with determinants severely perturbed on proinsulin and desasparagine-desalanine insulin but stabilized on nickel-insulin and zinc-insulin. Since the connecting peptide of proinsulin is probably in apposition to the A-chain residues on the solvent surface, the more effective reaction of proinsulin with ABR than with ABH is submitted as evidence that ABR are directed toward residues on the B-chain surface of insulin. Because ABR are more effective inducers of hyperglycemia than are ABH, it is proposed that the degree of hyperglycemia induced by antibodies in vivo is a result of interactions with determinants on the B-chain surface of insulin. These results support the possibility that insulin in vivo is more accessible for interaction with antibodies directed to the B-chain of insulin. It is also possible that ABR, which are directed to B-chain determinants, are of higher affinity than is the affinity between insulin and receptors or that the active site of insulin for maintaining euglycemia includes the B-chain surface residues.
Diabetes 1980 May
PMID:Induction of hyperglycemia with insulin antibodies to B-chain determinants. 615 99

There is accumulating evidence that the metabolism of several trace elements is altered in insulin-dependent diabetes mellitus and that these nutrients might have specific roles in the pathogenesis and progress of this disease. Magnesium deficiency is the most evident disturbance of metal metabolism in diabetes mellitus. Hypomagnesemia might increase the risk of ischemic heart disease and severe retinopathy. Increased urinary loss of zinc is a commonly encountered feature of diabetes. High-dose oral zinc might enhance wound healing, although data regarding diabetes are lacking. Chromium increases tissue sensitivity to insulin and tends to raise high-density lipoprotein (HDL) cholesterol and the HDL:low-density lipoprotein ratio. Selenium is involved in processes which protect the cell against oxidative damage by peroxides produced from lipid metabolism. There is one report of elevated serum selenium in diabetic children although the clinical significance of this finding is still unclear. An insulin-like effect has recently been attributed to vanadium in experimental animals, a finding of potential interest to man. Current knowledge does not implicate iron, iodine, manganese, cobalt, nickel, silicone, fluoride, molybdenum or tin in the pathophysiology of diabetes. Appropriate trace element supplementation might prove beneficial in ameliorating some physiological deficiencies associated with diabetes and prevent or retard secondary complications. However, properly designed and well-documented trials, especially on magnesium supplementation, need to be performed before rationales for such supplementation are developed. The potential roles of vanadium, chromium and selenium in diabetes constitute challenging areas for further experimental and clinical research.
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PMID:The role of trace elements in juvenile diabetes mellitus. 640 Apr 52


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