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

The susceptibility to competitive ganglionic blocking agents such as hexamethonium (C6), tetraethylammonium bromide (TEAB), mecamylamine and d-tubocurarine (d-TC), of the superior cervical ganglion in cats with pancreatectomy and spontaneous diabetes or in animals treated with contrainsular drugs such as cortisone or dihydrochlorothiazide, was found to be decreased as compared to the reactivity of normal controls. The increased tolerance to ganglioplegics was not correlated with the elevation of the blood sugar level, and proved to be resistant to an acute administration of insulin. The results could not be explained by a decrease in the specific cholinesterase activity of the ganglionic tissue due to diabetes. Alteration of the peripheral autonomic synaptic transmission may be an early sign of diabetic neuropathy.
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PMID:Diabetes-induced alterations of autonomic nerve function in the cat. 3 32

The clinical phenotype of Werner's syndrome (WS) includes short stature, premature cataracts, skin atrophy, osteoporosis, graying and loss of hair, neoplasia, diabetes mellitus, and arteriosclerosis. Cultured cells from patients with this autosomal recessive disorder exhibit chromosomal instability and a markedly reduced replicative lifespan and growth rate. To elucidate the cell cycle alterations associated with the growth deficit, we continuously labeled lymphoid cell lines from five WS patients and from four healthy adult controls with 5-bromodeoxyuridine. Bivariate Hoechst 33258/ethidium bromide flow cytometry revealed a 2.4-h prolongation in the minimal duration of the S phase of WS cells (P less than 0.005). Moreover, the fraction of proliferating cells irreversibly arrested in the S phase (5.4% vs 1.4% in controls) was significantly elevated in WS (P less than 0.001). Other cell cycle compartments were not significantly affected in WS cell lines. As a partial test of the hypothesis that the WS phenotype is due to a defect in DNA topoisomerase I (topo I) or DNA topoisomerase II (topo II) we exposed lymphoid cells from a healthy control to the topo I inhibitor camptothecin or to the topo II inhibitor 4'-(9-acridinylamino)methanesulfon-m-anisidine. The cell kinetic alterations elicited by these compounds differed from that exhibited by untreated WS patients. Thus, a primary defect in topo I or II is unlikely in WS. Our cell cycle results, however, provide important evidence that the biochemical genetic lesion is in fact expressed in lymphoblastoid cell lines, the most readily available cells from such subjects.
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PMID:Impaired S-phase transit of Werner syndrome cells expressed in lymphoblastoid cell lines. 132 51

As aminoguanidine (AG) is known to prevent non-enzymatic glycosylation in various tissues, we have histologically and biochemically evaluated AG effects on the skin in control, SZ-diabetic and AG-treated (25 mg/kgbw/day, 10w) diabetic rats. HbA1c and plasma glucose levels in diabetic and AG-treated diabetic rats were maintained about two times higher than those in control rats during the 10 weeks of the experiment. Histological findings revealed that the dermis in diabetic rats was thin and edematous, associated with swelling and degeneration of collagen fibers. Necrobiotic changes were seen in the lower dermis. These changes were greatly improved in AG-treated diabetic rats. Skin glucose contents in diabetic and AG-treated diabetic rats were about 10 times higher than those in the controls, whereas there was no difference in the sorbitol contents between three groups. Dry weight of the skin and collagen content was well correlated (r = 0.9044) and collagen represented 78.0 +/- 2.3% of the dry weight. By SDS-PAGE analysis of cyanogen bromide digests it was shown that high molecular weight peptides were increased in diabetic rats, but were decreased in AG-treated diabetic rats. The mean of glycosaminoglycan (GAG) contents of diabetic skin was 54% of that in the controls (1.58 +/- 0.09 vs. 2.94 +/- 0.39 micrograms/mg dry weight, P < 0.0025), which increased significantly in AG-treated diabetic rats (1.75 +/- 0.07 microgram/mg dry weight, P < 0.01 vs. diabetic).(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes Res 1992
PMID:Amelioration of dermal lesions in streptozotocin-induced diabetic rats by aminoguanidine. 134 7

The molecular basis of eight DR4 subtypes resides in several nucleotide substitutions in the third hypervariable region of the DR beta 1 chain. The typing of DR4 subsets using the mixed lymphocyte culture (MLC) assay or allele-specific oligonucleotide hybridization is expensive, cumbersome, and requires the use of radioisotopes. We have therefore developed a rapid and safe procedure for subtyping DR4-alleles that involves selective amplification of the second exon of the DR4-DRBI gene followed by unambiguous subtype discrimination after digestion with five allele-specific endonucleases [polymerase chain reaction (PCR)-restriction fragment length polymorphism (RFLP)] and visualization of the polymorphic fragments with silver or ethidium bromide staining. Validity of this subtyping procedure was initially examined by the use of cell lines of known subtypes. Three groups of DR4 patients with insulin-dependent diabetes mellitus (IDDM) from Chinese, Tunisian, and Caucasian populations were subtyped and the prevalence of subtype associations with IDDM was compared.
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PMID:A simple nonradioactive method of DNA typing for subsets of HLA-DR4: prevalence data on HLA-DR4 subsets in three diabetic population groups. 168 Aug 38

To investigate further the role of cytokines in the pathogenesis of type I insulin-dependent diabetes mellitus, the effects of interleukin-1 beta (IL-1), tumour necrosis factor-alpha (TNF) and gamma-interferon (IFN) were tested on rat insulinoma INS-1 cells. Whereas TNF and IFN had, respectively, a minor or no effect on insulin production, IL-1 caused a time- and dose-dependent decrease in insulin release and lowered the insulin content as well as the preproinsulin mRNA content of INS-1 cells. Both IL-1 and TNF exerted a cytostatic effect, estimated by a decrease in [3H]thymidine incorporation, while only IL-1 decreased cell viability as measured by the colorimetric 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) test. The glutathione content of INS-1 cells was shown to be modulated by the presence of 2-mercaptoethanol in the culture medium, but was not affected by IL-1 or TNF. In conclusion, INS-1 cell culture is considered to be a useful model for studying the effect of cytokines on insulin-producing cells. The differentiated features of these cells will permit several questions to be addressed regarding the mechanism of action of IL-1 and eventually other cytokines, both at the level of gene expression and of intracellular signalling.
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PMID:Effects of cytokines on rat insulinoma INS-1 cells. 173 60

The authors investigated the involvement of red blood cell aggregation in thrombosis by comparing erythrocyte aggregation in patients with myocardial infarction (28 patients) or cerebrovascular accidents (68 patients) with that in a normal control group (38 subjects). The erythrocyte aggregation was assessed by light transmission aggregometer, and aggregation was induced by hexadimethrine-bromide. Increased erythrocyte aggregation was detected in all patients with thrombotic disorders. In addition, patients with diabetes mellitus showed a marked increase in erythrocyte aggregation as compared with those without diabetes. The effect of ticlopidine on erythrocyte aggregation was also studied. It was demonstrated that ticlopidine inhibited aggregation in vitro. An inhibitory effect was shown to be dose dependent, with 10 microM ticlopidine inhibiting aggregation completely. After four weeks' oral administration of 200 mg ticlopidine, there was significant decrease of abnormally increased erythrocyte aggregation in patients with thrombosis.
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PMID:Effects of ticlopidine on erythrocyte aggregation in thrombotic disorders. 192 16

Insulin release is influenced by the autonomic nervous system. Regarding parasympathetic control, previous reports have shown that regulation of insulin release is executed exclusively through muscarinic receptors in the pancreatic islets. In the present study, however, we examined the effect on insulin release at the islet level of various agents affecting the parasympathetic nervous system, especially nicotinic receptor blockers. Pancreatic islets isolated from adult Wistar male rats were incubated with these agents and insulin release in the media was measured. Acetylcholine chloride (10(-5) M), as well as distigmine bromide (10(-6), 10(-5) M), both of which are cholinesterase inhibitors, stimulated insulin release, whereas atropine (5 x 10(-6), 5 x 10(-5) M) suppressed it. On the other hand, serum and IgG from myasthenia gravis patients, containing anti-acetylcholine receptor antibodies, affected insulin release, and alpha-bungarotoxin (10(-9)-10(-7) M), a nicotinic receptor blocker, stimulated insulin release dose-dependently. The present observations suggest that insulin release is influenced by the parasympathetic nervous system, mediated via not only muscarinic but also nicotinic receptors.
Diabetes Res Clin Pract 1990 Mar
PMID:Possible involvement of cholinergic nicotinic receptor in insulin release from isolated rat islets. 197 Dec 10

Techniques for freezing rat islets have been examined by the intensive use of the supravital stains fluorescein diacetate and ethidium bromide. By the use of a simple scoring system, the effect of the cooling rate, treatment with dimethyl sulfoxide (DMSO), rate of thawing, and postthaw culture were examined. These studies showed the most effective method to be a 24-h culture of islets, followed by partial incubation with 20% DMSO at 0 degrees C, followed by seeding at -8 degrees C in an alcohol bath. The islets were then cooled at a rate of -0.25 degrees C/min to -40 degrees C followed by quenching in liquid nitrogen at -196 degrees C. Rapid thawing at 37 degrees C was then followed by a 24-h culture. Islets from four Lewis rat donors were cryopreserved, counted, and transplanted intraportally into streptozocin-induced diabetic Lewis rats. Corresponding control transplants were performed with islets from four donors only cultured for 48 h. The results showed that reversal of hyperglycemia in severely diabetic rats was obtained at 5, 5, 6, 6, 6, or 8 days with cryopreserved islets from four donors, compared to reversal of diabetes at 1, 4, 5, 6, 7, and 12 days with islets from four donors subjected to culture alone. The new cryopreservation technique has several small modifications over previously described methods and results in a significant improvement in islet survival.
Diabetes 1989 Jan
PMID:Normalization of hyperglycemia in diabetic rats by intraportal transplantation of cryopreserved islets from four donors. 249 2

Although glycogen synthase is present in a highly inactivated state in hepatocytes from streptozocin-induced diabetic rats, glucagon, vasopressin, and vanadate are still able to further decrease the basal activity of the enzyme. This inactivation was observed with the low-to-high glucose 6-phosphate activity ratio assay. The inactivation of glycogen synthase occurred concomitantly with the activation of glycogen phosphorylase. When hepatocytes from diabetic rats were incubated with [32P]phosphate and then with the agents and when the 32P-labeled glycogen synthase was immunoprecipitated, we observed that the 32P bound to the 88,000-Mr subunit increased in all cases. All the [32P]phosphate was located in two cyanogen bromide fragments of the enzyme, indicating that the enzyme was phosphorylated at multiple sites. The fragments were precisely those phosphorylated by glycogenolytic hormones in hepatocytes from normal rats. These results demonstrated that hepatic glycogen synthase, although highly inactive, is under potential hormonal control in diabetes and that the enzyme has not reached its maximal level of phosphorylation. Furthermore, they indicated that vanadate behaves as a glycogenolytic agent regarding its effects on glycogen-metabolizing enzymes in hepatocytes from diabetic rats.
Diabetes 1989 Jun
PMID:Control of glycogen synthase and phosphorylase in hepatocytes from diabetic rats. Effects of glucagon, vasopressin, and vanadate. 249 42

The risk of congenital abnormality in diabetic pregnancy is about four times that for the normal population. Past clinical studies have suggested hyperglycemia and hyperketonemia as the factors responsible for these abnormalities, with no reference to the possible effects of low insulin levels. We examine the effect of hypoinsulinemia on rat embryonic growth and development in culture while normal glucose levels are maintained. With anti-insulin antibody bound to an affinity column containing cyanogen bromide-activated Sepharose 4B beads, insulin was selectively removed from the homologous culture serum eluted down the column. A culture of rat embryos from the early head-fold stage for 50 h in insulin-depleted normoglycemic homologous serum (insulin levels 0.055-0.18 ng/ml) showed retardation of growth and development when compared with control embryos. Adding physiological amounts (10 ng/ml) of insulin back into the insulin-depleted serum subsequently restored growth level to that of control embryos. We conclude that low insulin levels, encountered in newly diagnosed diabetic pregnancy, may be instrumental in increasing the risk of congenital abnormalities.
Diabetes 1989 Jun
PMID:Effects of low insulin levels on rat embryonic growth and development. 265 45


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