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

Growth and development of the thymus is dependent on secretions from the anterior pituitary, presumably growth hormone. Diabetes mellitus is known to reduce immunological competence. These studies compare the effects of bovine growth hormone (bGH) and the growth factor produced by plerocercoid larvae of the tapeworm, Spirometra mansonoides, on metabolism of lymphoid tissue, thymus and spleen, in hypophysectomized rats made diabetic with a single intraperitoneal injection of alloxan. Whereas the control diabetic-hypophysectomized rats gradually lost weight throughout the experimental period, both bGH and plerocercoid infection caused significant weight gains during the experimental period. The diabetic-hypophysectomized rats treated with bGH had significantly heavier thymuses and spleens than controls. Plerocercoid infection also caused significant increases in thymus weights. Both bGH and plerocercoids stimulated the metabolic activity of thymocytes isolated from treated rats and tested for their ability to incorporate 3H-thymidine into DNA in vitro. Thus, these growth factors have similar effects on the lymphoid tissue of diabetic-hypophysectomized rats which are apparently independent of normal insulin levels. Whether this anabolic effect is direct or mediated by somatomedin remains to be determined.
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PMID:Comparison of the effects of the growth factor produced by Spirometra mansonoides and growth hormone in diabetic-hypophysectomized rats: lymphoid tissue. 66 Mar 78

Antibodies to single stranded (SS-) and double stranded (DS-) DNA and RNA were determined by a passive microhemagglutination assay in sera from 80 children with juvenile-onset diabetes mellitus (JDM) and 129 children with asthma. The latter group was chosen for comparison with the JDM group because of their increased susceptibility to viral infection and the nonautoimmune nature of the disease. We found that JDM patients had increased titers of antibodies to SS-DNA (61.3%), synthetic polyadenylicpolyuridylic acid (Poly A-U) (78.8%), synthetic polyinosinicpolycytidylic acid (Poly I-C) (62.5%), and DS-RNA of statolon virus (51.3%) and reovirus (27.3%), respectively, in contrast to asthmatics (15.5, 34.9, 3.9, 20.2, and 2.3%, respectively) or to healthy controls. The difference of the incidence of antibodies among the groups is statistically significant (P less than 0.001). Presence of SS-DNA antibody found in two thirds of cases of JDM further support the increased prevalence of autoimmune phenomenon in that disease. Furthermore, the increased prevalence of DS-RNA antibodies in patients with JDM, found especially in cases of recent onset, is suggestive of an active immune response against the underlying viral replications that may have led to beta cell injury in islets of pancreas.
Diabetes 1978 Nov
PMID:Antibodies to nucleic acids in juvenile-onset diabetes. 72 Jul 70

The effects of alloxan-induced diabetes on liver regeneration were investigated. Normal and diabetic rats were sacrificed at eight time periods between 16 hours and 4 weeks following two-thirds partial hepatectomy or sham operation. The results indicate that alloxan-induced diabetes delays but does not prevent liver regeneration following partial hepatectomy. This delay is indicated by a depressed synthesis of RNA, DNA and protein during the first post-operative day and a lack of mitotic figures in the 24-hour sample. In addition, the synthesis of these three cellular constituents did not return to control levels as rapidly in the diabetics. Compared with the sham operated animals, the concentrations of total serum protein remained depressed longer in the diabetic hepatectomized animals. The data indicate that the metabolic alterations associated with alloxan diabetes delay the onset of the regenerative process and prolong the recovery period.
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PMID:Liver regeneration in normal and alloxan-induced diabetic rats. 88 99

Streptozotocin-induced diabetes in the rat alters intestinal function, causes hyperphagia and arrests body growth, but stimulates intestinal growth, particularly in the mucosa. Therefore we measured several indices of epithelial cell proliferation to gain insight on possible factors responsible for the increased mucosal cell mass in the small intestine. We examined epithelial cell proliferation in upper jejunum and terminal ileum of weight-matched control and diabetic rats pair fed or eating ad libitum. Cell proliferation was measured two ways: (1) isolating whole crypts 1 hr after injection of [3H]thymidine ([3H]TdR) and calculating disintegrations per minute per crypt (dpm per crypt), and (2) autoradiography of mucosal sections to obtain labeled cells per crypt, total cells per crypt-villus column, and cell migration rates. Autoradiography showed diabetes: (1) increased cell number of crypt-villus columns and increased labeled cells per crypt section, primarily jejunum, and (2) did not alter cell migration except for an increase in the ileum of diabetics eating ad libitum. Cell proliferation measured as dpm per crypt virtually doubled in diabetics in both segments regarless of dietary regimen. Dpm per crypt is a three-dimensional measurement based on the whole crypt. The increase in cell number and labeled cells per crypt in jejunal sections is also consistent with increased cell division, but shows a much smaller effect. The nature of the histological technique (two-dimensional) limits its usefulness for measuring morphological changes, and this may explain the discrepancy. Hence, the primary effect of diabetes is increased DNA synthesis (dpm per crypt) and this appears to be the main explanation for stimulated mucosal growth.
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PMID:Proliferation rate and transit time of mucosal cells in small intestine of the diabetic rat. 91 75

Wound healing as a model for diabetic angiopathy has been studied by light and electron microscopy. Biochemical studies of the rate of incorporation of 3H-proline and 3H-thymidine into collagen and DNA, respectively, have confirmed the morphologic observations. In both the normal and the diabetic, there was a marked decrease in the rate of collagen and DNA synthesis, suggesting that most of the cells in the biopsies were stunned by the injury and ceased DNA replication during the initial phase. In control mice this decrease was followed by a modest but significant burst of DNA replication, which peaked at two hours and by the fourth hour had returned to the one-hour level. In the diabetic this burst of DNA replication was absent and no capillary morphogenesis was seen at two, four, and eight hours. At 16 hours, there were only a few abnormal nascent vessels observed in the diabetic and antiserum-treated mice. The peak in the rate of collagen synthesis at four hours correlated well with the condensation of collagen at the wound margin and the fibroblast rough-endoplasmic-reticulum (RER) proliferation. In the diabetic mice, there was a significantly attenuated rate of collagen synthesis for the entire 16-hour period. The lack of DNA replication, capillary morphogenesis, fibroblast RER proliferation, and decreased collagen synthesis in the diabetic mouse can be considered interrelated and significant factors in the diabetic's impaired response to cellular injury. In view of the increased frequency and severity of injury to the circulation of the diabetic and the impaired response to repair such injury, it is likely that wound healing is a promising model for diabetic angiopathy.
Diabetes 1976
PMID:Wound healing: a model for the study of diabetic angiopathy. 97 88

Non-insulin-dependent (type II) diabetes mellitus (NIDDM) is characterized by hyperglycaemia and insulin resistance, and affects nearly 5% of the general population. Inherited factors are important for its development, but the genes involved are unknown. We have identified a large pedigree in which NIDDM, in combination with a sensorineural hearing loss, is maternally inherited. The maternal inheritance and the observed decrease in mitochondrial enzyme activities of the respiratory chain indicate a genetic defect in the mitochondrial DNA. An A to G transition was identified at nucleotide 3,243, a conserved position in the mitochondrial gene for tRNA(Leu)(UUR). This mutation cosegregates with the disease in this family and is absent in controls, and indicates that a point mutation in mitochondrial DNA is a pathogenetic factor for NIDDM.
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PMID:Mutation in mitochondrial tRNA(Leu)(UUR) gene in a large pedigree with maternally transmitted type II diabetes mellitus and deafness. 128 50

Exponentially growing rat islet cells (RINr) and hamster islet cells (HIT T-15) were incubated in presence of tolbutamide (10-1000 microM), gliclazide (0.1-10 microM) or glibenclamide (0.01-10 microM) for 15 hrs. Accumulation of insulin in culture medium was estimated by RIA. Effects of sulfonylureas (SU) on cell proliferation were assessed by 3H-thymidine (3H-T) incorporation into cellular DNA. All of SUs used stimulated insulin production in RIN and HIT cell cultures (with an exception of tolbutamide, which markedly suppressed insulin secretion in HIT cells at 1000 microM). 3H-T incorporation into RIN cells was elevated only in presence of gliclazide (10 microM), whereas tolbutamide at 1000 M significantly inhibited RIN cell proliferation. Gliclazide (0.1 microM) and glibenclamide (0.01-10 microM) enhanced 3H-T incorporation into HIT cells. Further detailed investigations of mechanisms of SU effects on islet cell reproduction will be of use for designing optimal strategy of hypoglycemizing therapy of diabetes mellitus.
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PMID:[The insulin-secreting and proliferative activity of established islet cells in the presence of sulfonylurea]. 128 6

Recently, human amniotic fluid (HAF) from healthy women was found to stimulate growth and function of pancreatic B-cells. Here, the effect of HAF and serum from healthy probands (HS) was compared with that from probands with gestational (GD), noninsulin-dependent (NIDDM), or insulin-dependent diabetes (IDDM) on islet function and replication. Rat islets were cultured in the presence of either HAF or HS for 7 d. Insulin content and basal insulin release were not different after exposure of the islets to HAF or HS from healthy or diabetic women. In contrast to HS, HAF provoked the islets to deliver significantly more insulin during culture. Additionally, the same islets exhibited a more intense response to a glucose challenge. The degree of HAF-induced insulin release was not influenced by the type of diabetes. HAF and HS from GD and NIDDM women did not influence the islet DNA synthesis in comparison to HAF and HS from healthy pregnant women. However, HAF but not HS from IDDM pregnant women, elicited a significant increase in islet replication. Most effective in stimulating islet cell replication were HAFs from IDDM pregnant women belonging to the White D-type. It was shown that the relatively high concentration of insulin in the HAFs was not directly responsible for the observed increase of the islet DNA synthesis. HAF from women with long-term diabetes is supposed to contain factor(s) that might directly or indirectly enhance islet replication.
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PMID:Human amniotic fluid obtained from diabetic women. A potent stimulator of islet cell replication. 128 18

Defects of the mitochondrial respiratory chain form a clinically and biochemically heterogeneous group of diseases. Mitochondrial diseases include myopathies and multisystem disorders that are defined either by biochemical abnormalities of the mitochondria or by the presence of "ragged red fibers" in muscle-biopsy specimens stained with modified Gomori's trichrome stain. Several syndromes have been identified. Typical Kearns-Sayre syndrome is a sporadic condition that is characterized by an onset before the age of 20, progressive external ophthalmoplegia, pigmentary retinopathy and cardiac disorders. Mitochondrial DNA deletions were found in patient with Kearns-Sayre syndrome. We report the case of a 33 year-old woman, with neuromuscular syndrome of the Kearns-Sayre type, insulin-sensitive diabetes and complete heart block, who was implanted a pacemaker.
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PMID:[Mitochondrial disease and complete heart block. Kearns-Sayre syndrome. Description of a case]. 130 Apr 76

The application of molecular scanning techniques to the detection of potentially pathogenic mutations in candidate genes in patients with non-insulin-dependent diabetes has revealed a number of molecular variants of uncertain pathophysiologic significance. The determination of the significance of such variants requires large-scale population studies of the prevalence of the mutant in affected and control groups. Herein, we describe two adaptations of the technique of single nucleotide primer extension (SNuPE) which allow the simultaneous examination of large numbers of alleles at multiple loci. The usefulness of these adaptations is illustrated by their application to the simultaneous detection of three point mutations, two in the tyrosine kinase domain of the insulin receptor and one in the insulin-responsive glucose transporter (GLUT4) in a highly insulin-resistant NIDDM population. By pooling genomic or amplified DNA and performing the SNuPE reactions with three primers of different length we could readily examine 300 alleles on a single 20 lane gel. Using pooled SNuPE, we also examined a large British Caucasian control population for the prevalence of GLUT4 Ile383, a variant which has previously been reported only in NIDDM. GLUT4 Ile383 was detected in 2/42 of the highly insulin-resistant NIDDM subjects and 4/240 middle-aged blood donors. Family studies and examination of the expressed mutant transporter will be necessary to establish whether this mutation is of functional significance. Pooled and multiplex SNuPE are powerful techniques with wide applicability to population genetic studies of specific mutations.
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PMID:Rapid and simultaneous detection of multiple mutations by pooled and multiplex single nucleotide primer extension: application to the study of insulin-responsive glucose transporter and insulin receptor mutations in non-insulin-dependent diabetes. 130 12


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