Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Temporal changes in non-B cell populations were determined during the period of B cell hyperplasia in diabetes-resistant C57BL/6J mice. Pancreases from normal and db/db mice between 3 and 20 weeks of age were stained immunocytochemically for glucagon, somatostatin and pancreatic polypeptide (PP), and changes in A, D and PP cell volume densities quantified by image analysis. Further, islet volumes, D cell volumes and actual D cell numbers per islet were determined by analysis of serial sections through entire islets. The volume of db/db islets was three- and ten-fold elevated above normal by 8 and 20 weeks, respectively, due mainly to B cell hyperplasia. D cell volume density exhibited a transient increase during the initial phase of B cell hyperplasia, but then showed a gradual reduction; the average number and absolute volume of D cells per islet was comparable in db/db and normal islets from older mice. In contrast, PP cell volume density remained stable throughout, suggesting that this cell type kept pace with B cell hyperplasia. A cells showed a reduced volume density throughout and were distinguished from other islet cells which all responded positively to a degree, albeit non-coordinately, to the mitogenic stimulus exerted by db gene expression. The finding that A cells shared with certain neuroectodermally-derived cell types a differentially high concentration of sn-glycerol-3-phosphate dehydrogenase further underscored the uniqueness of the A cell from other cell types.
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PMID:Temporal changes in pancreatic islet composition in C57BL/6J-db/db (diabetes) mice. 636 Jul 82

In 120 patients with diabetes mellitus the indices of the blood and erythrocytic acid-alkali balance, glycemia level, blood lactate and pyruvate concentrations, the activity of serum malate dehydrogenase and lactate dehydrogenase, as well as of succinate dehydrogenase and alpha-glycerophosphate dehydrogenase in lymphocytic mitochondria were studied. A remarkable difference of the indices examined, depending on the disease severity, duration or compensation state of carbohydrate metabolism, was noted comparatively to those of normal. Insulin therapy and the diet No. 9, combined with hyperbaric oxygenation, was accompanied by a rapid (within 12 to 18 days) compensation of carbohydrate metabolism and good dynamics of all the tests. The results obtained are indicative of a significant improvement of the tissue metabolism both on the glycolysis level and in the cycle of tricarboxylic acids.
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PMID:[Effect of insulin therapy and hyperbaric oxygenation on the enzyme activity of tissue metabolism in diabetes mellitus]. 676 Jan 77

Homogenates of isolated pancreatic islets contain 40-70 times as much flavin-linked glycerol-3-phosphate dehydrogenase (EC 1.1.99.5) as homogenates of whole pancreas, liver, heart, or skeletal muscle when the activity is assayed with either iodonitrotetrazolium or with dichloroindophenol as an electron acceptor. Intact mitochondria from islets release 3HOH from [2-3H]glycerol phosphate 7 times faster than do skeletal muscle mitochondria. The activity of the cytosolic, NAD-linked, glycerol phosphate dehydrogenase (EC 1.1.1.8) in pancreatic islets is comparable to that of the mitochondrial dehydrogenase so a glycerol phosphate shuttle is possible in pancreatic islets. Diazoxide, an inhibitor of insulin release in vivo and in vitro, inhibits the islet mitochondrial glycerol phosphate dehydrogenase in all three of the assays mentioned above at concentrations that inhibit insulin release and CO2 formation from glucose by isolated pancreatic islets. Diazoxide does not inhibit the dehydrogenase in mitochondria from skeletal muscle, liver, and heart. A slight inhibition in mitochondria from whole pancreas can be accounted for as inhibition of the islet dehydrogenase because no inhibition is observed in mitochondria from pancreas of rats treated with alloxan, an agent that causes diabetes by destroying pancreatic beta cells. The results of this study are compatible with the hypothesis that the mitochondrial glycerol phosphate dehydrogenase has a key role in stimulus-secretion coupling in the pancreatic beta cell during glucose-induced insulin release.
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PMID:High content of mitochondrial glycerol-3-phosphate dehydrogenase in pancreatic islets and its inhibition by diazoxide. 679 May 37

Diabetes induced during gestation has previously been demonstrated to increase adipose accretion in the fetal pig. The present experiment examined whether maternal diabetes alters the proliferation and differentiation of the fetal preadipocyte. Seven crossbred gilts were injected with alloxan (50 mg/kg) at d 75 of gestation to induce diabetes and seven additional gilts were injected with buffer (controls). All gilts underwent Caesarean section of d 105 of gestation. Cells obtained from adipose tissue of fetuses of diabetic swine (FDS) at d 105 of gestation demonstrated a greater (P < .05) proliferative response (57%) and higher (P < .05) rates of differentiation as determined by sn-glycerol-3-phosphate dehydrogenase (142% increase) and lipoprotein lipase (80% increase) activities than cells acquired from fetuses of control swine (FCS). Adipogenic activity of the sera from these two groups of fetuses did not differ when tested on adipose tissue from fetuses at 105 d of gestation. However, use of these sera on cells derived from normal fetuses at 75 d of gestation resulted in detection of an increase (P < .05) in adipogenic activity within the sera from FDS. This study suggests that maternal diabetes causes alterations in the preadipocyte fraction of cells within the developing adipose tissue that result in formation of more adipocytes and thus permits greater capacity for lipid accumulation in the growing fetus of the diabetic pig. These alterations in the preadipocyte result from the activity of factors that transitionally function during the latter half of gestation.
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PMID:The onset of maternal diabetes in swine induces alterations in the development of the fetal preadipocyte. 760 56

A deficient activity of the mitochondrial FAD-linked glycerophosphate dehydrogenase (m-GDH) in the pancreatic islet B-cell may represent a contributing factor in the pathogenesis of non-insulin-dependent (Type 2) diabetes. This enzyme controls circulation in the glycerol phosphate shuttle and, hence, plays a key role in the B-cell glucose-sensing device. An impaired activity of this enzyme in pancreatic islets was documented in several, but not all, animal models of inherited or acquired non-insulin-dependent diabetes. Enzymatic studies conducted in lymphocytes or islets from diabetic patients, as well as a search for possible mutations of the m-GDH gene, were recently undertaken to extend these observations to human subjects.
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PMID:Non-insulin-dependent diabetes mellitus and islet B-cell mitochondrial glycerophosphate dehydrogenase deficiency. 764 19

The monomethyl ester of succinic acid (SME) was recently proposed as a novel tool for stimulation of proinsulin biosynthesis and insulin release in animal models of non-insulin-dependent diabetes mellitus. In the present study, either saline or SME (14 mmol/day) was infused for 3 days to control rats, animals injected with streptozotocin during the neonatal period, and Goto-Kakizaki rats with inherited diabetes. The infusion of SME failed to correct the anomalies found in the islets of diabetic rats, namely, a decreased activity of the mitochondrial FAD-linked glycerophosphate dehydrogenase, a low insulin content, and an impaired secretory response to various nutrient secretagogues including D-glucose, 2-ketoisocaproate, and the combination of L-leucine and L-glutamine. These findings raise the question of whether a more prolonged administration of SME is required to raise the insulin store and improve the secretory potential of the endocrine pancreas in animals with type 2 diabetes.
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PMID:Enzymatic and secretory activities in pancreatic islets of non-insulin-dependent diabetic rats after short-term infusion of succinic acid monomethyl ester. 771 Jul 67

The aim of the present study is to compare normal and tumoral pancreatic islet cells in terms of both the activity of selected cytosolic and mitochondrial enzymes participating to nutrient catabolism and the intrinsic properties of FAD-glycerophosphate dehydrogenase. The activity of the glycolytic enzymes hexokinase and lactate dehydrogenase was higher in tumoral (RINm5F) than normal islet cells. The opposite was seen for glutamate decarboxylase, glutamate-oxaloacetate transaminase, glutamate-pyruvate transaminase, glutamate dehydrogenase, 2-ketoglutarate dehydrogenase and FAD-glycerophosphate dehydrogenase (m-GDH). These findings are consistent with the high rates of glycolysis and protein synthesis seen in tumoral islet cells compared with normal islet cells, which favour mitochondrial oxidative events associated with the catabolism of D-glucose and amino acids. The intrinsic catalytic properties of m-GDH were comparable, albeit not identical, in normal and tumoral islet cells. Since a deficiency of m-GDH in pancreatic islets may represent a contributing factor in the pathogenesis of non-insulin-dependent diabetes, it is proposed that RINm5F cells may readily yield sufficient islet m-GDH for purification and further gene cloning.
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PMID:Activity of cytosolic and mitochondrial enzymes participating in nutrient catabolism of normal and tumoral islet cells. 776 86

This review reevaluates the possible roles of glut-2 underexpression, glucokinase gene mutation, glucose-6-phosphate hyperactivity, glycerophosphate dehydrogenase (FAD-linked) deficiency and glycogen accumulation in the pancreatic B-cell as contributive factors in the pathogenesis of Type 2 diabetes.
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PMID:Physiology and pathology of islet metabolism. 780 57

Impairment of glucose-induced insulin secretion in non-insulin-dependent diabetes mellitus (NIDDM) may be caused by GLUT 2 underexpression in the pancreatic beta cell, a mutation of the glucokinase gene, glucose 6-phosphatase overactivity, FAD-linked glycerophosphate dehydrogenase deficiency, a mitochondrial DNA defect and/or a secondary phenomenon of so-called glucotoxicity possibly involving glycogen accumulation in the beta-cell. It is proposed tht the methyl esters of succinic acid and related molecules may represent new tools with which to bypass these defects in glucose transport, phosphorylation and further catabolism and, hence, to stimulate both proinsulin biosynthesis and insulin release in NIDDM.
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PMID:The beta cell in NIDDM: giving light to the blind. 782 38

The mitochondrial FAD-linked enzyme glycerophosphate dehydrogenase plays a key role in the pancreatic B-cell glucose sensing device. In the present study, the activity of this enzyme was examined in islets of fa/fa rats in which inherited diabetes mellitus is associated with obesity, hyperinsulinism and severe insulin resistance. The specific activity of both FAD-linked glycerophosphate dehydrogenase and glutamate dehydrogenase were decreased in islet and liver homogenates prepared from fa/fa, as compared to Fa/Fa, rats, this coinciding with a low ratio between glutamateoxalacetate and glutamate-pyruvate transaminase activity in both islet and liver extracts, islet hyperplasia, hyperinsulinemia and hepatic steatosis in the hyperglycemic fa/fa rats. It is speculated that a low activity of FAD-linked glycerophosphate dehydrogenase in the pancreatic B-cell may participate to the perturbation of glucose homeostasis in fa/fa rats, like in other animal models of non-insulin-dependent diabetes mellitus.
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PMID:Impaired FAD-glycerophosphate dehydrogenase activity in islet and liver homogenates of fa/fa rats. 783 41


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