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

The effect of diabetes on rat hepatic ornithine decarboxylase (ODC) activity was studied in male rats 4 h to 8 days after the ip or iv administration of streptozotocin. Hepatic ODC activity increased 4-fold above control on the fourth day of diabetes. Increased ODC activity was observed with a dose of streptozotocin (70 mg/kg iv) which increased plasma ketones and glucagon and reduced plasma insulin. No change was seen with doses causing only mild hyperglycemia without change in plasma ketones, glucagon, or insulin. Insulin therapy prevented the increase in hepatic ODC activity in diabetic rats. Adrenalectomy or hypophysectomy also prevented the diabetes-associated increase of ODC activity. The studies suggest that insulin deficiency may result in increased hepatic polyamine synthesis.
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PMID:Effect of streptozotocin-induced diabetes on hepatic ornithine decarboxylase activity in the rat. 74 42

Renal hypertrophy and hyperfiltration are early manifestations of human and experimental diabetes that may contribute to the late development of diabetic nephropathy. The biochemical events resulting in kidney growth in the diabetic state are completely unknown. Since growth of various tissues is accompanied by increased formation of polyamines, we studied whether polyamines were involved in the growth of the kidney observed in diabetic rats. This was done by measuring the activity of the rate-limiting enzyme in the polyamine pathway (ornithine decarboxylase; ODC) in kidneys from control, diabetic and insulin-treated diabetic animals. The ODC activity in the kidney was increased in the diabetic animals with a maximal rise 24 h after diabetes induction (6-fold, P less than 0.01); the activity thereafter declined. However, on day 14 the activity was still significantly elevated (2.5-fold, P less than 0.05). In insulin-treated diabetic animals the kidney ODC activity was only increased 3-fold (P less than 0.05) after 24 h, and for the rest of the study period the activity was about 1.8-fold higher than in control rats. After 14 days the kidneys from diabetic rats were significantly larger than kidneys from both control and insulin-treated diabetic rats, 1066 +/- 43 mg vs. 904 +/- 16 mg and 959 +/- 36 mg, respectively (P less than 0.01). For comparison, the ODC activity was also investigated in muscle. However, in muscle from diabetic animals the ODC activity declined steadily during the 14 days to 34% of control values (P less than 0.01), and insulin treatment completely normalized the ODC activity in muscle.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased ornithine decarboxylase activity in kidneys undergoing hypertrophy in experimental diabetes. 151 80

The effect of exogenous insulin treatment on the pancreatic regeneration after major pancreatectomy was evaluated in dogs. More than 92% of the pancreas was removed near the duodenum with the main pancreatic duct left intact. All 26 dogs developed diabetes mellitus (DM) immediately after surgery, and these dogs were divided into two groups: insulin-treated group (n = 19) and noninsulin-treated group (n = 7). All seven dogs in the noninsulin-treated group died within seven weeks after surgery, whereas all dogs in the insulin-treated group survived until the twelfth week, except for six dogs sacrificed on the seventh week, and finally seven (53.8%) of 13 dogs recovered from DM. DNA and polyamine syntheses in the remnant pancreatic tissue at the third day increased more significantly in the insulin-treated group than in the noninsulin-treated group. Sigma IRI in IV-GTT was maintained more significantly in the insulin-treated group, and the regeneration rate at the seventh week was also significantly higher in the insulin-treated group than in the noninsulin treated group. Furthermore, the regeneration rate of the remnant pancreas at seventh week correlated well with DNA synthesis and ornithine decarboxylase activity on the third day. The exogenous insulin treatment after major pancreatectomy enhanced the proliferation of the remnant pancreas within the first week, and it maintained endogenous insulin secretion, promoting pancreatic regeneration.
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PMID:Effect of insulin treatment on the regeneration of the remnant pancreas after major pancreatectomy in dogs. 174 42

1. The present study was designed to investigate if the aldose reductase inhibitor ponalrestat is capable of preventing the impairment of the response of ornithine decarboxylase (ODC) to nerve crush in streptozotocin (STZ)-diabetic rats. 2. ODC activity was measured in the dorsal root ganglia of crushed and uncrushed contralateral sciatic nerve of non-diabetic, ponalrestat-treated non-diabetic, STZ-diabetic and ponalrestat-treated STZ-diabetic rats. 3. Twenty four hours after crush, a significant (P less than 0.001) increase in the ratio of ODC activity in ganglia of crushed relative to uncrushed nerves was found in non-diabetic but not in diabetic rats, as expected. In the ponalrestat-treated diabetic rats the ratio was significantly higher (P less than 0.001) than that in the untreated diabetic rats and was not different from that in the non-diabetic group. 4. Ponalrestat also significantly decreased absolute levels of ODC activity in ganglia of uncrushed nerves from diabetic and non-diabetic animals. Despite the near-normal induction of ODC activity by nerve crush in the ponalrestat-treated diabetic animals, absolute ODC activity remained lower than that in ganglia of uncrushed nerves from non-diabetics. 5. We conclude that ponalrestat is able to prevent the impaired induction of ODC in experimental diabetes. The results, however, call into question the relationship between impaired ODC induction and diabetes-induced defects in nerve regeneration, which are insensitive to ponalrestat.
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PMID:Impaired induction of nerve ornithine decarboxylase activity in the streptozotocin-diabetic rat is prevented by the aldose reductase inhibitor ponalrestat. 212 96

Diabetes mellitus causes a more profound reduction of left ventricular weight (LVW) in the spontaneously hypertensive rat (SHR) than it does in nonhypertensive strains. Diabetes also depresses the activity of cardiac ornithine decarboxylase (ODC), an index of cell growth. We measured ODC activity, of ventricular homogenates obtained from diabetic SHR and nonhypertensive WKY rats, with and without chronic treatment with insulin or triiodothyronine (T3). Left ventricular ODC activities of nondiabetic SHR and WKY rats were not different from each other. Streptozotocin-induced diabetes (8 weeks) reduced left ventricular ODC activity of SHR and WKY rats to the same extent; the effect was characterized by a reduction in apparent Vmax with no change in apparent Km. Both T3 and insulin therapy prevented the decline in ventricular ODC activity in both strains, although only the effect of insulin was correlated with LVW. The results suggest that the effects of diabetes on LVW and ODC activity are independent of attendant reductions in serum thyroid hormone levels. However, the results did not reveal any strain-selective effects of diabetes on ODC activity which might have contributed to the pronounced loss of LVW in the SHR strain.
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PMID:Cardiac ornithine decarboxylase of diabetic spontaneously hypertensive rat: effects of insulin and thyroid hormone treatment. 214 35

Injury of the rat sciatic nerve is accompanied by an increased activity of the enzyme ornithine decarboxylase (ODC) in dorsal root ganglia. This increase is impaired in streptozotocin-induced diabetes, in which retrograde axonal transport of proteins is reduced. In order to confirm the relationship between altered axonal transport and ODC induction we treated rats with acrylamide i.p. to cumulative doses of 150 and 350 mg/kg. One sciatic nerve was crushed under anaesthesia and 24 h later dorsal root ganglia were removed and assayed for ODC activity by a dual-label radioenzymatic method. The ratio of activity of 2.41 +/- 0.57 (crushed side over control side) was reduced to 1.66 +/- 0.9 and 1.7 +/- 0.65 after acrylamide treatment at 150 and 350 mg/kg, respectively. The results are consistent with the postulated role of retrograde axonal transport in the cell body responses to nerve injury and may explain the effect of acrylamide on nerve regeneration.
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PMID:The effect of acrylamide on the induction of ornithine decarboxylase in the dorsal root ganglion of the rat. 240 Sep 13

Rat dorsal root ganglia respond to sciatic nerve injury with an increase in the activity of the enzyme ornithine decarboxylase (ODC). The increase is impaired under certain conditions (e.g. diabetes, Vinca alkaloid treatment) where retrograde axonal transport is reduced. The purpose of the experiments was to determine if the neurotoxin 2,5-hexanedione, also known to interfere with retrograde axonal transport, similarly affected ODC induction. Rats were treated with 2,5-hexanedione i.p. to a cumulative dose of 6 and 8 g/kg. One sciatic nerve was crushed under anaesthesia and 24 h later the dorsal root ganglia were removed and assayed for ODC activity by a radioenzymatic method. The ratio of ODC activity of 1.57 +/- 0.58 (crushed side over control side) was reduced to 1.02 +/- 0.41 1.08 +/- 0.39 after 2,5-hexanedione at 6 g and 8 g/kg, respectively. The enzyme was not inhibited by addition of 2,5-hexanedione in vitro. The results confirm the role of retrograde axonal transport in nerve cell responses to injury and are consistent with the effects of 2,5-hexanedione on nerve regeneration.
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PMID:The effect of 2,5-hexanedione on the induction of ornithine decarboxylase in the dorsal root ganglion of the rat. 240 39

Streptozotocin-induced diabetes of 7 weeks duration increased male Sprague-Dawley rat kidney ornithine decarboxylase activity by 4.8-fold but did not affect the liver enzyme. Hydrazine treatment of 4 hr duration stimulated equally kidney ornithine decarboxylase activities of nondiabetic and diabetic rats. Hydrazine treatment increased liver ornithine decarboxylase activity in the nondiabetic rat but did not increase it in the diabetic rat. Since hydrazine stimulates ornithine decarboxylase activity prior to polyamine and protein syntheses, we speculate that the lack of hydrazine stimulation of ornithine decarboxylase in the diabetic liver may be related in part to the unrestrained gluconeogenesis and depressed Kreb's cycle activity: the latter being required for protein synthesis.
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PMID:Hydrazine stress in the diabetic: ornithine decarboxylase activity. 321 30

The effect of diabetes on some enzymes of polyamine metabolism was studied in male rats 1-12 days after administration of streptozotocin. Hepatic ornithine decarboxylase activity decreased in the first days after the administration, but increased thereafter. The decrease was not due to an alteration of the ODC-antizyme concentration, nor to a posttranslational modification catalyzed by transglutaminase. S-adenosylmethionine decarboxylase and ornithine transaminase were both increased. Spermidine acetyltransferase activity was practically unchanged, while its inactivating factor was markedly decreased.
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PMID:Activity of some enzymes involved in the metabolism of polyamines in the liver of streptozotocin-diabetic rats. 615 27

1. Concentrations of polyamines, amino acids, glycogen, nucleic acids and protein, and activities of ornithine decarboxylase and S-adenosylmethionine decarboxylase, were measured in livers from control, streptozotocin-diabetic and insulin-treated diabetic rats. 2. Total DNA per liver and protein per mg of DNA were unaffected by diabetes, whereas RNA per mg of DNA and glycogen per g of liver were decreased. Insulin treatment of diabetic rats induced both hypertrophy and hyperplasia, as indicated by an increase in all four of these constituents to or above control values. 3. Spermidine content was increased in the livers of diabetic rats, despite the decrease in RNA, but it was further increased by insulin treatment. Spermine content was decreased by diabetes, but was unchanged by insulin treatment. Thus the ratio spermidine/spermine in the adult diabetic rat was more typical of that seen in younger rats, whereas insulin treatment resulted in a ratio similar to that seen in rapidly growing tissues. 4. Ornithine decarboxylase activity was variable in the diabetic rat, showing a positive correlation with endogenous ornithine concentrations. This correlation was not seen in control or insulin-treated rats. Insulin caused a significant increase in ornithine decarboxylase activity relative to control or diabetic rats. 5. S-Adenosylmethionine decarboxylase activity was increased approx. 2-fold by diabetes and was not further affected by insulin. 6. Hepatic concentrations of the glucogenic amino acids, alanine, glutamine and glycine were decreased by diabetes. Their concentrations and that of glutamate were increased by injection of insulin. Concentrations of ornithine, proline, leucine, isoleucine and valine were increased in livers of diabetic rats and were decreased by insulin. Diabetes caused a decrease in hepatic concentration of serine, threonine, lysine and histidine. Insulin had no effect on serine, lysine and histidine, but caused a further fall in the concentration of threonine.
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PMID:Polyamine and amino acid content, and activity of polyamine-synthesizing decarboxylases, in liver of streptozotocin-induced diabetic and insulin-treated diabetic rats. 616 56


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