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

Pancreatic islets from healthy (control) and neonatally streptozocin-induced diabetic (STZ-D) rats, a model for non-insulin-dependent diabetes mellitus, were incubated with 3H2O and 5.5 or 16.7 mM glucose. At 5.5 mM glucose, no detectable [3H]glucose was formed. At 16.7 mM, 2.2 patom.islet-1.h-1 of 3H was incorporated into glucose by the control islets and 5.4 patom.islet-1.h-1 by STZ-D islets. About 75% of the 3H was bound to carbon-2 of the glucose. Glucose utilization was 35.3 pmol.islet-1.h-1 by the control and 19.0 pmol.islet-1.h-1 by the STZ-D islets. Therefore, 4.5% of the glucose-6-phosphate formed by the control islets and 15.7% by the STZ-D islets was dephosphorylated. This presumably occurred in the beta-cells of the islets catalyzed by glucose-6-phosphatase. An increased glucose cycling, i.e., glucose----glucose-6-phosphate----glucose, in islets of STZ-D rats may contribute to the decreased insulin secretion found in these animals.
Diabetes 1990 Apr
PMID:Glucose cycling in islets from healthy and diabetic rats. 218 Jul 57

After induction of diabetes with streptozocin (STZ-D) in rats, we measured vasoactive intestinal polypeptide (VIP) content in sciatic nerve and spinal cord obtained from nondiabetic, untreated STZ-D, and insulin-treated STZ-D rats. Eight weeks after the onset of diabetes, caudal nerve conduction velocity (NCV) in the untreated STZ-D rats (n = 13) was slower than in the controls (n = 11; mean +/- SE 30.9 +/- 0.6 vs. 41.4 +/- 1.8 m/s, P less than 0.001). The decrease in NCV was less marked in the insulin-treated STZ-D rats (n = 11; 36.3 +/- 0.9 m/s, P less than 0.05 vs. control). VIP content in sciatic nerve decreased in the untreated STZ-D rats (1.33 +/- 0.23 ng/g wet wt) compared with the other groups (control, 3.10 +/- 0.44, P less than 0.01; insulin-treated STZ-D, 2.44 +/- 0.55, P less than 0.05). However, in spinal cord, VIP content was not significantly different among the three groups. The VIP levels in sciatic nerve showed a positive correlation with NCV (r = 0.430, P less than 0.01). In addition, an inverse correlation between VIP levels and blood glucose levels was observed (r = -0.5624, P less than 0.001). NCV was also inversely correlated with blood glucose levels (r = -0.7662, P less than 0.001). Together with a previous morphological study, these findings suggest a possible causal relationship between reduced VIP content and diabetic neuropathy.
Diabetes 1990 May
PMID:Decreased VIP content in peripheral nerve from streptozocin-induced diabetic rats. 218 11

The effect on skeletal muscle proteolysis of acute (20-hour) glucocorticoid treatment (dexamethasone 1.5 mg/kg, subcutaneously [SC]) was tested using the eviscerated rat preparation. According to this method, the peripheral tissues (primarily the skeletal muscles) are isolated by functional hepatectomy-nephrectomy. Total proteolysis is estimated from the rate of rise of plasma tyrosine concentration in the presence of cycloheximide to block protein synthesis. Myofibrillar proteolysis is measured from the rate of release into the plasma of the nonreutilized, nonmetabolized amino acid 3-methylhistidine (3MH), in the absence of cycloheximide. In normal rats, dexamethasone increased total proteolysis by 20% and myofibrillar proteolysis by 75% (both P less than .025 v saline controls). In diabetic-adrenalectomized rats prepared 2 weeks earlier (65 mg/kg streptozocin [STZ] followed by adrenalectomy), dexamethasone caused much greater increments in rates of total proteolysis (94%) and myofibrillar proteolysis (240%) (both P less than .001 v saline controls). Because diabetic animals are extremely sensitive to glucocorticoid-induced proteolysis, we also examined whether the acute proteolytic effect of diabetes itself might be mediated by adrenal cortical hormones. Previously adrenalectomized rats studied 20 hours after STZ showed a 40% augmentation of total proteolysis (P less than .01), an effect similar to that produced by acute diabetes in rats with intact adrenals. We conclude that glucocortical hormones cause a catabolic effect on total and myofibrillar skeletal muscle protein which is exaggerated when the counteracting action of insulin is reduced, but that the excess proteolysis of acute insulin deficiency is independent of the endogenous glucocorticoids secretion.
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PMID:Influence of glucocorticoids on skeletal muscle proteolysis in normal and diabetic-adrenalectomized eviscerated rats. 219 Nov 92

Semicarbazide-sensitive amine oxidase (SSAO) activity was investigated in serum and tissues of streptozotocin diabetic rats. Diabetes was induced by a single intraperitoneal injection of streptozotocin (STZ, 60 mg/kg) and rats were killed at 1, 3, 7, 9, 14, 28 and 56 days after treatment. STZ increased serum glucose and serum SSAO activity at all time points with a maximal increase (2 to 3 fold) at day 7. Kidney SSAO activity showed significant increases on days 9 and 14 (2.5 and 4 fold, respectively). SSAO activity of aorta, lung and pancreas was not changed significantly. Kinetic analysis showed that the elevation in both serum and kidney SSAO activity was due to an increased Vmax with no change in Km. SSAO activity appears to be selectively increased in the serum and kidney of STZ diabetic rats which may be indicative of a relationship between serum SSAO and early renovascular damage in this animal model of diabetes mellitus.
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PMID:Semicarbazide-sensitive amine oxidase activity in streptozotocin diabetic rats. 221 72

In a group of rats with streptozotocin induced diabetes the excretion of calcium, magnesium, phosphorus and creatinine in urine was investigated and the calcium, magnesium and phosphorus content of bone in relation to the duration of the disease. The authors observed that in diabetic rats the urinary losses of calcium, magnesium and phosphorus increase significantly. The creatinine excretion is also significant but lower in relation to calciuria and therefore the value of Nordin's index in diabetic rats rises markedly. Bone of diabetic rats in the early stage of diabetes (32 days) loses magnesium, while the calcium and phosphorus content does not change significantly. During longer persistence of severe diabetes (70 days) a significant drop of all three minerals in bone was observed. The bones of diabetic animals on the 70th experimental day were macroscopically smaller and were very fragile. The authors' findings suggest a marked influence of streptozotocin diabetes on calcium phosphate metabolism and bone metabolism, in particular on account of STZ diabetes, on an early drop of magnesium in bone. The possible impact of this finding for clinical practice will have to be tested further.
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PMID:[The effect of streptozotocin-induced diabetes treated with insulin on the metabolism of calcium, magnesium and phosphorus]. 221 56

In situ perfusion of the fetal side of the anesthetized rat placenta was used to monitor glucose fluxes in nondiabetic, streptozocin-induced diabetic (STZ-D), acutely hyperglycemic nondiabetic, and acutely normoglycemic STZ-D rats. STZ-D resulted in increased accumulation of glucose in the perfusate during a single passage through the fetal vasculature compared with nondiabetic rats, and this increase was maintained in normoglycemic STZ-D rats, indicating glucose release from placental stores. The fractional clearance of 3-O-[14C]methylglucose, a nonmetabolizable glucose analogue, across the placenta was decreased in both STZ-D groups compared with nondiabetic rats but unchanged in hyperglycemic nondiabetic rats, implying a reduction in glucose transporters in diabetic placentas. The difference between the transfer of D-[3H]glucose and 3-O-[14C]methylglucose indicated that 17% of the glucose was retained while traversing the placenta of nondiabetic rats, whereas a smaller percentage (8%) but a larger absolute amount (9 vs. 6 mumol/h) of glucose was retained by the placentas of the severely STZ-D rats. This retention was markedly enhanced in hyperglycemic nondiabetic rats and STZ-D rats when rendered normoglycemic. The net accumulation of perfusate glucose was less than that predicted from radiolabeled transfer data, indicating that glucose is also back transferred from the perfusate to the mother's placenta. We conclude that maternal diabetes markedly affects placental glucose flux.
Diabetes 1990 Mar
PMID:Effects of maternal diabetes on placental transfer of glucose in rats. 230 92

The present study has indicated that significant shifts in plasma, urinary, and tissue taurine and in non-taurine dialyzable amines occur in the STZ-induced diabetic rat, especially in the kidney. Taurine administration at relatively low dosage ameliorated only kidney taurine concentration. Anticipated alterations in plasma glucose and creatinine were observed but neither of these changes was affected by taurine administration. Similarly, urinary output of creatinine, glucose, and NAG increased significantly among diabetic rats, but none of these were detectably influenced by taurine. Increases in plasma triglycerides observed in STZ-induced diabetes appear to be attenuated by taurine administration, and although cholesterol concentrations were lower in taurine-treated rats, the differences were not statistically significant. These findings should encourage further studies of these effects in rats as a useful model for several complications of human diabetes including atherosclerosis, retinopathy, and nephropathy.
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PMID:Supplemental taurine in diabetic rats: effects on plasma glucose and triglycerides. 231 Jun 8

Brain regional glucose metabolism and regional blood flow were measured from autoradiographs by the uptake of [3H]-2-deoxy-D-glucose and [14C]iodoantipyrine in streptozocin-induced diabetic (STZ-D) rats. After 2 days of diabetes, glucose metabolism in the neocortex, basal ganglia, and white matter increased by 34, 37, and 8%, respectively, whereas blood flow was unchanged. After 4 mo, glucose metabolism in the same three regions was decreased by 32, 43, and 60%. This reduction was paralleled by a statistically nonsignificant reduction in blood flow in neocortex and basal ganglia. It is suggested that the decrease of brain glucose metabolism in STZ-D reflects increased ketone body oxidation and reduction of electrochemical work.
Diabetes 1990 Apr
PMID:Regional brain glucose metabolism and blood flow in streptozocin-induced diabetic rats. 231 47

The mechanisms responsible for hyperfiltration in diabetes mellitus (DM) as well as for the initiation and progression of diabetic nephropathy are not fully elucidated. Enhanced prostaglandin E2 (PGE2) production has been invoked in the former and thromboxane (TXB2) and hyperlipidemia in the latter. Fish oil (FO)-enriched diets can favorably alter eicosanoid synthesis and serum lipid profiles. We therefore examined the effects of a FO-enriched diet on glomerular filtration (GFR), proteinuria, glomerular eicosanoid production, and serum lipids in rats with streptozotocin-induced DM (STZ-DM). Groups of 5-8 rats with STZ-DM were maintained on low insulin and then pair-fed with isocaloric diets enriched with either FO (20% w/w) or beef tallow (BT; 20% w/w). GFR was determined in the same animals at onset of diet and after 8 and 20 weeks on the respective diets by [14C]inulin clearance using implanted osmotic minipumps each time. Significant hyperfiltration was present initially and GFR did not change on either diet for 20 weeks, in spite of a significant and greater than 50% decrease in all prostaglandins (PGE2, TXB2, PGF2 alpha, 6-keto, PGF1 alpha) produced by glomeruli isolated from DM/FO as compared to DM/BT or control rats. FO diet completely corrected the hypertriglyceridemia of diabetes and significantly reduced the mild and early proteinuria of DM. The decrease in proteinuria and the correction of hyperlipidemia of DM by a FO-enriched diet may be beneficial in the long term not only for the development of diabetic glomerulopathy, but also for the accelerated atherosclerosis of DM.
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PMID:Effects of fish oil on glomerular function in rats with diabetes mellitus. 240 55

Exocrine secretory function in response to 10 pM to 10 nM synthetic secretin was evaluated in perfused pancreas isolated from control, streptozocin-induced diabetic (STZ-D), alloxan-induced diabetic (ALX-D), and insulin-treated STZ-D rats. In STZ-D rats, the basal rate of pancreatic juice flow was significantly increased (10.3 +/- 1.0 microliters/20 min) compared with control rats (4.4 +/- 0.2 microliters/20 min). The basal rate of amylase output as well as pancreatic amylase content were significantly decreased to less than 5% of control values. The basal rates of protein and trypsinogen outputs were similar in both groups. In both control and diabetic rats, secretin caused a dose-dependent increase in exocrine secretion. Secretin (10 pM to 10 nM) induced 1.1- to 11.7-fold increases in exocrine secretion in STZ-D rats. These increases were significantly lower than the 2.1- to 20.8-fold increases in control rats. Furthermore, there was no significant increase in exocrine secretion from STZ-D rats in response to 10 pM secretin, although this concentration of secretin caused a significant increase in control rats. Secretin-induced exocrine secretion in ALX-D rats was similar to that in STZ-D rats. In insulin-treated STZ-D rats, the basal rates of pancreatic secretion were not significantly different from those of control rats. These results suggest that insulin resistance in this patient was due to a circulating factor of low molecular weight that uncoupled insulin stimulation of glucose transport from receptor binding and phosphorylation. The factor appears to increase the binding activity of the alpha-subunit of the insulin receptor without affecting the kinase activity of the beta-subunit.
Diabetes 1988 Sep
PMID:Secretin-induced exocrine secretion in perfused pancreas isolated from diabetic rats. 245 29


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