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

Streptozotocin treatment (125 mg/kg) in the Chinese hamster induced hyperglycaemia, hypoinsulinaemia, hyperglucagonaemia and changes in body, liver, pancreas, stomach, kidney and adipose tissue weights. The pancreatic reserves of insulin and glucagon in the diabetic animals were low, but stomach glucagon high. These animals showed high levels of phosphoenolpyruvate carboxykinase and low levels of glucokinase, hexokinase, isocitrate dehydrogenase and malic enzyme, but normal levels of pyruvate kinase in the liver. Increases in lactate dehydrogenase subunit B and isozymes 2, 3 and 4 were also observed in the liver, but not in the epididymal fat pad, of the diabetic animals. N-Acetyl-beta-D-glucosaminidase was elevated in plasma, liver and heart, but not in the kidney of the treated animals. Renal alpha-galactosidase and beta-glucosidase were depressed, whereas beta-galactosidase and alpha-glucosidase remained essentially normal. These features indicated that there were considerable differences between the biochemical disorders associated with streptozotocin-diabetes in the Chinese hamster and the published observations in the rat.
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PMID:Streptozotocin-induced diabetes in the Chinese hamster. Biochemical and endocrine disorders. 59 Jun 51

Vitreous fluorophotometry was used to evaluate the integrity of the blood-retinal barrier to fluorescein in hooded rats. Streptozotocin-induced diabetes mellitus caused a breakdown of this barrier within ten days. Normalization of blood glucose levels with insulin significantly reduced (P less than .005) the increased permeability. This functional microangiopathy might prove to be the earliest detectable change in the retinal circulation in experimental diabetes.
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PMID:Alteration of the blood-retinal barrier in experimental diabetes mellitus. 65 25

The activity of several regulatory enzymes representing the pathways of glycolysis, gluconeogenesis, NADPH generation and lipogenesis was measured in rat placenta maternal and foetal livers on the 20th day of gestation. Streptozotocin diabetes, induced on the 12th day of gestation, or 48 h of fasting did not induce adaptive changes in the activity of placental enzymes while producing a typical insulin deficiency pattern in maternal liver. Foetal liver enzyme activities were unaffected by fasting and in diabetes showed changes suggestive of foetal hyperinsulinaemia. A small increase was observed in the activity of placental pyruvate kinase and a small decrease in that of PEP carboxylase in diabetic and in glucocorticoid-treated rats; these changes were reciprocal to those in the maternal liver and were attributed to hyperglycaemia, as was the increase in placental glycogen. Lack of response to insulin deficiency and to other endocrine alterations indicates that placenta is not sensitive to stimuli which induce adaptive alterations in hepatic enzymes. The only consistent change found in placental enzyme activities was a decrease associated with gestational age.
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PMID:Placental enzymes of glycolysis, gluconeogenesis and lipogenesis in the diabetic rat and in starvation. Comparison with maternal and foetal liver. 72 Jul 82

Streptozotocin-induced diabetes suppressed the normal development of the nine glycolytic and lipogenic enzyme activities measured. With the exception of NADP-isocitrate dehydrogenase, insulin replacement therapy induced increased activities of the enzymes in streptozotocin-treated rats. Insulin appeared to have a specific effect on the activities of glucokinase, ATP-citrate lyase, malic enzyme, and glucose-6-P-dehydrogenase.
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PMID:Effect of streptozotocin diabetes and insulin administration on some liver enzyme activities in the post-weaning rat. 72 37

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

Blood lipids and glucose were studied in streptozotocin diabetic rats during hyperthermia. Blood glucose, free fatty acids (F.F.A.) and glycerol of diabetic rats with a rectal temperature of 42 degrees C (hyperthermic) were elevated significantly above those values found in normothermic (TR = 38 degrees C) diabetic or normothermic non-diabetic rats as well as hyperthermic non-diabetic rats. Streptozotocin diabetes caused an elevation in blood triglycerides of normothermic rats, but this hypertriglyceridemia was depressed in diabetic rats during hyperthermia. As in the case of diabetic animals, hyperthermia also caused a depression in the blood triglycerides of non-diabetic rats. However, unlike in the diabetic animals, the blood F.F.A. of non-diabetic rats were depressed during hyperthermia. Although hyperthermia caused a significant increase in the blood glucose of the diabetic animals, no significant change in blood glucose was shown in the hyperthermic non-diabetic rats. Blood cholesterol did not change significantly in the non-diabetic or diabetic animals during hyperthermia. The blood changes of these "energy substrates" are discussed with respect to their possible role in the extreme sensitivity of diabetics to high environmental temperature and "heat stress".
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PMID:Metabolic effect of high environment temperature on non-diabetic and diabetic rats. 92 47

The effects of experimental induced diabetes on the production, metabolism and transport of androgens in the rat testis were examined. Streptozotocin diabetes diminishes the serum and testicular levels of testosterone and increases the enzymic activity that converts testosterone to 5 alpha reduced metabolites, in the seminiferous tubules. The concentration of the androgen binding protein (ABP) in caput epididymis was also reduced in diabetic animals. Although the changes observed could be attributed to differences in gonadotropin production, these phenomena appear to be related to insulin deficiency, since the testes from diabetic rats treated for two weeks with insulin were capable to restore the parameters studied at levels comparable to that observed in normal animals. These data indicate that the testicular function may be regulated by the action of insulin.
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PMID:Endocrine function of the testis in streptozotocin diabetic rats. 105 2

The expression and regulation of IGF-I is tissue-specific in diabetes mellitus in the rat. These studies were designed to examine if similar tissue specificity exists for IGF-BPs in the diabetic milieu. Diabetes mellitus was induced by a single i.p. injection of STZ (100 mg/kg body weight). Rats were treated with either vehicle--insulin, vanadate, or phlorizin for 7-14 days. Tissues were analyzed for IGF-BPs by ligand blotting and by affinity cross-linking and immunoprecipitation. In liver tissue from nondiabetic control rats, multiple forms of IGF-BPs were noted, ranging from 48,000 to 25,000 M(r). In diabetic rat liver tissue, the 25,000-M(r) form was unchanged, whereas the higher M(r) forms (48,000-42,000 M(r)) were decreased, and the 30,000-M(r) form was increased. Insulin therapy of diabetic rats decreased all forms to below control levels. In the kidney tissue of control rats, faint IGF-BP bands were seen at 30,000 and 25,000 M(r). In diabetic rat kidney tissue, the 30,000-M(r) form again was increased (as in liver) and restored to control levels with insulin therapy. In contrast, only a 30,000-M(r) band was seen in control pituitary tissue, which was slightly increased in the diabetic rats and also was decreased below control levels by insulin. In hypothalamus and cerebral cortex tissue, bands at 30,000 and 25,000 M(r) were noted, and neither was altered by diabetes or insulin treatment. Treatment of diabetic rats with vanadate and phlorizin resulted in comparable blood glucose levels, which were only slightly higher than those achieved with insulin therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1992 Dec
PMID:Differential tissue regulation of insulin-like growth factor binding proteins in experimental diabetes mellitus in the rat. 128 Feb 36

The steady-state levels of mRNA encoding for the alpha 1(IV) collagen chain, laminin B1 and B2 chains, basement membrane HSPG, and alpha 1(I) and alpha 1(III) collagen chains were examined in rat glomeruli at 4, 12, and 24 wk after injection of STZ. The mRNA levels for the alpha 1(IV) collagen chain, laminin B1 and B2 chains, and alpha 1(I) and alpha 1(III) collagen chains increased significantly with age in the STZ-induced diabetic rats before morphological thickening of basement membrane occurred. In contrast, the mRNA levels for HSPG decreased markedly 4 wk after STZ injection and then increased with age compared with those for control rats. The mRNA levels for these ECM components showed a continuous decline with age in controls. Treating the diabetic rats with insulin for 4 wk ameliorated the abnormally regulated ECM gene expression in the glomeruli. These data suggest that the abnormal regulation of ECM gene expression in the glomeruli may contribute to the expansion of mesangial matrix and basement membrane thickening in diabetic rats, and that hyperglycemia may play a role in the abnormal ECM gene expression.
Diabetes 1992 Dec
PMID:ECM gene expression and its modulation by insulin in diabetic rats. 128 Feb 37

Insulinopenic states in rodents are known to cause an increase in the number of hepatic insulin receptors. To determine if this change is related to an abnormality in insulin receptor gene expression, insulin receptor binding, insulin receptor mRNA levels, and insulin receptor gene transcription rates have been measured in livers from rats rendered hypoinsulinemic by STZ administration (65 mg/kg) or fasting. In the two groups of experimental rats, insulin binding to liver plasma membranes was increased (approximately 40 and 25%, respectively) relative to control, normoinsulinemic animals. Northern blot analysis of either total or poly (A)+ RNA from livers of hypo- and normoinsulinemic rats revealed two major insulin receptor mRNA species of 9.5 and 7.5 kbs. In hypoinsulinemic rats, insulin receptor mRNA levels were increased > or = 10-fold, with similar effects on the two mRNA species. The effects of STZ administration and fasting on insulin receptor binding and insulin receptor mRNA levels were fully reversed by insulin treatment or refeeding, respectively. Injection of ACT D, an inhibitor of gene transcription, decreased insulin receptor mRNA levels by > or = 80% in control and diabetic rats and suppressed the overexpression of mRNA seen in diabetic rats. In vitro nuclear transcription assays showed that the rate of transcription of the insulin receptor gene was increased 2-fold in STZ-induced diabetic rats and fasted rats relative to control animals. Taken together, these results suggest that the upregulation of the insulin receptor induced by chronic insulinopenia results, at least in part, from an increase in insulin receptor gene transcription.
Diabetes 1992 Dec
PMID:Effects of STZ-induced diabetes and fasting on insulin receptor mRNA expression and insulin receptor gene transcription in rat liver. 128 Feb 38


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