Short-term insulin treatment prevents the diabetogenic action of streptozotocin in rats

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Short-term insulin treatment prevents the diabetogenic action of streptozotocin in rats. / Thulesen, J; Orskov, C; Holst, J J; Poulsen, Steen Seier.

In: Endocrinology, Vol. 138, No. 1, 01.1997, p. 62-68.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Thulesen, J, Orskov, C, Holst, JJ & Poulsen, SS 1997, 'Short-term insulin treatment prevents the diabetogenic action of streptozotocin in rats', Endocrinology, vol. 138, no. 1, pp. 62-68.

APA

Thulesen, J., Orskov, C., Holst, J. J., & Poulsen, S. S. (1997). Short-term insulin treatment prevents the diabetogenic action of streptozotocin in rats. Endocrinology, 138(1), 62-68.

Vancouver

Thulesen J, Orskov C, Holst JJ, Poulsen SS. Short-term insulin treatment prevents the diabetogenic action of streptozotocin in rats. Endocrinology. 1997 Jan;138(1):62-68.

Author

Thulesen, J ; Orskov, C ; Holst, J J ; Poulsen, Steen Seier. / Short-term insulin treatment prevents the diabetogenic action of streptozotocin in rats. In: Endocrinology. 1997 ; Vol. 138, No. 1. pp. 62-68.

Bibtex

@article{caf451d06c3811dcbee902004c4f4f50,
title = "Short-term insulin treatment prevents the diabetogenic action of streptozotocin in rats",
abstract = "Streptozotocin, which induces diabetes mellitus in experimental animals, has been reported to be taken up by beta-cells by means of the glucose transporter 2 (GLUT2) and then reduce the cellular level of NAD+, leading to necrosis of the beta-cells. We investigated the effect of insulin pretreatment on the diabetogenic action of streptozotocin (60 mg/kg). Four groups of rats were studied: 1) a group that received streptozotocin (STZ), 2) a group that received insulin pretreatment and streptozotocin (INS + STZ), 3) a group that received insulin (INS), and 4) a control group (CTRL). Insulin treatment reduced the beta-cell immunoreactivity (IR) of insulin and GLUT2, which, thus, was reduced in INS + STZ rats at the time of streptozotocin injection. In STZ rats, plasma insulin concentrations after 3 weeks as well as insulin concentrations in pancreatic tissue samples were significantly lower than those in CTRL rats [plasma, 274.3 +/- 101.9 vs. 1078.8 +/- 254.9 pmol/liter (P <0.05); tissue, 0.46 +/- 0.02 vs. 117.0 +/- 28.4 nmol/g (P <0.01)]. INS + STZ rats did not become hyperglycemic, and the plasma and tissue levels of insulin were higher than those in STZ rats [plasma, 538.3 +/- 80.1 vs. 274.3 +/- 101.9 pmol/liter (P = 0.08); tissue, 0.46 +/- 0.02 vs. 37.90 +/- 2.13 nmol/g (P <0.05)]. The immunohistochemical findings of insulin IR in the pancreatic tissues were in accordance with the results obtained by RIA. We conclude that exogenous insulin suppresses the expression of GLUT2 and insulin in beta-cells, and this may prevent the diabetogenic effect of streptozotocin.",
keywords = "Animals, Blood Glucose, Body Weight, Diabetes Mellitus, Experimental, Female, Glucagon, Glucose Transporter Type 2, Immunohistochemistry, Insulin, Monosaccharide Transport Proteins, Pancreas, Rats, Rats, Wistar, Streptozocin",
author = "J Thulesen and C Orskov and Holst, {J J} and Poulsen, {Steen Seier}",
year = "1997",
month = "1",
language = "English",
volume = "138",
pages = "62--68",
journal = "Endocrinology",
issn = "0013-7227",
publisher = "Oxford University Press",
number = "1",

}

RIS

TY - JOUR

T1 - Short-term insulin treatment prevents the diabetogenic action of streptozotocin in rats

AU - Thulesen, J

AU - Orskov, C

AU - Holst, J J

AU - Poulsen, Steen Seier

PY - 1997/1

Y1 - 1997/1

N2 - Streptozotocin, which induces diabetes mellitus in experimental animals, has been reported to be taken up by beta-cells by means of the glucose transporter 2 (GLUT2) and then reduce the cellular level of NAD+, leading to necrosis of the beta-cells. We investigated the effect of insulin pretreatment on the diabetogenic action of streptozotocin (60 mg/kg). Four groups of rats were studied: 1) a group that received streptozotocin (STZ), 2) a group that received insulin pretreatment and streptozotocin (INS + STZ), 3) a group that received insulin (INS), and 4) a control group (CTRL). Insulin treatment reduced the beta-cell immunoreactivity (IR) of insulin and GLUT2, which, thus, was reduced in INS + STZ rats at the time of streptozotocin injection. In STZ rats, plasma insulin concentrations after 3 weeks as well as insulin concentrations in pancreatic tissue samples were significantly lower than those in CTRL rats [plasma, 274.3 +/- 101.9 vs. 1078.8 +/- 254.9 pmol/liter (P <0.05); tissue, 0.46 +/- 0.02 vs. 117.0 +/- 28.4 nmol/g (P <0.01)]. INS + STZ rats did not become hyperglycemic, and the plasma and tissue levels of insulin were higher than those in STZ rats [plasma, 538.3 +/- 80.1 vs. 274.3 +/- 101.9 pmol/liter (P = 0.08); tissue, 0.46 +/- 0.02 vs. 37.90 +/- 2.13 nmol/g (P <0.05)]. The immunohistochemical findings of insulin IR in the pancreatic tissues were in accordance with the results obtained by RIA. We conclude that exogenous insulin suppresses the expression of GLUT2 and insulin in beta-cells, and this may prevent the diabetogenic effect of streptozotocin.

AB - Streptozotocin, which induces diabetes mellitus in experimental animals, has been reported to be taken up by beta-cells by means of the glucose transporter 2 (GLUT2) and then reduce the cellular level of NAD+, leading to necrosis of the beta-cells. We investigated the effect of insulin pretreatment on the diabetogenic action of streptozotocin (60 mg/kg). Four groups of rats were studied: 1) a group that received streptozotocin (STZ), 2) a group that received insulin pretreatment and streptozotocin (INS + STZ), 3) a group that received insulin (INS), and 4) a control group (CTRL). Insulin treatment reduced the beta-cell immunoreactivity (IR) of insulin and GLUT2, which, thus, was reduced in INS + STZ rats at the time of streptozotocin injection. In STZ rats, plasma insulin concentrations after 3 weeks as well as insulin concentrations in pancreatic tissue samples were significantly lower than those in CTRL rats [plasma, 274.3 +/- 101.9 vs. 1078.8 +/- 254.9 pmol/liter (P <0.05); tissue, 0.46 +/- 0.02 vs. 117.0 +/- 28.4 nmol/g (P <0.01)]. INS + STZ rats did not become hyperglycemic, and the plasma and tissue levels of insulin were higher than those in STZ rats [plasma, 538.3 +/- 80.1 vs. 274.3 +/- 101.9 pmol/liter (P = 0.08); tissue, 0.46 +/- 0.02 vs. 37.90 +/- 2.13 nmol/g (P <0.05)]. The immunohistochemical findings of insulin IR in the pancreatic tissues were in accordance with the results obtained by RIA. We conclude that exogenous insulin suppresses the expression of GLUT2 and insulin in beta-cells, and this may prevent the diabetogenic effect of streptozotocin.

KW - Animals

KW - Blood Glucose

KW - Body Weight

KW - Diabetes Mellitus, Experimental

KW - Female

KW - Glucagon

KW - Glucose Transporter Type 2

KW - Immunohistochemistry

KW - Insulin

KW - Monosaccharide Transport Proteins

KW - Pancreas

KW - Rats

KW - Rats, Wistar

KW - Streptozocin

M3 - Journal article

VL - 138

SP - 62

EP - 68

JO - Endocrinology

JF - Endocrinology

SN - 0013-7227

IS - 1

ER -

ID: 1124001