Effect of diabetes, insulin, and glucose load on lipid peroxidation in the rat

Michael P. Habib; Frank D. Dickerson; Arshag D. Mooradian

doi:10.1016/0026-0495(94)90042-6

Effect of diabetes, insulin, and glucose load on lipid peroxidation in the rat

Michael P. Habib, Frank D. Dickerson, Arshag D. Mooradian

Medicine, College of

Research output: Contribution to journal › Article

45 Scopus citations

Abstract

Lipid peroxidative activity in rats made diabetic with streptozocin and rats made acutely hyperglycemic by intraperitoneal dextrose administration was determined by measurement of exhaled ethane during exposure in vivo to ethane-free air (EFA). Diabetic rats demonstrated increased ethane in the expired breath while breathing EFA (5.82 ± 0.56 pmol / min /100 g) compared with control rats (4.02 ± 0.23 pmol/ min/ 100 g). Insulin treatment of diabetic rats attenuated the ethane produced (4.88 ± 0.23 pmol/ min /100 g). Acute hyperglycemia increased exhaled ethane to levels higher than those seen in diabetic rats (9.87 ± 0.98 pmol/ min/ 100 g). Saline injected intraperitoneally to control rats produced ethane levels similar to those of untreated nondiabetic controls (4.11 ± 0.52 pmol/ min / 100 g). Chronic uncontrolled hyperglycemia and acute hyperglycemia are associated with increased in vivo ethane production.

Original language	English (US)
Pages (from-to)	1442-1445
Number of pages	4
Journal	Metabolism
Volume	43
Issue number	11
DOIs	https://doi.org/10.1016/0026-0495(94)90042-6
State	Published - Nov 1994

ASJC Scopus subject areas

Endocrinology, Diabetes and Metabolism
Endocrinology

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Habib, M. P., Dickerson, F. D., & Mooradian, A. D. (1994). Effect of diabetes, insulin, and glucose load on lipid peroxidation in the rat. Metabolism, 43(11), 1442-1445. https://doi.org/10.1016/0026-0495(94)90042-6

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title = "Effect of diabetes, insulin, and glucose load on lipid peroxidation in the rat",

abstract = "Lipid peroxidative activity in rats made diabetic with streptozocin and rats made acutely hyperglycemic by intraperitoneal dextrose administration was determined by measurement of exhaled ethane during exposure in vivo to ethane-free air (EFA). Diabetic rats demonstrated increased ethane in the expired breath while breathing EFA (5.82 ± 0.56 pmol / min /100 g) compared with control rats (4.02 ± 0.23 pmol/ min/ 100 g). Insulin treatment of diabetic rats attenuated the ethane produced (4.88 ± 0.23 pmol/ min /100 g). Acute hyperglycemia increased exhaled ethane to levels higher than those seen in diabetic rats (9.87 ± 0.98 pmol/ min/ 100 g). Saline injected intraperitoneally to control rats produced ethane levels similar to those of untreated nondiabetic controls (4.11 ± 0.52 pmol/ min / 100 g). Chronic uncontrolled hyperglycemia and acute hyperglycemia are associated with increased in vivo ethane production.",

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N2 - Lipid peroxidative activity in rats made diabetic with streptozocin and rats made acutely hyperglycemic by intraperitoneal dextrose administration was determined by measurement of exhaled ethane during exposure in vivo to ethane-free air (EFA). Diabetic rats demonstrated increased ethane in the expired breath while breathing EFA (5.82 ± 0.56 pmol / min /100 g) compared with control rats (4.02 ± 0.23 pmol/ min/ 100 g). Insulin treatment of diabetic rats attenuated the ethane produced (4.88 ± 0.23 pmol/ min /100 g). Acute hyperglycemia increased exhaled ethane to levels higher than those seen in diabetic rats (9.87 ± 0.98 pmol/ min/ 100 g). Saline injected intraperitoneally to control rats produced ethane levels similar to those of untreated nondiabetic controls (4.11 ± 0.52 pmol/ min / 100 g). Chronic uncontrolled hyperglycemia and acute hyperglycemia are associated with increased in vivo ethane production.

AB - Lipid peroxidative activity in rats made diabetic with streptozocin and rats made acutely hyperglycemic by intraperitoneal dextrose administration was determined by measurement of exhaled ethane during exposure in vivo to ethane-free air (EFA). Diabetic rats demonstrated increased ethane in the expired breath while breathing EFA (5.82 ± 0.56 pmol / min /100 g) compared with control rats (4.02 ± 0.23 pmol/ min/ 100 g). Insulin treatment of diabetic rats attenuated the ethane produced (4.88 ± 0.23 pmol/ min /100 g). Acute hyperglycemia increased exhaled ethane to levels higher than those seen in diabetic rats (9.87 ± 0.98 pmol/ min/ 100 g). Saline injected intraperitoneally to control rats produced ethane levels similar to those of untreated nondiabetic controls (4.11 ± 0.52 pmol/ min / 100 g). Chronic uncontrolled hyperglycemia and acute hyperglycemia are associated with increased in vivo ethane production.

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