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Tumor necrosis factor-α alters glucose metabolism in suckling rats

Authors
Journal
Journal of Laboratory and Clinical Medicine
0022-2143
Publisher
Elsevier
Volume
133
Issue
6
Identifiers
DOI: 10.1016/s0022-2143(99)90188-9

Abstract

Abstract Tumor necrosis factor-α (TNF-α), an important mediator of endotoxic shock, induces hypoglycemia and shock in adult animals. Indomethacin ameliorates TNF-α-induced hypoglycemia in the adult. However, effects of TNF-α on glucose metabolism in the newborn have not been well documented. The present study showed that in 10-day-old rats injected with TNF-α (4.5 × 107 U/kg, intraperitoneally) the plasma glucose concentration increased from 4.1 ± 0.3 mmol/L to 6.9 ± 0.5 mmol/L (P < .05) at 2 hours and subsequently decreased to 1.4 ± 0.5 mmol/L (P < .05) at 6 hours, although plasma lactate concentration increased from 1.1 ± 0.1 mmol/L to 5.5 ± 0.3 mmol/L (P < .05) at 6 hours. Plasma insulin concentration remained unchanged throughout the experiment. TNF-α increased GLUT 1 messenger RNA (mRNA) abundance in the brain, liver, muscle, and fatty tissue (P < .05). Glucose uptake increased in association with the increase of GLUT1 mRNA abundance. TNF-α decreased mRNA abundance of GLUT 2 and phosphoenolpyruvate carboxykinase (PEPCK) in liver, suggesting decreased gluconeogenesis. Indomethacin (1.5 mg/kg 20 minutes before TNF-α, intraperitoneally) attenuated the hypoglycemia, the lactacidemia, and the increase of GLUT1 mRNA abundance and glucose uptake. Indomethacin attenuated the decrease of PEPCK mRNA abundance. We concluded that TNF-α induced hypoglycemia, increasing GLUT1 mRNA abundance and glucose uptake and decreasing PEPCK mRNA abundance in 10-day-old rats. Indomethacin attenuated the TNF-α-induced glucose dyshomeostasis.

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