PMID- 10360633
OWN - NLM
STAT- MEDLINE
DCOM- 19990610
LR  - 20191103
IS  - 0022-2143 (Print)
IS  - 0022-2143 (Linking)
VI  - 133
IP  - 6
DP  - 1999 Jun
TI  - Tumor necrosis factor-alpha alters glucose metabolism in suckling rats.
PG  - 583-9
AB  - Tumor necrosis factor-alpha (TNF-alpha), an important mediator of endotoxic 
      shock, induces hypoglycemia and shock in adult animals. Indomethacin ameliorates 
      TNF-alpha-induced hypoglycemia in the adult. However, effects of TNF-alpha on 
      glucose metabolism in the newborn have not been well documented. The present 
      study showed that in 10-day-old rats injected with TNF-alpha (4.5 x 10(7) 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-alpha 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-alpha decreased mRNA abundance of GLUT 
      2 and phosphoenolpyruvate carboxykinase (PEPCK) in liver, suggesting decreased 
      gluconeogenesis. Indomethacin (1.5 mg/kg 20 minutes before TNF-alpha, 
      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-alpha induced 
      hypoglycemia, increasing GLUT1 mRNA abundance and glucose uptake and decreasing 
      PEPCK mRNA abundance in 10-day-old rats. Indomethacin attenuated the 
      TNF-alpha-induced glucose dyshomeostasis.
FAU - Battelino, T
AU  - Battelino T
AD  - Department of Pediatrics, University Medical Center Ljubljana, Slovenia.
FAU - Goto, M
AU  - Goto M
FAU - Krzisnik, C
AU  - Krzisnik C
FAU - Zeller, W P
AU  - Zeller WP
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Lab Clin Med
JT  - The Journal of laboratory and clinical medicine
JID - 0375375
RN  - 0 (Blood Glucose)
RN  - 0 (Glucose Transporter Type 1)
RN  - 0 (Insulin)
RN  - 0 (Monosaccharide Transport Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Slc2a1 protein, rat)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 33X04XA5AT (Lactic Acid)
RN  - EC 4.1.1.49 (Phosphoenolpyruvate Carboxykinase (ATP))
RN  - IY9XDZ35W2 (Glucose)
RN  - XXE1CET956 (Indomethacin)
SB  - IM
MH  - Animals
MH  - Animals, Suckling
MH  - Blood Glucose/metabolism
MH  - Gene Expression Regulation, Developmental
MH  - Glucose/*metabolism
MH  - Glucose Transporter Type 1
MH  - Indomethacin/pharmacology
MH  - Insulin/blood
MH  - Lactic Acid/blood
MH  - Monosaccharide Transport Proteins/genetics/metabolism
MH  - Organ Specificity
MH  - Phosphoenolpyruvate Carboxykinase (ATP)/metabolism
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Tumor Necrosis Factor-alpha/pharmacology/*physiology
EDAT- 1999/06/09 00:00
MHDA- 1999/06/09 00:01
CRDT- 1999/06/09 00:00
PHST- 1999/06/09 00:00 [pubmed]
PHST- 1999/06/09 00:01 [medline]
PHST- 1999/06/09 00:00 [entrez]
AID - S0022-2143(99)90188-9 [pii]
AID - 10.1016/s0022-2143(99)90188-9 [doi]
PST - ppublish
SO  - J Lab Clin Med. 1999 Jun;133(6):583-9. doi: 10.1016/s0022-2143(99)90188-9.