Hepatic production and intestinal uptake of IGF-I: Response to infection

Charles H. Lang, Robert A. Frost, Joseph Ejiofor, D. Brooks Lacy, Owen P. McGuinness

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

The role of the liver and gut in contributing to the infection-induced fall in circulating insulin-like growth factor I (IGF-I) was examined in chronically catheterized conscious dogs. Two weeks before study, catheters and Doppler flow probes were implanted to assess hepatic and gut balance of IGF-I. To control nutrient intake, dogs were placed on total parenteral nutrition (TPN) as their sole caloric source. After dogs received TPN for 5 days, net hepatic and intestine IGF-I balances were assessed. A hypermetabolic infected state was then induced by the intraperitoneal implantation of a fibrin clot containing Escherichia coli. TPN was continued, and organ IGF-I balance was assessed 24 and 48 h after induction of infection. Arterial IGF-I levels were significantly decreased following infection (111 ± 18, 62 ± 10, and 63 ± 8 ng/ml before and 24 and 48 h after, respectively). Net hepatic IGF-I output decreased markedly (221 ± 73, to 73 ± 41 and 41 ± 17 ng · kg-1 · min-1 before and 24 and 48 h after, respectively). The infection-induced decrease in hepatic IGF-I output could not be explained by concomitant alterations in plasma cortisol or insulin levels. The gut demonstrated a net uptake of IGF-I before infection (178 ± 29 ng · kg-1 · min-1). However, after infection, intestinal IGF-I uptake was completely suppressed (-10 ± 15 and -8 ± 36 ng · kg-1 · min-1). In summary, infection decreases net hepatic IGF-I release 65- 80% and completely suppresses net IGF-I uptake by the intestine. As a consequence of these reciprocal changes in IGF-I balance across the liver and intestine, splanchnic production of IGF-I was unchanged by infection. These data suggest that changes in the clearance and/or production of IGF-I by extrasplanchnic tissues contribute to the infection-induced decrease in circulating IGF-I levels.

Original languageEnglish (US)
Pages (from-to)G1291-G1298
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Volume275
Issue number6 38-6
StatePublished - Dec 1 1998

Fingerprint

Insulin-Like Growth Factor I
Liver
Infection
Total Parenteral Nutrition
Intestines
Dogs
Viscera
Fibrin
Hydrocortisone
Catheters

All Science Journal Classification (ASJC) codes

  • Physiology
  • Hepatology
  • Gastroenterology
  • Physiology (medical)

Cite this

Lang, C. H., Frost, R. A., Ejiofor, J., Brooks Lacy, D., & McGuinness, O. P. (1998). Hepatic production and intestinal uptake of IGF-I: Response to infection. American Journal of Physiology - Gastrointestinal and Liver Physiology, 275(6 38-6), G1291-G1298.
Lang, Charles H. ; Frost, Robert A. ; Ejiofor, Joseph ; Brooks Lacy, D. ; McGuinness, Owen P. / Hepatic production and intestinal uptake of IGF-I : Response to infection. In: American Journal of Physiology - Gastrointestinal and Liver Physiology. 1998 ; Vol. 275, No. 6 38-6. pp. G1291-G1298.
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Lang, CH, Frost, RA, Ejiofor, J, Brooks Lacy, D & McGuinness, OP 1998, 'Hepatic production and intestinal uptake of IGF-I: Response to infection', American Journal of Physiology - Gastrointestinal and Liver Physiology, vol. 275, no. 6 38-6, pp. G1291-G1298.

Hepatic production and intestinal uptake of IGF-I : Response to infection. / Lang, Charles H.; Frost, Robert A.; Ejiofor, Joseph; Brooks Lacy, D.; McGuinness, Owen P.

In: American Journal of Physiology - Gastrointestinal and Liver Physiology, Vol. 275, No. 6 38-6, 01.12.1998, p. G1291-G1298.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Hepatic production and intestinal uptake of IGF-I

T2 - Response to infection

AU - Lang, Charles H.

AU - Frost, Robert A.

AU - Ejiofor, Joseph

AU - Brooks Lacy, D.

AU - McGuinness, Owen P.

PY - 1998/12/1

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N2 - The role of the liver and gut in contributing to the infection-induced fall in circulating insulin-like growth factor I (IGF-I) was examined in chronically catheterized conscious dogs. Two weeks before study, catheters and Doppler flow probes were implanted to assess hepatic and gut balance of IGF-I. To control nutrient intake, dogs were placed on total parenteral nutrition (TPN) as their sole caloric source. After dogs received TPN for 5 days, net hepatic and intestine IGF-I balances were assessed. A hypermetabolic infected state was then induced by the intraperitoneal implantation of a fibrin clot containing Escherichia coli. TPN was continued, and organ IGF-I balance was assessed 24 and 48 h after induction of infection. Arterial IGF-I levels were significantly decreased following infection (111 ± 18, 62 ± 10, and 63 ± 8 ng/ml before and 24 and 48 h after, respectively). Net hepatic IGF-I output decreased markedly (221 ± 73, to 73 ± 41 and 41 ± 17 ng · kg-1 · min-1 before and 24 and 48 h after, respectively). The infection-induced decrease in hepatic IGF-I output could not be explained by concomitant alterations in plasma cortisol or insulin levels. The gut demonstrated a net uptake of IGF-I before infection (178 ± 29 ng · kg-1 · min-1). However, after infection, intestinal IGF-I uptake was completely suppressed (-10 ± 15 and -8 ± 36 ng · kg-1 · min-1). In summary, infection decreases net hepatic IGF-I release 65- 80% and completely suppresses net IGF-I uptake by the intestine. As a consequence of these reciprocal changes in IGF-I balance across the liver and intestine, splanchnic production of IGF-I was unchanged by infection. These data suggest that changes in the clearance and/or production of IGF-I by extrasplanchnic tissues contribute to the infection-induced decrease in circulating IGF-I levels.

AB - The role of the liver and gut in contributing to the infection-induced fall in circulating insulin-like growth factor I (IGF-I) was examined in chronically catheterized conscious dogs. Two weeks before study, catheters and Doppler flow probes were implanted to assess hepatic and gut balance of IGF-I. To control nutrient intake, dogs were placed on total parenteral nutrition (TPN) as their sole caloric source. After dogs received TPN for 5 days, net hepatic and intestine IGF-I balances were assessed. A hypermetabolic infected state was then induced by the intraperitoneal implantation of a fibrin clot containing Escherichia coli. TPN was continued, and organ IGF-I balance was assessed 24 and 48 h after induction of infection. Arterial IGF-I levels were significantly decreased following infection (111 ± 18, 62 ± 10, and 63 ± 8 ng/ml before and 24 and 48 h after, respectively). Net hepatic IGF-I output decreased markedly (221 ± 73, to 73 ± 41 and 41 ± 17 ng · kg-1 · min-1 before and 24 and 48 h after, respectively). The infection-induced decrease in hepatic IGF-I output could not be explained by concomitant alterations in plasma cortisol or insulin levels. The gut demonstrated a net uptake of IGF-I before infection (178 ± 29 ng · kg-1 · min-1). However, after infection, intestinal IGF-I uptake was completely suppressed (-10 ± 15 and -8 ± 36 ng · kg-1 · min-1). In summary, infection decreases net hepatic IGF-I release 65- 80% and completely suppresses net IGF-I uptake by the intestine. As a consequence of these reciprocal changes in IGF-I balance across the liver and intestine, splanchnic production of IGF-I was unchanged by infection. These data suggest that changes in the clearance and/or production of IGF-I by extrasplanchnic tissues contribute to the infection-induced decrease in circulating IGF-I levels.

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