Effects of glucose-insulin-potassium on intestinal hemodynamics and substrate utilization during endotoxemia

C. H. Lang, R. J. Alteveer

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Abstract

This study examined the effects of endotoxin on small intestinal hemodynamics and metabolism with and without an infusion of glucose-insulin-potassium (GIK). Glucose uptake and lactate release were determined by arteriovenous differences across a segment of canine ileum, which was vascularly isolated in vivo, and by the direct measurement of intestinal blood flow. Free fatty acid (FFA) utilization by intestinal tissue was assessed by the constant infusion of albumin-bound [14C]palmitate and [3H]oleate. Endotoxemic dogs showed a sustained reduction of mean arterial blood pressure (MABP) and intestinal blood flow. In contrast, endotoxemic dogs infused with GIK demonstrated a decreased intestinal vascular resistance and an increased blood flow (two-fold), whereas MABP was transiently improved. Intestinal glucose uptake was not different from control values in endotoxemic animals, however, a sixfold increase was seen in shocked dogs treated with GIK. The endotoxin-induced increase in the plasma lactate concentration and intestinal lactate release was similar between dogs infused with saline or GIK. After endotoxin, the arterial FFA concentration remained unchanged and whole-body FFA turnover was decreased. FFA uptake by the gut was reduced, but FFA oxidation was not altered. Similar changes in FFA metabolism were seen in endotoxemic animals infused with GIK. The metabolic pattern after endotoxin suggests an elevated rate of aerobic glycolysis by the gut that increases the availability of lactate to the liver. Compared with saline-infused endotoxemic animals, GIK produced an elevation in glucose uptake without a further increase in lactate output, suggesting an increased storage of glucose by this tissue.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Volume251
Issue number3
StatePublished - Jan 1 1986

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Endotoxemia
Nonesterified Fatty Acids
Potassium
Hemodynamics
Lactic Acid
Insulin
Glucose
Endotoxins
Arterial Pressure
Dogs
Palmitates
Glycolysis
Oleic Acid
Ileum
Vascular Resistance
Canidae
Albumins
Liver

All Science Journal Classification (ASJC) codes

  • Physiology
  • Hepatology
  • Gastroenterology
  • Physiology (medical)

Cite this

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abstract = "This study examined the effects of endotoxin on small intestinal hemodynamics and metabolism with and without an infusion of glucose-insulin-potassium (GIK). Glucose uptake and lactate release were determined by arteriovenous differences across a segment of canine ileum, which was vascularly isolated in vivo, and by the direct measurement of intestinal blood flow. Free fatty acid (FFA) utilization by intestinal tissue was assessed by the constant infusion of albumin-bound [14C]palmitate and [3H]oleate. Endotoxemic dogs showed a sustained reduction of mean arterial blood pressure (MABP) and intestinal blood flow. In contrast, endotoxemic dogs infused with GIK demonstrated a decreased intestinal vascular resistance and an increased blood flow (two-fold), whereas MABP was transiently improved. Intestinal glucose uptake was not different from control values in endotoxemic animals, however, a sixfold increase was seen in shocked dogs treated with GIK. The endotoxin-induced increase in the plasma lactate concentration and intestinal lactate release was similar between dogs infused with saline or GIK. After endotoxin, the arterial FFA concentration remained unchanged and whole-body FFA turnover was decreased. FFA uptake by the gut was reduced, but FFA oxidation was not altered. Similar changes in FFA metabolism were seen in endotoxemic animals infused with GIK. The metabolic pattern after endotoxin suggests an elevated rate of aerobic glycolysis by the gut that increases the availability of lactate to the liver. Compared with saline-infused endotoxemic animals, GIK produced an elevation in glucose uptake without a further increase in lactate output, suggesting an increased storage of glucose by this tissue.",
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