These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Liver metabolism and glucogenesis in trauma and sepsis.
    Author: Imamura M, Clowes GH, Blackburn GL, O'Donnell TF, Trerice M, Bhimjee Y, Ryan NT.
    Journal: Surgery; 1975 Jun; 77(6):868-80. PubMed ID: 1145447.
    Abstract:
    The relationship of glucogenesis and other energy-requiring functions of the liver to the proteolysis which is characteristic of trauma and sepsis was studied in conscious pigs following laporotomy and after the induction of intraperitoneal sepsis. By means of appropriately placed thermal dilution catheters, portal and hepatic arterial blood flows, hepatic oxygen consumption, glucogenesis, and uptake of the fuel, substrates were measured. No animal was in shock. Despite significant increases of lactate and aminoacids delivered to the liver, the blood concentrations were maintained in the normal range. The rate of glucogenesis was proportional (r equals 0.71) to the sum of the glucogenic precursors (lactate, pyruvate, glycerol, and alanine) taken up by the liver. Higher rates of glucose production were accompanied by elevated blood insulin values. Hepatic oxygen consumption and the uptake of free fatty acids also were related directly to the glucogenic rate, the correlation coefficients being 0.69 and 0.74, respectively. In the absence of shock, the liver function and hepatic energy production remained normal in post-traumatic and septic states. Under the conditions insulin-resistant muscle in the presence of reduced free fatty acid availability mobilize protein to satisfy local energy requirements. Skeletal muscle can oxidize only branch chain aminoacids; other aminoacids, including alanine, are transported to the liver for glucogenesis or other purposed. This concept accounted for failure of glucose infusion to eliminate post-traumatic and septic proteolysis, since alanine is cleared only from blood by conversion in the liver to glucose. Thus it is concluded that in sepsis the release of glucogenic substrates because of altered metabolism in peripheral tissues determines the rate of hepatic glucogenesis. This relationship constitutes an important metabolic homeostatic mechanism.
    [Abstract] [Full Text] [Related] [New Search]