The effect of hemorrhagic stress on liver gluconeogenesis. An isolated rat liver perfusion study with three-carbon units as substrates.
This effect of hypovolemic stress on hepatic gluconeogenesis has been studied using isolated perfused organs obtained from starved rats subjected to 60 min hemorrhagic hypotension at 70 mmHg. Four different substrates were used: lactate, pyruvate, glycerol and alanine. The substrates were added without any stress endocrine stimulation in the perfusate. Using a recirculating system and supraoptimal substrate availability, a significant higher rate of gluconeogenesis was confirmed for the stressed donor livers: glycerol (+100%), alanine (+97%), lactate (+64%) and pyruvate (+62%). Glucose accumulation was linear for all control and experimental groups. In the absence of added stress hormones, known to stimulate gluconeogenesis, the findings are concordant with an in vivo hormone activation of key enzymes in the gluconeogenic pathway, persisting for the 60 min duration of the in vitro perfusion.
D000409:Alanine / Q000378:metabolism; D000818:Animals; D005943:Gluconeogenesis; D005947:Glucose / Q000378:metabolism; D005990:Glycerol / Q000378:metabolism; D007773:Lactates / Q000378:metabolism; D008099:Liver / Q000378:metabolism*; D008297:Male; D010477:Perfusion; D011773:Pyruvates / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D012771:Shock, Hemorrhagic / Q000378:metabolism*
D007773:Lactates; D011773:Pyruvates; D005947:Glucose; D000409:Alanine; D005990:Glycerol