Initial glucose kinetics and hormonal response to a gastric glucose load in unrestrained post-absorptive and starved rats.
A gastric [U-14C]glucose load (4.8 mg/g body wt.) was delivered to unrestrained post-absorptive or 30 h-starved rats bearing peripheral and portal vein catheters and continuously perfused with [3-3H]glucose, in order to compare their metabolic and hormonal responses. In the basal state, portal and peripheral glycaemia were less in starved rats than in rats in the post-absorptive period (P less than 0.01), whereas blood lactate was similar. Portal insulinaemia (P less than 0.05) and protal glucagonaemia (P less than 0.005) were lower in starved rats, but insulin/glucagon ratio was higher in post-absorptive rats (P less than 0.005). The glucose turnover rate was decreased by starvation (P less than 0.005). After glucose ingestion, blood glucose was similar in post-absorptive and starved rats. A large portoperipheral gradient of lactate appeared in starved rats. Portal insulinaemia reached a peak at 9 min, and was respectively 454 +/- 68 and 740 +/- 65 mu-units/ml in starved and post-absorptive rats. Portal glucagonaemia remained stable, but was higher in post-absorptive rats (P less than 0.05). At 60 min after the gastric glucose load, 30% of the glucose was delivered at the periphery in both groups. The total glucose appearance rate was higher in starved rats (P less than 0.05), as was the glucose utilization rate (P less than 0.05), whereas the rate of appearance of exogenous glucose was similar. This was due to a non-suppressed hepatic glucose production in the starved rats, whereas it was totally suppressed in post-absorptive rats. At 1 h after the glucose load, the increase in both liver and muscle glycogen concentration was greater in starved rats. Thus short-term fasting induces an increased portal lactate concentration after a glucose load, and produces a state of liver insulin unresponsiveness for glucose production, whereas the sensitivity of peripheral tissues for glucose utilization is unchanged or even increased. This might allow preferential replenishment of the peripheral stores of glycogen.
Centre de Recherche sur la Nutrition, CNRS, Meudon-Bellevue, France.
C
C
Smadja
J
J
Morin
P
P
Ferré
J
J
Girard
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D005260:Female; D005502:Food; D005774:Gastrostomy; D005934:Glucagon / Q000097:blood*; D005947:Glucose / Q000008:administration & dosage / Q000494:pharmacology*; D006003:Glycogen / Q000378:metabolism; D007328:Insulin / Q000097:blood*; D007700:Kinetics; D007773:Lactates / Q000097:blood; D019344:Lactic Acid; D008099:Liver / Q000378:metabolism; D009132:Muscles / Q000378:metabolism; D011169:Portal Vein; D051381:Rats; D013217:Starvation / Q000378:metabolism*
D001786:Blood Glucose; D007328:Insulin; D007773:Lactates; D019344:Lactic Acid; D006003:Glycogen; D005934:Glucagon; D005947:Glucose