Modification of glycogen deposition by priming glucose loads: the second-meal phenomenon.
Glucose priming modifies tolerance and oxidation of subsequent loads. To assess effects in glycogenesis, rats were given a D-[U14C]-glucose load, either alone or preceded by one or two unlabeled hourly doses. The incorporation of 14C into total liver glycogen was 8.6 +/- 0.4% of the glucose dose and was little changed by priming loads. Total liver glycogen was 169 +/- 10 mg after one load and 276 +/- 12 mg after two; after three it fell to 243 +/- 20 mg. In muscle, net incorporation of 14C was 9.6 +/- 0.6% of the first but fell to 6.9 +/- 0.4% of the third glucose 14C dose/100 g. Muscle glycogen concentration rose at a decremental rate with priming. Net incorporation of glucose 14C into hepatic glycogen remains constant after repeated loads even after storage is reduced. In keeping with the reported peripheral resistance to glucose uptake in the second-meal phenomenon, repeated loading is associated with reduction of 14C-glucose incorporation into muscle glycogen.
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D005947:Glucose / Q000378:metabolism / Q000494:pharmacology*; D006003:Glycogen / Q000378:metabolism*; D008112:Liver Glycogen / Q000378:metabolism*; D008297:Male; D009132:Muscles / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains
D001786:Blood Glucose; D008112:Liver Glycogen; D006003:Glycogen; D005947:Glucose