We interrogated the hypothesis of a Postprandial Lactate Shuttle (PLS) in young, healthy men and women (n=15). Participants reported to the lab (5:00 AM) following an overnight fast and had the forearm vein catheterized for primed continuous infusions of [6,6-2H]glucose and [3-13C]lactate stable isotope tracers. The contralateral hand vein was warmed and catharized for arterialized blood sampling. After a 90-minute (min) equilibration period participants underwent a 75 g oral glucose tolerance test (OGTT). Arterialized [lactate] rose from baseline (0.60sup>). We estimate carbon flow from the OGTT from the rates of appearance of glucose, lactate and GNG from lactate. At 120-min the 75 g load was accounted for as follows: 29 g as blood lactate, 24 g of glucose from hepatic glucose release, 8 g of glucose from GNG, and 14 g withheld in the liver. Because blood [lactate] and Ra rose before [glucose] and Ra, evidence of an Enteric PLS is provided. Because secondary increments in blood [lactate] and Ra coincided with those of glucose, results are interpreted to indicate presence of a larger, secondary Systemic PLS phase. Antiquated ideas of lactate production due to hypoxia in skeletal muscles need to be supplanted because glycolysis proceeds to lactate in fully aerobic tissues, and because dietary carbohydrate is processed via lactate shuttling. In humans, lactate is a major vehicle for carbohydrate carbon distribution and metabolis. NIH grant R01 AG059715. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.
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