We evaluated the relative contribution of oral glucose to arterial lactate and the relative role of the splanchnic bed in converting glucose to lactate in normal healthy dogs. After an oral glucose load (1.2 g/kg) spiked with [U-14C]glucose (16.9 μCi/kg; protocol 1, n = 7), arterial blood lactate increased from 0.43 ± 0.03 mM at basal to a peak of 1.04 ± 0.07 mM at 45 min and then slowly decreased to 0.47 ± 0.07 mM at 240 min. Arterial blood [14C]lactate peaked at 60 min and then decreased slowly to ∼35% of the peak at 4 h. When arterial blood lactate peaked at 45 min, the proportion of arterial lactate that was derived from oral glucose was 34 ± 3%. The integrated area under the curve of lactate derived from exogenous glucose was 40 ± 2% of that of total lactate. The splanchnic bed released lactate and [14C]lactate during the initial 2 h after oral [14C]glucose. Thus, the splanchnic bed apparently contributed to the conversion of exogenous glucose to lactate. In the matched experiments (protocol 2, n = 5), dogs were given the same amount of oral glucose but no [14C]glucose, and [U-14C]lactate was infused into the right atrium to match the splanchnic [14C]lactate release from the first experiment. Despite a well-matched splanchnic [14C]lactate contribution, arterial concentrations of [14C]lactate were markedly lower in protocol 2 compared with protocol 1. The integrated area under the [14C]lactate profile in protocol 2 was only 11 ± 1% of that in protocol 1. These results indicate that the splanchnic bed is responsible for only 11% of arterial blood lactate that was derived from oral glucose. We concluded that 1) after oral glucose loading, a major portion of circulating lactate has its origin not in exogenous glucose but in endogenous sources, and 2) the splanchnic bed is not the major site of oral glucose conversion to lactate after glucose ingestion.

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