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Quantification of the metabolism of dietary glucose by the splanchnic tissues is incomplete. Whether habitual carbohydrate intake affects splanchnic glucose metabolism is not known. Female mice were offered isoenergetic and isonitrogenous quantities of diets containing high (HCD) or low (LCD) amounts of carbohydrate, 5% of which was [U-13C]-glucose. Four mice from each dietary group were killed after 24, 48 and 120 h. The 13C-isotopomer distribution in blood glucose, lactate and alanine and in hepatic alanine and glycogen was measured by selected ion monitoring mass spectrometry. [U-13C]-Glucose and its products, [U-13C]-lactate and alanine, were in complete isotopic equilibrium in the blood. The tracer:tracee ratio of hepatic [U-13C]-alanine was significantly higher (P < 0.01) than that of circulating alanine. In both groups, the tracer:tracee ratio of circulating [U-13C]-glucose was significantly (P < 0.001) lower than that of the dietary carbohydrate, and the ratio of [13C3]-glucose:[U-13C]-glucose [0.57 (HCD) and 0.78 (LCD); diet effect P < 0.05], a measure of glucose metabolic cycling, was between two- and fivefold higher than published values obtained with intravenous tracer glucose. The tracer:tracee ratio of [U-13C]-glycogen glucose was significantly (P < 0.05) higher than that of arterial glucose. We conclude the following: 1) dietary glucose is extensively recycled, via pyruvate, within the liver; 2) this metabolic cycle is maintained in mice consuming low carbohydrate diets; and 3) dietary carbohydrate is channelled to hepatic glycogen. We speculate that the metabolic cycling of enteral glucose is related to the hepatic catabolism of dietary protein.

To investigate the contribution of dietary carbohydrate to glutamate and acetyl CoA synthesis, two groups of adult mice were fed a high- (HCD) or a low-carbohydrate diet (LCD) in which 5% of the carbohydrate was [U-13C]-glucose. Four animals from each dietary group were killed after 1, 2 and 5 d. The tracer:tracee ratios of [13C3] and [13C6]blood glucose and of the [13C2] and [13C3] isotopomers of blood, mucosal, hepatic and muscle alanine and glutamate were used to calculate the fractional contribution of glucose to the 3-carbon, acetyl CoA and oxaloacetate pools of each tissue. In the HCD mice, glucose contributed 66, 33 and 31% of the acetyl CoA pool of muscle, liver and mucosa, respectively. The contribution of glucose to acetyl CoA was lowered by 33% (P < 0.05) and 55% (P < 0.01) in the liver and muscle of the LCD group, respectively, but was unaltered in the mucosa. Glucose made a minor contribution to glutamate synthesis via oxaloacetate in the liver (23%) and muscle (10%) of the HCD group. The fraction of hepatic and muscle glutamate synthesis derived from glucose was not affected by the diet. We conclude that glucose oxidation in liver and muscle parallels the contribution of carbohydrate to dietary energy and that glucose is not a major carbon precursor for muscle glutamate synthesis. Net glutamate synthesis in extraintestinal tissues is preserved when dietary carbohydrate is restricted.

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