Abstract
Excessive sugar intake including high-fructose corn syrup (HFCS) is implicated in the rise of obesity, insulin resistance and non-alcoholic fatty liver disease. Liver glycogen synthesis is influenced by both fructose and insulin signaling. Therefore, the effect of HFCS on hepatic glycogenesis was evaluated in mice feeding ad-libitum. Using deuterated water: the fraction of glycogen derived from triose-P sources, Krebs cycle substrates, and direct pathway + cycling, was measured in 9 normal-chow fed mice (NC) and 12 mice fed normal chow plus a 55% fructose/45% glucose mix in the drinking water at 30% w/v (HFCS-55). This was enriched with [U-13C]fructose or [U-13C]glucose to determine the contribution of each to glycogenesis. For NC, direct pathway + cycling, Krebs cycle, and triose-P sources accounted for 66 ± 0.7%, 23 ± 0.8% and 11 ± 0.4% of glycogen synthesis, respectively. HFCS-55 mice had similar direct pathway + cycling (64 ± 1%) but lower Krebs cycle (12 ± 1%, p < 0.001) and higher triose-P contributions (24 ± 1%, p < 0.001). HFCS-55-fructose contributed 17 ± 1% via triose-P and 2 ± 0% via Krebs cycle. HFCS-55-glucose contributed 16 ± 3% via direct pathway and 1 ± 0% via Krebs cycle. In conclusion, HFCS-55 supplementation resulted in similar hepatic glycogen deposition rates. Indirect pathway contributions shifted from Krebs cycle to Triose-P sources reflecting HFCS-55-fructose utilization, while HFCS-55-glucose was incorporated almost exclusively by the direct pathway.
Highlights
Excessive sugar intake including high-fructose corn syrup (HFCS) is implicated in the rise of obesity, insulin resistance and non-alcoholic fatty liver disease
The aim of this study was to compare hepatic glycogen synthesis in mice fed with standard chow to mice where the standard chow was supplemented with a mixture of fructose and glucose in the drinking water corresponding to HFCS-55
The mean weight of the mice whose chow was supplemented with fructose and glucose in the drinking water, hereafter referred to as HFCS-55 mice, was not significantly different from the group fed normal chow, hereafter referred to as normal-chow fed mice (NC) mice (34.0 ± 3.5 g vs 35.7 ± 4.2 g, p = 0.34)
Summary
Excessive sugar intake including high-fructose corn syrup (HFCS) is implicated in the rise of obesity, insulin resistance and non-alcoholic fatty liver disease. Using deuterated water: the fraction of glycogen derived from triose-P sources, Krebs cycle substrates, and direct pathway + cycling, was measured in 9 normal-chow fed mice (NC) and 12 mice fed normal chow plus a 55% fructose/45% glucose mix in the drinking water at 30% w/v (HFCS-55). This was enriched with [U-13C]fructose or [U-13C]glucose to determine the contribution of each to glycogenesis. In the setting of high sucrose or HFCS feeding, the effects of the fructose component on hepatic glycogen synthesis rates and on the conversion of dietary glucose to glycogen are unclear. By integrating deuterated water (2H2O) measurements of hepatic glycogen sources under natural feeding c onditions[9,11,12,18] with 13C-tracers of the glucose and fructose present in the drinking water (Fig. 1), the specific contributions of the HFCS-55 glucose and fructose components to hepatic glycogen synthesis were determined
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