Research Article Details

Article ID: A06827
PMID: 32733017
Source: Sci Rep
Title: Determining the contribution of a high-fructose corn syrup formulation to hepatic glycogen synthesis during ad-libitum feeding in mice.
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&#8201;+&#8201;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&#8201;+&#8201;cycling, Krebs cycle, and triose-P sources accounted for 66&#8201;&#177;&#8201;0.7%, 23&#8201;&#177;&#8201;0.8% and 11&#8201;&#177;&#8201;0.4% of glycogen synthesis, respectively. HFCS-55 mice had similar direct pathway&#8201;+&#8201;cycling (64&#8201;&#177;&#8201;1%) but lower Krebs cycle (12&#8201;&#177;&#8201;1%, p&#8201;<&#8201;0.001) and higher triose-P contributions (24&#8201;&#177;&#8201;1%, p&#8201;<&#8201;0.001). HFCS-55-fructose contributed 17&#8201;&#177;&#8201;1% via triose-P and 2&#8201;&#177;&#8201;0% via Krebs cycle. HFCS-55-glucose contributed 16&#8201;&#177;&#8201;3% via direct pathway and 1&#8201;&#177;&#8201;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.
DOI: 10.1038/s41598-020-69820-3