科研之友
微信
新浪微博
Facebook
分享链接
摘要
During feeding, dietary galactose is a potential source of hepatic glycogen synthesis; but its contribution has not been measured to date. In the presence of deuterated water ((H2O)-H-2), uridine diphosphate (UDP)-glucose derived from galactose is not enriched, whereas the remainder derived from glucose-6-phosphate (G6P) is enriched in position 2 to the same level as body water, assuming complete G6P-fructose-6-phosphate (F6P) exchange. Hence, the difference between UDP-glucose position 2 and body water enrichments reflects the contribution of galactose to glycogen synthesis relative to all other sources. In study 1, G6P-F6P exchange in 6 healthy subjects was quantified by supplementing a milk-containing breakfast meal with 10 g of [U-H-2(7)]glucose and quantifying the depletion of position 2 enrichment in urinary menthol glucuronide. In study 2, another 6 subjects ingested (H2O)-H-2 and acetaminophen followed by an identical breakfast meal with 10 g of [1-C-13]glucose to resolve direct/indirect pathways and galactose contributions to glycogen synthesis. Metabolite enrichments were determined by H-2 and C-13 nuclear magnetic resonance. In study 1, G6P-F6P exchange approached completion; therefore, the difference between position 2 and body water enrichments in study 2 (0.20% +/- 0.03% vs 0.27% +/- 0.03%, P %26lt; .005) was attributed to galactose glycogenesis. Dietary galactose contributed 19% +/- 3% to glycogen synthesis. Of the remainder, 58% +/- 5% was derived from the direct pathway and 22% 4% via the indirect pathway. The contribution of galactose to hepatic glycogen synthesis was resolved from that of direct and indirect pathways using a combination of (H2O)-H-2 and [1-C-13]glucose tracers.
- 出版日期2012-2
