Assessment of postprandial hepatic glycogen synthesis from uridine diphosphoglucose kinetics in obese and lean non-diabetic subjects

BACKGROUND: Obese patients are frequently characterized by insulin resistance and decreased insulin-mediated glycogen synthesis in skeletal muscle. Whether they also have impaired postprandial hepatic glycogen synthesis remains unknown. AIM: To determine whether postprandial hepatic glycogen synthes...

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Published inInternational Journal of Obesity Vol. 24; no. 10; pp. 1297 - 1302
Main Authors Paquot, N, Schneiter, P, Scheen, A.J, Lefebvre, P.J, Tappy, L
Format Journal Article Web Resource
LanguageEnglish
Published England Nature Publishing Group 01.10.2000
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ISSN0307-0565
1476-5497
1476-5497
DOI10.1038/sj.ijo.0801386

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Summary:BACKGROUND: Obese patients are frequently characterized by insulin resistance and decreased insulin-mediated glycogen synthesis in skeletal muscle. Whether they also have impaired postprandial hepatic glycogen synthesis remains unknown. AIM: To determine whether postprandial hepatic glycogen synthesis is decreased in obese patients compared to lean subjects. METHODS: Lean and obese subjects with impaired glucose tolerance were studied over 4 h after ingestion of a glucose load. Hepatic uridine diphosphoglucose kinetics were assessed using 13C-galactose infusion, with monitoring of urinary acetaminophen-glucuronide isotopic enrichment to estimate hepatic glycogen kinetics. RESULTS: Estimated net hepatic glycogen synthesis amounted to 18.6 and 22.6% of the ingested load in lean and obese subjects, respectively. CONCLUSION: Postprandial hepatic glycogen metabolism is not impaired in non-diabetic obese subjects.
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scopus-id:2-s2.0-0033774947
ISSN:0307-0565
1476-5497
1476-5497
DOI:10.1038/sj.ijo.0801386