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Effects of fructose overfeeding on intrahepatic lipid accumulation and hepatic insulin sensitivity in healthy humans
Author(s) -
Lecoultre Virgile,
Egli Leonie,
Boss Andreas,
Carrel Guillaume,
Theytaz Fanny,
Zwygart Karin,
Kreis Roland,
Schneiter Philippe,
Boesch Chris,
Tappy Luc
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.630.16
Subject(s) - medicine , fructose , endocrinology , insulin resistance , insulin , carbohydrate metabolism , chemistry , lipid metabolism , insulin sensitivity , metabolism , biochemistry
Added sugars may contribute to the development of insulin resistance in metabolic diseases. It is further suspected that this is related to fructose‐induced intrahepatic fat deposition. How it relates to daily fructose intake, and what the relative roles of fructose, glucose and excess energy are, remains however controversial. We therefore evaluated the effects of short term overfeeding with various amounts of fructose, glucose, or saturated fat on hepatic insulin sensitivity (HIS) and lipid content (IHCL) in healthy male subjects. Data collected in several studies were pooled. Fasting hepatic glucose production (HGP), HIS and IHCL were measured after both 6–7 days on a weight‐maintenance diet (control, C; n=53) and 6–7 days of overfeeding with 1.5 (F 1.5, n=7), 3 (F3, n=17), or 4g fructose/kg/day (F4, n=10), with 3g glucose/kg/day (G3, n=11), or with 30% excess energy as saturated fat (fat 30%, n=8). F3, F4, G3 and fat 30% all significantly increased IHCL as compared to C (all p<0.05). F4 and G3 significantly increased HGP, (both p<0.05), and F3 and F4 significantly decreased HIS (both p<0.01). In contrast, there was no significant effect of fat 30% on HGP or HISI. Overfeeding with large amounts of fructose or glucose impairs fasting hepatic glucose metabolism and increases hepatic fat content within 6–7 days. This indicates short‐term regulation of hepatic glucose metabolism by simple carbohydrates.