möglich sobald bei der ZB eingereicht worden ist.
Nutritional strategy to prevent fatty liver and insulin resistance independent from obesity by reducing glucose-dependent insulinotropic polypeptide responses in mice.
Diabetologia 58, 374-383 (2015)
AIMS/HYPOTHESIS:High intake of carbohydrates, particularly sucrose, in western societies is associated with the development of non-alcoholic fatty liver (NAFL) and diabetes mellitus. It is unclear whether this is related primarily to the carbohydrate quantity or to the hormonal responses, particularly glucose-dependent insulinotropic polypeptide (GIP), which is released in the proximal intestine. Therefore, we investigated the role of GIP by comparing two glucose-fructose dimers, sucrose and Palatinose (isomaltulose), resorbed proximally or distally. METHODS: The glycaemic and incretin responses to sucrose and Palatinose were studied by oral gavage and meal tests. We then analysed phenotypic and metabolic diet-induced changes in C57Bl/6J mice exposed to isoenergetic diets differing in carbohydrate type. Studies were repeated in GIP receptor knockout (Gipr -/-) mice and their wild-type littermates. RESULTS: Compared with sucrose, Palatinose intake resulted in slower glucose absorption and reduced postprandial insulin and GIP levels. After 22 weeks, Palatinose feeding prevented hepatic steatosis (48.5%) compared with sucrose and improved glucose tolerance, without differences in body composition and food intake. Ablation of GIP signalling in Gipr -/- mice completely prevented the deleterious metabolic effects of sucrose feeding. Furthermore, our microarray analysis indicated that sucrose increased 2.3-fold the hepatic expression of Socs2, which is involved in the growth hormone signalling pathway and participates in the development of NAFL. CONCLUSIONS/INTERPRETATION: Our results suggest that the site of glucose absorption and the GIP response determine liver fat accumulation and insulin resistance. GIP may play a role in sucrose induced fatty liver by regulating the expression of Socs2.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Fatty Liver ; Gip Response ; Palatinose; Diet-induced Obesity; Lipid-metabolism; Disease; Gip; Palatinose; Rats; Isomaltulose; Receptor; Steatohepatitis; Adiponectin
ISSN (print) / ISBN 0012-186X
Quellenangaben Band: 58, Heft: 2, Seiten: 374-383
Verlagsort Berlin ; Heidelberg [u.a.]
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Experimental Genetics (IEG)