Heat-treated high-fat diet modifies gut microbiota and metabolic markers in apoe-/- mice
Research output: Contribution to journal › Article
BACKGROUND: High-fat diet has been known to have adverse effects on metabolic markers, as well as the gut microbiota. However, the effect of heat processing of high-fat diet, which leads to formations of advanced glycation end products (AGEs) has not been clearly distinguished from the effect of unheated fat. This study compared the effect of high-fat diet with heat-treated high-fat diet on adiposity, atherosclerosis and gut microbiota composition in the caecum of apoe (-/-) mice.
METHOD: Male apoe (-/-) mice were fed either low-fat (LF) control diet, high-fat (40 E% saturated fat, HF) control diet, or heat-treated high-fat (200 °C for 10 min, HT) diet, for 8 weeks. The plasma samples were used in the analysis of Nε-carboxy-methyl-lysine (CML) and Nε-carboxy-ethyl-lysine (CEL). The heart samples were analysed for atherosclerotic plaques, and the DNA from caecum was extracted and analysed for microbiota composition using 16S rRNA gene sequencing on a Miseq instrument. Additionally, the functions of microbial communities were also predicted based on the bacterial 16S rRNA gene sequence using Phylogenetic Investigation of Communities by Reconstruction of Unobserved States (PICRUSt).
RESULTS: Here we found that HT modifies gut microbiota composition and host adiposity. Prediction of bacterial gene functions based on 16S rRNA gene sequence revealed that HF increased bacterial genera enriched in lipid metabolism genes, while HT did not. Plasma CML and CEL increased 1.7 and 2.5 times, respectively, in mice fed HT as compared to mice fed HF. Despite lower adiposity, mice fed HT maintained atherosclerosis and displayed enlarged spleens.
CONCLUSIONS: The results suggested that heat processing of high-fat diet modifies the substrates reaching the lower gut of apoe (-/-) mice, resulting in different effects on gut microbiota composition. AGEs seem to maintain the effect on atherosclerosis, despite lower adiposity, and causing enlarged spleens, which possibly reflect elevated levels of inflammation in the body.
|Research areas and keywords||
Subject classification (UKÄ) – MANDATORY
|Journal||Nutrition & Metabolism|
|Publication status||Published - 2016|
Patrick Adlercreutz, Irini Lazou Ahrén, Siv Ahrné, Said Alhamimi, Kristina E Andersson, Kristina E Andersson, Anna Månberger, Ulrika Axling, Ulrika Axling, Björn Bergenståhl, Karin Berger, Inger Björck, Camilla Bränning, Fredrik Bäckhed, Yoghatama Cindya Zanzer, Anders Danielsson, Birgitta Danielsson, Eva Degerman, Petr Dejmek, Estera Dey, Anestis Dougkas, Linda Ekström, Ann-Charlotte Eliasson, Christer Fahlgren, Peter Falck, Peter Falck, Tannaz Ghaffarzadegan, Yvonne Granfeldt, Carl Grey, Ulrika Gunnerud, Åsa Håkansson, Åsa Håkansson, Frida Hållenius, Frida Hållenius, Lina Haskå, Lina Haskå, Emilia Heimann, Per Hellstrand, Lovisa Heyman, Cecilia Holm Wallenberg, Ann-Kristin Holmén-Pålbrink, Olle Holst, Tina Immerstrand, Peter Immerzeel, Greta Jakobsdottir, Bengt Jeppsson, Elin Johansson, Maria Johansson, Maria Johansson, Margareta Johansson, Ulla Johansson, Helena Jones, E N Karlsson, Petia Kovatcheva-Datchary, Evelina Kulcinskaja, Mona Landin-Olsson, Caroline Linninge, Ali Marefati, Nittaya Marungruang, Göran Molin, Anne Nilsson, Einar Nilsson, Ulf Nilsson, Margareta Nyman, Eva Ohlson, Crister Olsson, Rickard Öste, Elin Östman, Lisbeth Persson, Stefan Persson, Merichel Plaza, Olena Prykhodko, Karl Radeborg, Marilyn Rayner, Liza Rosén, Margareta Sandahl, Jonna Sandberg, Malin Sjöö, Kerstin Skog, Peter Spégel, Henrik Stålbrand, Olov Sterner, Julia Svensson, Eden Tareke, Juscelino Tovar, Charlotta Turner, Björn Weström, Jie Xu & Yadong Zhong
2007/07/01 → 2018/01/31