title: Diet-induced obesity in ad libitum-fed mice: food texture overrides the effect of macronutrient composition.
abstract: Diet-induced obesity in mice can be achieved through the use of diets with different macronutrient compositions and textures. We aimed at determining the contribution of macronutrient composition to obesity development and associated pathophysiological changes in mice. C57BL/6N mice were offered a control, a high-fat or a Western-style diet, either as pellet (H for hard) or with identical composition in powder form (S for soft), resulting in C-S, C-H, HF-H, HF-S, W-H and W-S groups, respectively. Body fat distribution, expression levels of selected target genes in adipose tissues, clinical chemistry and hormone concentration in the blood, as well as liver TAG content were measured. The most striking finding was that all mice fed the different powder diets developed obesity with similar weight gain, whereas among the mice fed the pellet diets, only those given the HF and W diets became obese. This allowed us to separate diet-specific effects from obesity-mediated effects. Irrespective of the food texture, the W diet induced a more severe hepatosteatosis and higher activities of serum transaminases compared with the two other diets. Adipose tissue gene expression analysis revealed that leptin and adiponectin levels were not affected by the dietary composition per se, whereas uncoupling protein 1 and 11β-hydroxysteroid dehydrogenase type 1 levels were decreased by both dietary composition and changes in body weight. In conclusion, diets differing in macronutrient composition elicit specific pathophysiological changes, independently of changes in body weight. A diet high in both fat and sugars seems to be more deleterious for the liver than a HF diet.
authors.affiliation: Molecular Nutrition Unit, ZIEL-Research Center for Nutrition and Food Sciences, Technische Universität München (TUM), Gregor-Mendel-Strasse 2, 85350 Freising-Weihenstephan, Germany. charles.desmarchelier@univ-amu.fr
authors.forename: Charles
authors.initials: C
authors.lastname: Desmarchelier
authors.forename: Tobias
authors.initials: T
authors.lastname: Ludwig
authors.forename: Ronny
authors.initials: R
authors.lastname: Scheundel
authors.forename: Nadine
authors.initials: N
authors.lastname: Rink
authors.forename: Bernhard L
authors.initials: BL
authors.lastname: Bader
authors.forename: Martin
authors.initials: M
authors.lastname: Klingenspor
authors.forename: Hannelore
authors.initials: H
authors.lastname: Daniel
mesh_terms: D043205:11-beta-Hydroxysteroid Dehydrogenase Type 1 / Q000235:genetics / Q000378:metabolism; D052242:Adiponectin / Q000097:blood* / Q000378:metabolism; D000273:Adipose Tissue / Q000378:metabolism*; D000704:Analysis of Variance; D000818:Animals; D050218:Body Fat Distribution / Q000009:adverse effects; D001835:Body Weight / Q000502:physiology; D004032:Diet / Q000009:adverse effects*; D004041:Dietary Fats / Q000009:adverse effects / Q000378:metabolism*; D019422:Dietary Sucrose / Q000009:adverse effects; D015870:Gene Expression; D007328:Insulin / Q000097:blood; D007473:Ion Channels / Q000235:genetics / Q000378:metabolism; D020738:Leptin / Q000097:blood* / Q000378:metabolism; D008099:Liver / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D024101:Mitochondrial Proteins / Q000235:genetics / Q000378:metabolism; D009765:Obesity / Q000209:etiology*; D009929:Organ Size / Q000502:physiology; D052243:Resistin / Q000097:blood; D000071256:Uncoupling Protein 1
chemical_list: D052242:Adiponectin; D004041:Dietary Fats; D019422:Dietary Sucrose; D007328:Insulin; D007473:Ion Channels; D020738:Leptin; D024101:Mitochondrial Proteins; D052243:Resistin; C000604372:Ucp1 protein, mouse; D000071256:Uncoupling Protein 1; D043205:11-beta-Hydroxysteroid Dehydrogenase Type 1