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Replication of Obesity and Associated Signaling Pathways Through 1624 Diabetes Volume 63, May 2014 Frank A. Duca,1,2,3 Yassine Sakar,1,2 Patricia Lepage,1,2 Fabienne Devime,1,2 Bénédicte Langelier,1,2 Joël Doré,1,2 and Mihai Covasa1,2,4,5 Replication of Obesity and Associated Signaling Pathways Through Transfer of Microbiota From Obese-Prone Rats AS Aberrations in gut microbiota are associated with animals harbored specifi c speciesH from Oscillibacter metabolic disorders, including obesity. However, and Clostridium clustersE XIVa and IV that were whether shifts in the microbiota profile during obesity completelyL absent from OR animals. In conclusion, are a characteristic of the phenotype or susceptibilityC to obesity is characterized by an D a consequence of obesogenic feeding remains Iunfavorable microbiome predisposing the host to fl E elusive. Therefore, we aimed to determine differencesT peripheral and central in ammationT and promoting in the gut microbiota of obese-prone (OP)R and obese- weight gain and adiposity during obesogenic resistant (OR) rats and examinedA the contribution of feeding. C Diabetes 2014;63:1624–1636 | DOI: 10.2337/db13-1526 OBESITY STUDIES this microbiota to the behavioral and metabolic A characteristicsI duringS obesity. We found that OP rats R displayH a gut microbiota distinct from OR rats fed the T Tsame high-fat diet, with a higher Firmicutes-to- EThe overabundance of energy-dense foods in developed Bacteroidetes ratio and significant genera R westernized societies has transformed obesity from an differences. Transfer of OP but not OR microbiota to American burden to a worldwide epidemic, with grave germ-free (GF) mice replicatedN the characteristics of health and socioeconomic consequences. Recent the OP phenotype, includingE reduced intestinal and advancements in DNA sequencing techniques and meta- hypothalamic satiationE signaling, hyperphagia, genomic profiling have established a link between the increasedB weight gain and adiposity, and enhanced trillions of microbial inhabitants of the gut (i.e., gut lipogenesis and adipogenesis. Furthermore, microbiota) and the development of obesity-related increased gut permeability through metabolic dysregulations (1). Gut microbiota are signifi- conventionalization resulted in inflammation by cantly altered in humans and animal models of obesity, proinflammatory nuclear factor (NF)-kB/inhibitor of with reduction in bacterial diversity (2) as well as overall NF-kB kinase subunit signaling in adipose tissue, compositional shifts, such as a reduced abundance of liver, and hypothalamus. OP donor and GF recipient Bacteroidetes and a proportional increase in Firmicutes 1UMR1913-Microbiologie de l’Alimentation au Service de la Santé, l’Institut Corresponding author: Mihai Covasa, [email protected]. National de la Recherche Agronomique, Jouy-en-Josas, France Received 3 October 2013 and accepted 5 January 2014. 2UMR1913-Microbiologie de l’Alimentation au Service de la Santé, This article contains Supplementary Data online at http://diabetes AgroParisTech, Jouy-en-Josas, France .diabetesjournals.org/lookup/suppl/doi:10.2337/db13-1526/-/DC1. 3Doctoral School of Physiology and Pathophysiology, University Pierre and Marie Currie, Paris, France F.A.D. and Y.S. contributed equally to this study. 4Department of Basic Medical Sciences, College of Osteopathic Medicine, © 2014 by the American Diabetes Association. See http://creativecommons Western University of Health Sciences, Pomona, CA .org/licenses/by-nc-nd/3.0/ for details. 5Department of Human Health and Development, University of Suceava, Suceava, Romania diabetes.diabetesjournals.org Duca and Associates 1625 phylum (3–6). Gut microbiota regulate several host a HF diet (4.2 kcal/g; D12334B; Research Diets, New metabolic functions, and microbial dysbiosis is associated Brunswick, NJ) for 12 weeks, until sacrifice (11). Addi- with altered energy homeostasis (1). Obesity is charac- tional OP (n = 5) and OR (n = 4) rats, kept in the same terized by an enrichment in genes encoding enzymes housing conditions, were maintained on chow through- responsible for extracting calories from otherwise in- out and used for microbiota analysis. digestible polysaccharides (2,4). In addition to increased Mice energy harvest, the microbial metabolic byproducts, such as short-chain fatty acids (FAs), modulate secre- Male C57BL/6J GF mice (n = 20) from our GF colonies tion and gene expression of gut peptides controlling (Animalerie Axénique de Micalis, Jouy-en-Josas, France) satiety, such as glucagon like peptide-1 (GLP-1) and were used for inoculation studies. Two groups (n =10 peptideYY(PYY),byactingonG-coupledprotein each) were housed separately in two Trexler-type iso- receptors (GPRs) in intestinal enteroendocrine cells, lators (Igenia, France), with animals housed individually suggesting a role for gut microbiota in modulating sa- in polycarbonate cages with cedar bedding. tiation (7). Obesity and high-fat (HF) feeding are also Conventionalization associated with intestinal, systemic, and adipose tissue inflammation (1). Intestinal inflammation is an early GF mice (n = 10 for each phenotype) were con- consequence of HF feeding, present before the onset of ventionalized (CV) with fecal microbiota from one OP obesity and insulin resistance (8), supporting a direct, and OR donor rat, both maintained on the HF diet. Feces causal role for HF-induced microbiota changes in the from each donor were freshly collected, quickly diluted, development of obesity. and homogenized in liquid casein yeast mediumS (1:100 Conventionalization studies have demonstrated the w/v) in anaerobic conditions. GF mice (12 weeks old) were inoculated immediately thereafterA by oral gavage contribution of the gut microbiota to the development of metabolic disease because the metabolic phenotype is (250 mL) and maintained onH standard chow (2.83 kcal/g; transmissible by gut microbiota transplantation (3,4,9). R03, Safe Diets)E for 4 weeks in separate gnotobiotic These early studies investigated the effect of gut micro- isolators.L Afterward, half of each group was switched to biota using genetic, transgenic, or HF-fed models of Ca HF diet (4.73 kcal/g; D12451, Research Diets) for D obesity, none of which are an accurate reflection of hu-I 8 weeks, while the remaining half was fed chow. All animals were killed and tissue collected forE analyses. man obesity that encompasses the interaction betweenT T genes and the environment (3,4,9,10).R Therefore, in the Quantitative RT-PCR and WesternC Blotting current study, we examined theA role of the gut micro- biota in obese-prone (OP) and obese-resistant (OR) rats, For all experiments,A protein and RNA extraction, and S subsequent Western blotting and quantitative (q)PCR a model thatI closely mimics the characteristics of the R humanH obese phenotype, including a polygenic mode of wereT performed as previously described (11). Briefly, Tinheritance, whereby some, but not all, individuals areERNA was extracted by using TRiZol, quantified, 10 mg susceptible to weight gain when exposed toR an obeso- RNA was reverse transcribed, and cDNA was diluted genic environment (10). First, by using both chow- and fivefold for qRT-PCR using TaqMan gene expression HF-fed OP and OR rats, we determinedN whether micro- assays (Applied Biosystems). Data are expressed as the biota shifts solely resultE from consumption of an obe- relative mRNA normalized to b-actin and analyzed –DDCT sogenic diet orE are a manifestation of the obese according to the 2 method. phenotype.B Second, we transplanted microbiota from OP For Western blotting, tissues were thawed on ice and and OR rats fed a HF diet into germ-free (GF) mice to suspended in 1 mL radioimmunoprecipitation assay examine the capacity of microbiota to influence pheno- buffer containing protease inhibitors (Sigma-Aldrich, type and associated metabolic and molecular changes, Lyon, France). Cells were lysed, homogenized, and including gut–brain satiation signaling, lipid storage, and centrifuged for 20 min at 14,000g at 4°C. After quanti- systemic and hypothalamic inflammation. fying, soluble protein (25–100 mg) was run on SDS-PAGE gels containing 8–12% acrylamide, transferred to nitro- RESEARCH DESIGN AND METHODS cellulose membranes, and probed with antibodies (Santa Animals Cruz Biotechnology and Abcam). Immune complexes were detected by chemiluminescence and quantified by All experiments were done in accordance with the European scanning densitometry using ImageJ software against Guidelines for the Care and Use of Laboratory Animals. b-actin (cytosolic proteins) or Ras-related nuclear protein Rats (nucleus proteins) as internal controls. OP-CD (n = 7) and OR-CD (n = 4) rats from Charles River Laboratories (Wilimington, MA) were used. Ani- Plasma Analysis mals were housed individually in a temperature- Plasma was analyzed for glucose, triglycerides, total controlled vivarium with 12:12-h light/dark cycle (lights cholesterol, and total HDL by an AU 400 automated on at 0700). Starting at 8 weeks of age, rats were fed biochemical analyzer (Olympus). Gut hormones and 1626 Microbiota Transfer and Obesity Diabetes Volume 63, May 2014 cytokines were determined in duplicate using a mouse acquired with an inverted confocal microscope LSM510 gut hormone panel or mouse cytokine magnetic bead with 340 oil-immersed objective and processed by panel (Millipore), measured with Luminex technology AxioVision SE64 Rel.4.8 software. Controls were run for (St. Antoine, Paris, France), following the manufacturers’ false negatives or positives of the first and secondary instructions.
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