Essere magri può anche essere determinato dalla flora batterica.
Una ricerca della Washington University's School of Medicine pubblicata su Science evidenzia come trasferendo batteri presenti nelle viscere di obesi nell'intestino di topi che non hanno flora batterica, questi ingrasseranno e accumuleranno più peso, viceversa trasferendo batteri di soggetti magri , gli obesi dimagriranno..
Si tratta del genere di batteri chiamato Bacteroidetes, che sembrano arricchire il microbiota di alcuni indivui magri, e che sembrano avere per loro anche un ruolo protettivo contro l'accumulo di grasso nei topi sottoposti ad alcuni regimi alimentari.
Per fare questa scoperta, gli scienziati statunitensi hanno studiato la flora intestinale di coppie di gemelli in cui uno fosse magro e l'altro obeso. Hanno poi prelevato il microbiota da ciascuno dei due fratelli, e lo hanno trapiantato in topi che erano stati privati della propria flora intestinale e cresciuti in ambiente sterile, in modo che non avessero microrganismi propri nell'intestino. E così si sono accorti che i topi che avevano ricevuto i batteri provenienti dal gemello grasso tendevano – con una dieta normale – a diventare più grassi rispetto agli altri. “Era impossibile attribuire questa differenza a differenze nel regime alimentare, uguale per tutti i roditori, e dunque ci si è resi conto che era il microbiota stesso a fare la differenza”, ha spiegato Jeffrey Gordon, direttore del Center for Genome Sciences and Systems Biology nell'ateneo statunitense. Questo, stando a quanto riportato nello studio, sarebbe dovuto al passaggio dai roditori più magri a quelli grassi di batteri del phylum Bacteroidetes.
ABSTRACT
Science 6 September 2013:
Vol. 341 no. 6150
DOI: 10.1126/science.1241214
Gut Microbiota from Twins Discordant for Obesity Modulate Metabolism in Mice
1. Vanessa K. Ridaura1,
2. Jeremiah J. Faith1,
3. Federico E. Rey1,
4. Jiye Cheng1,
5. Alexis E. Duncan2,3,
6. Andrew L. Kau1,
7. Nicholas W. Griffin1,
8. Vincent Lombard4,
9. Bernard Henrissat4,5,
10. James R. Bain6,7,8,
11. Michael J. Muehlbauer6,
12. Olga Ilkayeva6,
13. Clay F. Semenkovich9,
14. Katsuhiko Funai9,
15. David K. Hayashi10,
16. Barbara J. Lyle11,
17. Margaret C. Martini11,
18. Luke K. Ursell12,
19. Jose C. Clemente12,
20. William Van Treuren12,
21. William A. Walters13,
22. Rob Knight12,14,15,
23. Christopher B. Newgard6,7,8,
24. Andrew C. Heath2,
25. Jeffrey I. Gordon1,*
Introduction
Establishing whether specific structural and functional configurations of a human gut microbiota are causally related to a given physiologic or disease phenotype is challenging. Twins discordant for obesity provide an opportunity to examine interrelations between obesity and its associated metabolic disorders, diet, and the gut microbiota. Transplanting the intact uncultured or cultured human fecal microbiota from each member of a discordant twin pair into separate groups of recipient germfree mice permits the donors’ communities to be replicated, differences between their properties to be identified, the impact of these differences on body composition and metabolic phenotypes to be discerned, and the effects of diet-by-microbiota interactions to be analyzed. In addition, cohousing coprophagic mice harboring transplanted microbiota from discordant pairs provides an opportunity to determine which bacterial taxa invade the gut communities of cage mates, how invasion correlates with host phenotypes, and how invasion and microbial niche are affected by human diets.
Cohousing Ln and Ob mice prevents increased adiposity in Ob cage mates (Ob). (A) Adiposity change after 10 days of cohousing. *P < 0.05 versus Ob controls (Student’s t test). (B) Bacteroidales from Ln microbiota invade Ob microbiota. Columns show individual mice.
Methods
Separate groups of germfree mice were colonized with uncultured fecal microbiota from each member of four twin pairs discordant for obesity or with culture collections from an obese (Ob) or lean (Ln) co-twin. Animals were fed a mouse chow low in fat and rich in plant polysaccharides, or one of two diets reflecting the upper or lower tertiles of consumption of saturated fats and fruits and vegetables based on the U.S. National Health and Nutrition Examination Survey (NHANES). Ln or Ob mice were cohoused 5 days after colonization. Body composition changes were defined by quantitative magnetic resonance. Microbiota or microbiome structure, gene expression, and metabolism were assayed by 16S ribosomal RNA profiling, whole-community shotgun sequencing, RNA-sequencing, and mass spectrometry. Host gene expression and metabolism were also characterized.
Results and Discussion
The intact uncultured and culturable bacterial component of Ob co-twins’ fecal microbiota conveyed significantly greater increases in body mass and adiposity than those of Ln communities. Differences in body composition were correlated with differences in fermentation of short-chain fatty acids (increased in Ln), metabolism of branched-chain amino acids (increased in Ob), and microbial transformation of bile acid species (increased in Ln and correlated with down-regulation of host farnesoid X receptor signaling). Cohousing Ln and Ob mice prevented development of increased adiposity and body mass in Ob cage mates and transformed their microbiota’s metabolic profile to a leanlike state. Transformation correlated with invasion of members of Bacteroidales from Ln into Ob microbiota. Invasion and phenotypic rescue were diet-dependent and occurred with the diet representing the lower tertile of U.S. consumption of saturated fats, and upper tertile of fruits and vegetables, but not with the diet representing the upper tertile of saturated fats, and lower tertile of fruit and vegetable consumption. These results reveal that transmissible and modifiable interactions between diet and microbiota influence host biology. |
