THis is from PNAS. In short, obesity seems to be modulated in mice fed a high fat diet by a bacterium. Reduce the bacterial count, and the mice thin out. From the abstract
Obesity and type 2 diabetes are characterized by altered gut microbiota, inflammation, and gut barrier disruption. Microbial composition and the mechanisms of interaction with the host that affect gut barrier function during obesity and type 2 diabetes have not been elucidated. We recently isolated Akkermansia muciniphila, which is a mucin-degrading bacterium that resides in the mucus layer. The presence of this bacterium inversely correlates with body weight in rodents and humans. However, the precise physiological roles played by this bacterium during obesity and metabolic disorders are unknown. This study demonstrated that the abundance of A. muciniphila decreased in obese and type 2 diabetic mice. We also observed that prebiotic feeding normalized A. muciniphila abundance, which correlated with an improved metabolic profile. In addition, we demonstrated that A. muciniphila treatment reversed high-fat diet-induced metabolic disorders, including fat-mass gain, metabolic endotoxemia, adipose tissue inflammation, and insulin resistance. A. muciniphila administration increased the intestinal levels of endocannabinoids that control inflammation, the gut barrier, and gut peptide secretion. Finally, we demonstrated that all these effects required viable A. muciniphila because treatment with heat-killed cells did not improve the metabolic profile or the mucus layer thickness. In summary, this study provides substantial insight into the intricate mechanisms of bacterial (i.e., A. muciniphila) regulation of the cross-talk between the host and gut microbiota. These results also provide a rationale for the development of a treatment that uses this human mucus colonizer for the prevention or treatment of obesity and its associated metabolic disorders.
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A. muciniphila abundance is decreased in obese and diabetic mice, and prebiotic treatment restored A. muciniphila to basal levels and reversed metabolic endotoxemia and related disorders. (A) A. muciniphila abundance (log10 of bacteria per g of cecal content) measured in the cecal content of leptin-deficient (ob-ob) obese mice and their lean littermates (lean) (n = 5). (B) A. muciniphila abundance (log10 of bacteria per g of cecal content) measured in the cecal content of control diet-fed mice (CT) or CT diet-fed mice treated with prebiotics (CT-Pre) added to their drinking water and HF diet-fed mice (HF) or HF diet-fed mice treated with prebiotics (HF-Pre) added to their drinking water for 8 wk (n = 10). (C) A. muciniphila abundance (log10 of bacteria per g of cecal content) measured in the cecal content of obese mice fed a control diet (ob-CT) or treated with prebiotics (ob-Pre) for 5 wk (n = 10). (D) Portal vein serum LPS levels (n = 7–9). (E) mRNA expression of the adipose tissue macrophage infiltration marker CD11c (n = 10). (F) Total fat mass gain measured by time-domain NMR (n = 10). (G) Pearson’s correlation between log values of portal vein LPS levels and A. muciniphila abundance (log10 of bacteria per g of cecal content); (Inset) Pearson’s correlation coefficient (r) and the corresponding P value. Data are shown as means ± SEM; *P < 0.05 by two-tailed Student t test, data with different superscript letters are significantly different (P < 0.05) according to post hoc ANOVA one-way statistical analysis. PNAS Online First
This is very close to meeting Koch’s hypotheses: a replication of this in humans would be unethical. And it is the second disorder that I was told was psychosomatic that has become an intection: the first was gastric ulcers.
