Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Comment
. 2015 Oct 14;18(4):385-7.
doi: 10.1016/j.chom.2015.10.005.

Eat Your Curry

Purna C Kashyap  1
Affiliations
Comment

Eat Your Curry

Purna C Kashyap. Cell Host Microbe. .

Abstract

The role of gut bacteria in modulating gastrointestinal physiology is increasingly being appreciated. In a recent issue of Cell, Dey et al. (2015) report how a single dietary ingredient-turmeric-interacts with gut bacteria to alter gastrointestinal motility.

PubMed Disclaimer

Figures

Figure 1
Figure 1. Microbiota-mediated pathways that affect GI transit
Diet–gut microbiota interaction results in a large array of metabolites. In the presence of dietary turmeric, gut microbial communities with high bile-salt hydrolase activity make higher amounts of unconjugated bile acids, which influence enteric nervous system signaling and lead to faster GI transit. Dietary fermentation by gut microbiota results in formation of short chain fatty acids which affect GI motility by effects on gut neuromuscular apparatus and the host serotonergic pathway. LPS and other bacterial products are implicated in improving neuronal survival as well as affecting enteric neuron–muscularis macrophage crosstalk. Gut microbiota are required for the post-natal development and generation of new enteric glia. LPS, lipopolysaccharide; GDNF, glia derived neurotrophic factor; TLR-4, Toll like receptor 4; 5HTR, 4 5-hydroxytryptamine receptor-4; ICC, interstitial cells of Cajal.
See this image and copyright information in PMC

Comment on

References

    1. Anitha M, Vijay-Kumar M, Sitaraman SV, Gewirtz AT, Srinivasan S. Gut microbial products regulate murine gastrointestinal motility via Toll-like receptor 4 signaling. Gastroenterology. 2012;143:1006–1016 e1004. - PMC - PubMed
    1. Camilleri M. Advances in understanding of bile acid diarrhea. Expert Rev Gastroenterol Hepatol. 2014;8:49–61. - PMC - PubMed
    1. Dey N, Wagner VE, Blanton LV, Cheng J, Fontana L, Haque R, Ahmed T, Gordon JI. Regulators of Gut Motility Revealed by a Gnotobiotic Model of Diet-Microbiome Interactions Related to Travel. Cell. 2015;163:95–107. - PMC - PubMed
    1. Duboc H, Rainteau D, Rajca S, Humbert L, Farabos D, Maubert M, Grondin V, Jouet P, Bouhassira D, Seksik P, et al. Increase in fecal primary bile acids and dysbiosis in patients with diarrhea-predominant irritable bowel syndrome. Neurogastroenterol Motil. 2012;24:513–520. e246–517. - PubMed
    1. Duboc H, Rajca S, Rainteau D, Benarous D, Maubert MA, Quervain E, Thomas G, Barbu V, Humbert L, Despras G, et al. Connecting dysbiosis, bile-acid dysmetabolism and gut inflammation in inflammatory bowel diseases. Gut. 2013;62:531–539. - PubMed

Publication types