Microbiome and Nutrition
The complex community of bacteria, yeasts and viruses living in our intestines, collectively known as the gut microbiome, is shaped, in part, by what we eat. Genetics, environment, and other factors also influence an individual’s microbial community. Research at the NRI investigates these complex relationships and their impact on disease risk. We use animal models and bioinformatics to study the associations between nutritional metabolites, gut microbiome, and health. What happens in the gut doesn’t stay in the gut. Your microbiome can play a role in cardiovascular disease, obesity and diabetes, and even cancer. Our team envisions a future where analysis of your microbiome can determine disease risk, and medical foods can be prescribed to treat and prevent disease by regulating the microbiome.
Publications
Microbiome and Nutrition Publications
2020
Population studies of TMAO and its precursors may help elucidate mechanisms. Meyer K
2019
Association of dietary patterns with the gut microbiota in older, community-dwelling men. Meyer K
2018
Meta-analysis of human genome-microbiome association studies: the MiBioGen consortium initiative. Meyer K
Human microbiota, blood group antigens, and disease. Sumner S
2017
Trimethylamine N-Oxide, the Microbiome, and Heart and Kidney Disease. Zeisel S
2016
Diet and Gut Microbial Function in Metabolic and Cardiovascular Disease Risk. Meyer K
Antibiotic-mediated gut microbiome perturbation accelerates development of type 1 diabetes in mice. Sumner S
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The mechanism of discrimination between oxidized and reduced coenzyme in the aldehyde dehydrogenase domain of Aldh1l1
The mechanism of discrimination between oxidized and reduced coenzyme in the aldehyde dehydrogenase domain of Aldh1l1.
Tsybovsky Y, Malakhau Y, Strickland KC, Krupenko SA.
Chem Biol Interact. 2013 Feb 25;202(1-3):62-9. doi: 10.1016/j.cbi.2012.12.015. Epub 2013 Jan 5.
PMID: 23295222
JNK1/2 regulate Bid by direct phosphorylation at Thr59 in response to ALDH1L1
JNK1/2 regulate Bid by direct phosphorylation at Thr59 in response to ALDH1L1.
Prakasam A, Ghose S, Oleinik NV, Bethard JR, Peterson YK, Krupenko NI, Krupenko SA.
Cell Death Dis. 2014 Jul 31;5:e1358. doi: 10.1038/cddis.2014.316.
PMID: 25077544
A novel tumor suppressor function of glycine N-methyltransferase is independent of its catalytic activity but requires nuclear localization
A novel tumor suppressor function of glycine N-methyltransferase is independent of its catalytic activity but requires nuclear localization.
DebRoy S, Kramarenko II, Ghose S, Oleinik NV, Krupenko SA, Krupenko NI.
PLoS One. 2013 Jul 30;8(7):e70062. doi: 10.1371/journal.pone.0070062. Print 2013.
PMID: 23936142
Activation of p21-Dependent G1/G2 Arrest in the Absence of DNA Damage as an Antiapoptotic Response to Metabolic Stress
Activation of p21-Dependent G1/G2 Arrest in the Absence of DNA Damage as an Antiapoptotic Response to Metabolic Stress.
Hoeferlin LA, Oleinik NV, Krupenko NI, Krupenko SA.
Genes Cancer. 2011 Sep;2(9):889-99. doi: 10.1177/1947601911432495.
PMID: 22593801