Volume 28, Issue S1 1018.5
Nutrition
Free Access

Potential of glycated proteins produced during aging of cheddar cheese to modulate fecal bacteria from obese mice ex vivo and protect against colon inflammation (1018.5)

Jialing Yuan

Jialing Yuan

Food Science and Human nutrition, Washington State University, Pullman, WA, United States

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Katherine Noratto

Katherine Noratto

Washington State University, Pullman, WA, United States

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Gerhard Munske

Gerhard Munske

School of Molecular Biosciences, Washington State University, Pullman, WA, United States

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Paulina Pilla

Paulina Pilla

Panamerican School of Agriculture Zamorano, Francisco morazan, Honduras

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Indira Mohanty

Indira Mohanty

Food Science and Human nutrition, Washington State University, Pullman, WA, United States

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Diana Alcantara Zapata

Diana Alcantara Zapata

Food Science and Human nutrition, Washington State University, Pullman, WA, United States

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Giuliana Noratto

Giuliana Noratto

Food Science and Human nutrition, Washington State University, Pullman, WA, United States

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First published: 01 April 2014
Citations: 2

Abstract

Cheddar cheese aging promotes the production of glycated proteins with potential to improve intestinal health.

We investigated major changes on proteins of aged cheddar cheese (Cougar Gold) during ripening up to 24 months using HPLC/MS-MS. The proteins effects on fecal bacteria from obese mice after in vitro intestinal digestion, and the effects of metabolites produced during fecal fermentation were evaluated. We further assessed the effects of metabolites from fecal fermentation on production of reactive oxygen species (ROS) in colon epithelial HT-29 and the fibroblast CCD-18Co cells challenged with E. Coli lipopolysaccharides (LPS) following standard analytical procedures.

Results demonstrated that cheese aging (6-24 months) produced soluble glycosylated proteins of MW ~ 23 kDa mainly derived from α-S1- and β-casein. Cheese glycated proteins were resistant to in vitro gastrointestinal digestion and changed the relative abundances of fecal bacteria by increasing Bacteroidetes/Firmicutes ratio and Bifidobacterium compared to the casein fermented controls. These changes resembled relative abundances of bacteria in feces from lean mice control. Furthermore, metabolites produced during fecal fermentation protected both the HT-29 and CCD-18Co cells from LPS-induced ROS. We are currently investigating the molecular targets of glycated proteins and metabolites produced after fecal fermentation that protect colon cells from inflammation. These results are relevant for gut health.