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Effects of Epicatechin and its Gut Metabolites on Beta Cell Function, Survival and Proliferation
Author(s) -
Tessem Jeffery Sivert,
Rowley Thomas J.,
Ray Jason D.,
Herring Jacob A.,
Kener Kyle B.,
Bitner Benjamin F.,
Ross Mimi,
Lopez Moroni,
Bikman Benjamin T.,
Neilson Andrew P.
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.41.8
Subject(s) - secretion , insulin , beta cell , cell growth , cell , function (biology) , cell culture , chemistry , beta (programming language) , biology , microbiology and biotechnology , biochemistry , endocrinology , medicine , islet , genetics , computer science , programming language
An initiating factor of Type 2 diabetes (T2D) is beta cell dysfunction and the eventual loss of functional beta cell mass. Mechanisms that improve beta cell function could be used as a treatment for the millions of individuals with T2D. We have recently shown that the monomeric cocoa epicatechin is sufficient to enhance insulin secretion from the 832/13 INS‐1 derived beta cell line and primary rat islets through upregulating the Nrf2 pathway, enhancing mitochondrial protein expression, improving mitochondrial function and ultimately enhancing beta cell ATP production. Here we present data pertaining to the larger epicatechin forms (oligomeric and polymeric epicatechin) as well as gut microbe metabolites of epicatechin (Homovanillic Acid, Hippuric Acid, 5‐phenylvaleric Acid) on beta cell proliferation, survival and insulin secretion. While the monomeric form enhances insulin secretion, the oligomeric and polymeric forms inhibit insulin secretion. Interestingly, the gut metabolites of epicatechin all significantly enhance insulin secretion. These results suggest that cocoa derived monomeric epicatechin and its gut‐derived metabolites could be leveraged to enhance insulin secretion as a treatment modality for patients with T2D. Support or Funding Information This research has been funded by a grant to JST from the Diabetes Action Research and Education Foundation. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .