(LB04-05-26) Resistant Maltodextrin Starch May Promote Metabolic Health via Modulation of the Murine Microbiome and Metabolome

Tuesday, July 28, 2026

10:48 AM - 11:00 AM ET

Location: Maryland Ballroom D

Presenting Author(s)

Kari Melander, B.S.

PhD Candidate
University of California, Davis
Davis, California, United States

Disclosure(s): No relevant financial relationship(s) with ineligible companies to disclose.

Co-Author(s)

LE

Levi Evans

University of California, Davis, United States
David Klurfeld, PhD

Adjunct Professor
Indiana University School of Public Health-Bloomington
Glenwood, Maryland, United States
Marta L. Fiorotto, Ph.D.

Children's Nutrition Research Center, Baylor College of Medicine
Houston, Texas, United States
Jesse F. Gregory, III, PhD

Professor Emeritus of Food Science and Human Nutrition
University of Florida
Gainesville, Florida, United States
DK

Dohee Kim

University of California, Davis
Davis, United States
JN

John W. Newman, PhD

PWA-ARS WHNRC
Davis, California, United States
JR

Jennifer Rutkowsky, Ph.D.

University of California, Davis
Mary E. Kable, PhD

Research Scientist/Adjunct Assistant Professor
United States Department of Agriculture
Davis, California, United States
BB

Brian J. Bennett, Dr., PhD

Western Human Nutrition Research Center
Davis, California, United States

Disclosure(s):

Kari Melander, B.S.: No relevant financial relationship(s) with ineligible companies to disclose.

Objectives: This experiment examines whether adding Resistant Maltodextrin Starch (RMD) to the AIN93 formula will improve rodent metabolic health markers via cecal microbiome modulation.

Methods: This study used 36 C57/BL6J and 36 Swiss Webster mice with equal males and females per strain/diet group. Mice were group housed (n =3) and acclimated on the AIN-93G diet for two weeks. Post-acclimation, mice were sex- and weight-matched, singly housed, and fed either a control diet (AIN-93G) or an experimental diet containing 5% Fibersol®-2 for 13 weeks. Fasting plasma was collected at weeks 0 and 13 to measure albumin, ALT, creatinine, glucose, total and HDL cholesterol, and triglycerides. Mice were euthanized at 13wk and cecal content microbiome 16s RNA profiling, LC-MS/MS-based 2- to 12- carbon fatty acid profiling, colorimetric liver triglyceride determinations, and colon tissue MUC2, FFAR2, FFAR3, and GRP109a gene expression were evaluated. Body composition was assessed via Echo MRI at weeks 0, 7, and 13. Weekly food disappearance was recorded.

Results: No differences were found in weight gain, plasma markers, or body fat percentage between diet groups. The weight of food, but not energy, disappearance was significantly higher in C57BL/6J mice on the experimental diet. Ceca in the ASN2026 diet group were heavier and contained higher levels of the short chain fatty acids (SCFAs) acetate, propionate, 2-methyl-butyrate, isobutyrate, and isovalerate. These differences were associated with increased cecal tissue expression of MUC2, but not SCFA receptors. Tests of β diversity indicated diet-dependent changes in microbiome compositions, with greater evenness in AIN93 mice and dominance of Dubosiella newyorkensis in mice fed the experimental diet. While RMD did not significantly influence major metabolic health markers in this context, it did alter the cecal microbiome and SCFA profile.

Conclusions: Addition of a fermentable dietary fiber to the widely used AIN93 rodent diet had a limited impact on health phenotypes but did lead to significant changes in the cecal microbiome and SCFA profile.

Funding Sources: CRIS project 2032-10700-003-000D