(PTFS08-06-26) Dietary Açaí Selectively Restores Gut Barrier, Redox Homeostasis, and Microbial Composition Independent of Glycemic Improvement in a Diabetic Neuropathy Model

Sunday, July 26, 2026

12:50 PM - 12:54 PM ET

Location: Prince George's Hall B-E (The Hub) - Poster Theater 2 / Poster Board Number: PT2-6

Presenting Author(s)

XL

Xiaobo Liu, PhD

Post Doctorate Research Associate
Texas Tech University Health Sciences Center
Lubbock, Texas, United States

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

Co-Author(s)

PP

Patrick Q. Pham

Texas Tech University Health Sciences Center
Lubbock, Texas, United States
ME

Moamen M. Elmassry, PhD

Princeton University
Princeton, New Jersey, United States
SC

Stacy Cos

Texas Tech University Health Sciences Center
Lubbock, Texas, United States
JT

João Pedro Tôrres Guimarães

Texas Tech University Health Sciences Center
Lubbock, Texas, United States
RB

Rachel L. Babcock

Texas Tech University Health Sciences Center
Lubbock, Texas, United States
JD

Jannette Dufour, PhD

Texas Tech University Health Sciences Center
Lubbock, Texas, United States
CS

Chwan-Li Shen, PhD

Professor
Texas Tech University Health Sciences Center
lubbock, Texas, United States

Disclosure(s):

Xiaobo Liu, PhD: No relevant financial relationship(s) with ineligible companies to disclose.

Objectives: Diabetic neuropathy (DN) is a common complication of diabetes with limited therapies. Gut barrier dysfunction, dysbiosis, oxidative stress, and mitochondrial impairment contribute to DN pathogenesis. Functional foods rich in antioxidant and anti-inflammatory bioactives may help restore intestinal integrity and redox balance. Açaí is a polyphenol-rich berry with strong antioxidant properties. This study evaluated whether dietary açaí supplementation improves gut barrier function, redox signaling, and microbial composition in an HFD/STZ-induced rat model of DN.

Methods: DN was induced using HFD and a single STZ injection (40 mg/kg, i.p.). The diabetic rats were assigned to HFD+STZ or HFD+STZ+2% (w/w diet) açaí groups; the low-fat diet rats served as controls. Distal colon tissue was analyzed for gene expression of intestinal barrier (occluding, MUC2), antioxidant (NRF, SOD1), pro-inflammatory (IFNγ, TNFα, IL-6, IL-1β, CD11b), and mitochondrial biogenesis markers (PGC1α, TFAM) using RT-qPCR. Microbiome sequencing data of cecal feces were processed in QIIME2 with differential abundance testing using LOCOM with FDR correction. Pancreatic islet function was evaluated by serum and pancreatic insulin, HOMA-IR, HOMA-B, and histology.

Results: HFD+STZ reduced colonic occludin and MUC2 expression, both restored by açaí. NRF2 and SOD1 were downregulated by HFD+STZ and normalized with açaí. PGC1α and TFAM were unchanged by HFD+STZ, but açaí selectively increased PGC1α. Pro-inflammatory cytokines (IFNγ, TNFα, IL-6, IL-1β) were reduced in HFD+STZ and unchanged by açaí. NFκB remained unchanged, and CD11b showed an upward trend with açaí (0.05< p< 0.1). Microbiome α-diversity and richness were unchanged among three groups; however, LOCOM revealed significant HFD-induced compositional shifts, with selective normalization of specific taxa by açaí. Açaí did not significantly alter insulin levels, insulin resistance, β-cell function, or islet morphology in the diabetic rats.

Conclusions: Dietary açaí selectively restores gut barrier integrity and redox homeostasis with concurrent microbial remodeling, independent of systemic glycemic improvement.

Funding Sources: School of Medicine, Texas Tech University Health Sciences Center