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Research Abstract - Oral

Small Animal Internal Medicine

EN09 - Gut Microbial Whole Genome Gene-networks and Metabolic Pathways Analysis in Diabetic Cats

Thursday, June 23, 2022

1:45 PM – 2:00 PM CT

Location: ACC 18CD

CE: .25

Research Abstract - Oral Presenter(s)

AG

Arnon Gal, DVM BS MS PhD DACVIM (SAIM) DACVP (AP)

Assistant Professor in Small Animal Internal Medicine
Department of Veterinary Clinical Medicine, University of Illinois at Urbana-Champaign
Urbana, Illinois, United States

Proceedings/Handout

Abstract: Background: Gastrointestinal microbiota participate in regulating glucose homeostasis. Enteric microbiota dysbiosis has been associated with feline diabetes mellitus (DM), and with metabolic syndrome and DM in humans and other animals, but the functional association of microbial dysbiosis with feline DM has not been investigated.

Objectives: Compare gut microbial gene-networks and metabolic pathways between diabetic and nondiabetic cats.

Animals: 10 diabetic and 21 nondiabetic age-matched cats.

Methods: Whole-genome shotgun sequencing (Illumina NovaSeq) and HMP Unified Metabolic Analysis Network (HUMAnN v3.0) were used to generate fecal metagenomic microbiome profiles. Microbiome Multivariable Associations with Linear Models (MaAsLin v2) was used to compare the abundance of microbial genes and metabolic pathways between groups.

Results: The relative abundances of 849 microbial genes from 37 distinct bacterial species belonging to the phyla Firmicutes and Bacteroidetes were significantly decreased in diabetic cats (FDR < 0.05). Fecalibacterium prauznitsi (404/849; 47.6%) was the most common species associated with genes significantly under-represented in diabetic cats. Metabolic pathway analysis identified six distinct microbial metabolic pathways significantly under-represented in diabetic cats; five generate pyruvate and acetyl-CoA, and the sixth generates the urea cycle intermediates ornithine and agmatine.

Conclusions: In health, intestinal gluconeogenesis and ureagenesis critically downregulate hepatic gluconeogenesis and satiety that are deregulated in DM. We speculate that bacterial pyruvate and acetyl-CoA participate in the feline host intestinal gluconeogenesis, whereas ornithine and agmatine in the host's hepatic ureagenesis. Hence, deficiency in these bacterial metabolic pathways may contribute to the development and maintenance of feline DM through increased hepatic gluconeogenesis and decreased satiety.