Abstract
Obesity and inactivity are major risk factors of feline diabetes mellitus (FDM) and human type II diabetes mellitus (T2DM). In recent years, changes in the gut microbiota have been suggested as a contributing factor to T2DM. Whether the gut microbiota (GM) composition plays a role in FDM remains unknown. The aim of the current study was firstly a cross-sectional comparison of the GM of diabetic cats, to that of lean, and of obese/overweight non-diabetic cats of a similar age. Specifically, fecal samples from 82 privately-owned cats from Denmark and Switzerland were sequenced using 16S rRNA gene amplicon metabarcoding. Secondly dietary intervention data was generated, by obtaining additional samples from a subset of cats after placing them on a high-protein diet for four weeks. The GM diversity of diabetic cats was lower than that of lean cats in the cross-sectional study, and lower compared to lean and to overweight/obese cats after diet intervention. Diabetic cats also exhibited fewer Anaerotruncus, Dialister, and unknown Ruminococcaceae than lean cats. Serum fructosamine levels correlated negatively with Prevotellaceae abundance and positively with Enterobacteriaceae abundance. In summary the intestinal microbiota of diabetic cats was characterized by decreased GM diversity and loss of butyrate producing bacterial genera.
Highlights
Obesity and inactivity are major risk factors of feline diabetes mellitus (FDM) and human type II diabetes mellitus (T2DM)
In this study of cats sampled in two different European countries, we demonstrated that diabetic cats exhibited an overall significantly reduced richness of the gut microbiota (GM) compared to lean healthy cats
Following a 4-week dietary intervention with a high-protein commercial diet formulated for diabetic cats, the DM cats exhibited decreased richness and evenness compared to lean group (LN) cats, the microbial GM community of DM cats differed from that of LN and obese group (OB) cats, and a decreased evenness was seen in DM cats compared to OB cats
Summary
Obesity and inactivity are major risk factors of feline diabetes mellitus (FDM) and human type II diabetes mellitus (T2DM). Inconsistencies relating to the nature of the dysbiosis exist between studies, which could possibly relate to the ethnic, dietary or therapeutic differences that have been shown to directly influence the gut microbiota[6] In these studies, a decreased proportion of bacteria (such as Roseburia species and Faecalibacterium prausnitzii) known to produce the short chain fatty acid (SCFA) butyrate was seen in T2DM patients compared to controls[4,5,6]. A recent study in mice found that butyrate and propionate (through different mechanisms) both activate intestinal gluconeogenesis gene expression, while propionate acts directly as a substrate for intestinal gluconeogenesis[8] This may seem paradoxical, as an increase in gluconeogenic substrates intuitively should be associated with decreased glycemic control. In agreement with findings in rats and humans, the subacute administration of LPS - which mimics low-grade inflammation in cats - impairs insulin sensitivity but not pancreatic β-cell function[12]
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