The gastrointestinal (GI) microbiome of cats and dogs is increasingly recognized as a metabolically active organ inextricably linked to pet health. Food serves as a substrate for the GI microbiome of cats and dogs and plays a significant role in defining the composition and metabolism of the GI microbiome. The microbiome, in turn, facilitates the host’s nutrient digestion and the production of postbiotics, which are bacterially derived compounds that can influence pet health. Consequently, pet owners have a role in shaping the microbiome of cats and dogs through the food they choose to provide. Yet, a clear understanding of the impact these food choices have on the microbiome, and thus on the overall health of the pet, is lacking. Pet foods are formulated to contain the typical nutritional building blocks of carbohydrates, proteins, and fats, but increasingly include microbiome-targeted ingredients, such as prebiotics and probiotics. Each of these categories, as well as their relative proportions in food, can affect the composition and/or function of the microbiome. Accumulating evidence suggests that dietary components may impact not only GI disease, but also allergies, oral health, weight management, diabetes, and kidney disease through changes in the GI microbiome. Until recently, the focus of microbiome research was to characterize alterations in microbiome composition in disease states, while less research effort has been devoted to understanding how changes in nutrition can influence pet health by modifying the microbiome function. This review summarizes the impact of pet food nutritional components on the composition and function of the microbiome and examines evidence for the role of nutrition in impacting host health through the microbiome in a variety of disease states. Understanding how nutrition can modulate GI microbiome composition and function may reveal new avenues for enhancing the health and resilience of cats and dogs.

Selenium (Se) status in non-deficient subjects is typically assessed by the Se contents of plasma/serum. That pool comprises two functional, specific selenoprotein components and at least one non-functional, non-specific components which respond differently to changes in Se intake. A more informative means of characterizing Se status in non-deficient individuals is needed.

High-fat (HF) diets can produce obesity and have been linked to the development of nonalcoholic fatty liver disease and changes in the gut microbiome

Nitroxyl (HNO) can inhibit the glycolytic enzyme glyceraldehyde 3‐phosphate dehydrogenase (GAPDH). Because of the importance of glycolysis in many malignant cells, we thus propose that HNO can adversely affect tumor growth. This hypothesis was tested using in vitro and in vivo models of breast cancer. We report here for the first time that HNO suppresses the proliferation of both estrogen receptor (ER)‐positive and ER‐negative human breast cancer cell lines, in a dose dependent manner. Mice treated with HNO either injected into the tumor itself or via the intraperitoneal approach had smaller xenograft tumor size. In addition to significantly decreased blood vessel density in the HNO‐treated tumors, we observed lower levels of circulating serum vascular endothelial growth factor (VEGF). Accordingly, there was a decrease in total HIF‐1α (hypoxia‐inducible factor) protein in HNO‐treated tumor cells. Further studies showed inhibition of GAPDH activity in HNO‐treated human breast cancer cell lines and in HNO‐treated tumor tissue derived from xenografts. One explanation for the multiplicity of actions observed after HNO treatment could be the effect from the initial inhibition of GAPDH, providing a potential therapeutic avenue based upon blocking glycolysis resulting in decreased HIF‐1α, thus leading to angiogenesis inhibition. Therefore, HNO appears to act via mechanism(s) different from those of existing breast cancer drugs, making it a potential candidate to overcome known and emerging drug resistance pathways.

Dietary fiber is a key component in gastrointestinal health maintenance partly due to its fermentation by the gut microbiome. The food-dependent effects of a novel fiber bundle added to hydrolyzed meat (HM) or grain-rich (GR) foods in healthy dogs (n = 16) or those with chronic enteritis/gastroenteritis (n = 16) were examined. Addition of fiber to either food improved stool quality in dogs regardless of health status; microbiome diversity of dogs with chronic enteritis/gastroenteritis became more similar to healthy dogs. The abundance of bacteria mediating beneficial saccharolytic processes (eg, Lachnospiraceae) significantly increased on addition of fiber to the GR food, while those mediating detrimental proteolytic catabolism (eg, Desulfovibrionaceae) significantly decreased. Fiber addition to the HM food led to significant changes in saccharolytic/proteolytic bacteria. Higher levels of free saccharides in feces upon fiber addition to either food indicated increased saccharolysis. Fiber addition to the GR food decreased levels of fecal free amino acids, indicating decreased proteolysis. Addition of fiber decreased fecal pH for both foods but likely by different mechanisms: addition of fiber to the HM food led to increased straight-chain short-chain fatty acids (SCFAs) and no significant change in proteolytic branched-chain SFCAs, while in the GR food, fiber mainly led to decreased proteolytic branched-chain SFCAs. Other postbiotics related to intestinal health were consistently altered when fiber was added to either food. Plant-derived bioactive molecules were enriched in feces from dogs fed either food with added fiber, which could account for the observed modulation of the canine gut microbiome and shifts in metabolic capacity.