Increasing evidence suggests that metabolites produced by the gut microbiota play a crucial role in host–microbe interactions. Dietary tryptophan ingested by the host enters the gut, where indole-like metabolites such as indole propionic acid (IPA) are produced under deamination by commensal bacteria. Here, we summarize the IPA-producing bacteria, dietary patterns on IPA content, and functional roles of IPA in various diseases. IPA can not only stimulate the expression of tight junction (TJ) proteins to enhance gut barrier function and inhibit the penetration of toxic factors, but also modulate the immune system to exert anti-inflammatory and antioxidant effects to synergistically regulate body physiology. Moreover, IPA can act on target organs through blood circulation to form the gut–organ axis, which helps maintain systemic homeostasis. IPA shows great potential for the diagnosis and treatment of various clinical diseases, such as NAFLD, Alzheimer’s disease, and breast cancer. However, the therapeutic effect of IPA depends on dose, target organ, or time. In future studies, further work should be performed to explore the effects and mechanisms of IPA on host health and disease to further improve the existing treatment program.
Background: Excessive fat accumulation of pigs is undesirable. It severely affects economic return of modern pig industry. Studies in humans and mice have examined the role of the gut microbiome in host energy metabolism. Commercial Duroc pigs are often fed formula diets with high energy and protein. Whether and how the gut microbiome under this type of diets regulates swine fat accumulation is largely unknown.Results: In the present study, we systematically investigated the correlation of gut microbiome with pig lean meat percentage (LMP) in a total of 698 commercial Duroc pigs. We demonstrate that the gut microbiome of fat pigs was dominated by P. copri which occupied 23.53% and 5.76% of relative abundance in average in the discovery and validation cohort, respectively. High abundance of P. copri in the gut resulted in a higher abundance of serum metabolites associated with chronic inflammation, e.g., branched chain amino acids, aromatic amino acids, the metabolites of arachidonic acid metabolism and lipopolysaccharides. Host intestinal barrier permeability and chronic inflammation response were increased. A gavage experiment using germ-free mice confirmed that the P. copri isolated from experimental pigs was a causal species increasing host fat accumulation. Host colon, adipose tissue, and muscle transcriptomes indicated that P. copri colonization significantly upregulated the expression of the genes related to immune and inflammatory responses, lipogenesis, and fat accumulation, but attenuated the genes associated with lipolysis, lipid transport, and muscle growth.Conclusions: Taken together, we identified and confirmed that P. copri in the gut microbial communities of pigs fed by commercial formula diets results in the significantly increased fat deposition of pigs, and proposed a possible mechanism of P. copri affecting fat accumulation. The results provided fundamental knowledges for reducing pig fat accumulation through regulating the gut microbial composition in pig industry.
Background: Dominance and other non-additive genetic effects arise from the interaction between alleles, and historically these phenomena played a major role in quantitative genetics. However, today most genome-wide association studies (GWAS) assume alleles act additively. Methods: We systematically investigated both dominance - here representing any non-additive effect - and additivity across 574 physiological and gene expression traits in three mammalian models: a Pig F2 Intercross, a Rat Heterogeneous Stock and a Mouse Heterogeneous Stock. Results: In all species, and across all physiological traits, dominance accounts for about one quarter of the heritable variance. Hematological and immunological traits exhibit the highest dominance variance, possibly reflecting balancing selection in response to pathogens. Although most quantitative trait loci (QTLs) are detectable assuming additivity, we identified 154, 64 and 62 novel dominance QTLs in pigs, rats and mice respectively, that were undetectable as additive QTLs. Similarly, even though most cis-acting eQTLs are additive, we observed a large fraction of dominance variance in gene expression, and trans-acting eQTLs are enriched for dominance. Genes causal for dominance physiological QTLs are less likely to be physically linked to their QTLs but instead act via trans-acting dominance eQTLs. In addition, in HS rat transcriptomes, thousands of eQTLs associate with alternate transcripts and exhibit complex additive and dominant architectures, suggesting a mechanism for dominance. Conclusions: Although heritability is predominantly additive, many mammalian genetic effects are dominant and likely arise through distinct mechanisms. It is therefore advantageous to consider both additive and dominance effects in GWAS to improve power and uncover causality.
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