Type 2 diabetes mellitus (T2DM) is a prevalent metabolic disease, yet its pathogenesis remains inconclusive. Recent studies have revealed a close relationship between the gut microbiota and T2DM, and specific gut microbiota structures and metabolic characteristics are associated with the onset and progression of T2DM. Exercise is an effective intervention for the prevention and management of T2DM, capable of reversing the dysbiosis induced by T2DM and regulating gut metabolites. However, the effects of exercise on the gut microbiota in T2DM patients still present many unresolved issues. Furthermore, the regulation of gut microbiota by exercise in T2DM patients is closely linked to multiple organs and can exert alleviation effects on T2DM via various gut-organ axis pathways. This paper reviews the characteristics of gut microbiota in T2DM and the effects of exercise on the gut microbiota in T2DM, with a particular focus on the mechanisms by which exercise regulates the gut microbiota to ameliorate T2DM via the gut-organ axis. This review aims to provide a reference for elucidating the relationship between exercise, gut microbiota, and T2DM.

Galactose is a ubiquitous monosaccharide in nature, serving not only as a primary carbon source for bioenergy metabolism but also as a precursor for various biological synthesis reactions. In eukaryotic cells, galactose or its derivatives can act as signaling molecules to participate in intercellular communication. Recent studies have revealed that galactose can modulate bacterial virulence by regulating intracellular signal transduction. Accordingly, galactose is considered an underappreciated environmental regulator in bacterial infection. However, the specific regulatory mechanisms remain incompletely elucidated. This review integrates the latest research findings to summarize the bacterial galactose metabolic pathway, the biological implications of galactose metabolism in bacterial virulence and interactions with hosts, and the key proteins (enzymes) in the galactose metabolism pathway as potential targets for developing novel vaccines. It offers new insights and reference for comprehending bacterial infection mechanisms and exploring innovative antibacterial strategies.

Acinetobacter spp. are the common opportunistic pathogens worldwide and pose a threat to the health of humans and animals. As the resistance rate to carbapenems aggravates, tigecycline has become one of the last lines for the treatment of multidrug-resistant Acinetobacter spp. infection. The rapid dissemination of tigecycline resistance genes tet(X3), tet(X4), tet(X5), tet(X6), and other variants in recent years has seriously affected the clinical application of new tetracycline antibiotics such as tigecycline, eravacycline, and omadacycline, whereas there is a lack of review on the tet(X) genes in Acinetobacter spp. This article comprehensively expounds the mechanisms of action, epidemiological characteristics, transmission risks, and inhibitors of tet(X) genes in Acinetobacter spp. and evaluates the diversity of their variants, bacterial hosts, geographical distribution, and sampling sources, aiming to provide a theoretical basis for the prevention and control of tet(X)-positive Acinetobacter spp.

Adenosine diphosphate-ribosylation (ADPr) is a reversible post-translational modification that is catalyzed by adenosine diphosphate-ribosyltransferases (ARTs) and adenosine diphosphate- ribosylhydrolases (ARHs), and it widely occurs in eukaryotes and prokaryotes. ARHs are a class of key enzymes that can reverse ADPr modification of specific amino acid residues or specific sites/sequences of DNA and RNA. They can regulate the physiological metabolism, signal transduction, gene expression, and other key life processes in bacteria or hosts, playing an important role in the inter/intraspecific competition, stress responses, and pathogenicity of bacteria. This article reviews the classification, structural characteristics, and catalytic mechanisms of bacterial ARHs, aiming to enrich our understanding about the catalytic mechanisms and biological functions of ARHs in bacterial life.