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Alterations in the composition of the gut microbiota is thought to play a key role in causing type 2 diabetes, yet is not fully understood, especially at the strain level. Here, we used long-read DNA sequencing technology of 16S-ITS-23S rRNA genes for high-resolution characterization of gut microbiota in the development of type 2 diabetes. Gut microbiota composition was characterized from fecal DNA from 47 participants divided into 4 cohorts based on glycemic control: normal glycemic control (healthy; = 21), reversed prediabetes (prediabetes/healthy; = 8), prediabetes ( = 8), or type 2 diabetes ( = 10). A total of 46 taxa were found to be possibly related to progression from healthy state to type 2 diabetes. DSM 18228, DSM 20438, and ATCC 15703 could confer resistance to glucose intolerance. On the other hand, YIT 12061 may be pathogenic as it was found to be more abundant in type 2 diabetes participants than other cohorts. This research increases our understanding of the structural modulation of gut microbiota in the pathogenesis of type 2 diabetes and highlights gut microbiota strains, with the potential for targeted opportunistic pathogen control or consideration for probiotic prophylaxis and treatment.
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http://dx.doi.org/10.3390/microorganisms11030758 | DOI Listing |
Biomol Biomed
September 2025
Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China.
Coronary heart disease (CHD) is a leading cause of morbidity and mortality; patients with type 2 diabetes mellitus (T2DM) are at particularly high risk, highlighting the need for reliable biomarkers for early detection and risk stratification. We investigated whether combining the stress hyperglycemia ratio (SHR) and systemic inflammation response index (SIRI) improves CHD detection in T2DM. In this retrospective cohort of 943 T2DM patients undergoing coronary angiography, associations of SHR and SIRI with CHD were evaluated using multivariable logistic regression and restricted cubic splines; robustness was examined with subgroup and sensitivity analyses.
View Article and Find Full Text PDFAnnu Rev Pharmacol Toxicol
September 2025
1Department of Physiology and Pharmacology and Center for Molecular Medicine, Karolinska Institutet and University Hospital, Stockholm, Sweden; email:
In light of the success of blockbuster drugs for type 2 diabetes and obesity based on the GLP-1 hormone, drugmakers have concentrated their efforts on developing new and improved variations that address the route of administration, dosing, pathway selectivity, or polypharmacology. While some of these modifications have demonstrated improved efficacy in clinical studies and offered exciting opportunities for treating other diseases, drug-induced shifts to the conformational landscape of target receptors may have consequences for side effects. Our review summarizes advances in the understanding of the biochemistry, pharmacogenomics, and molecular pharmacology of incretins and their cognate receptors.
View Article and Find Full Text PDFSci Adv
September 2025
Department of Pediatrics, University of California San Diego, La Jolla, CA, USA.
Cell type-specific regulatory programs that drive type 1 diabetes (T1D) in the pancreas are poorly understood. Here, we performed single-nucleus multiomics and spatial transcriptomics in up to 32 nondiabetic (ND), autoantibody-positive (AAB), and T1D pancreas donors. Genomic profiles from 853,005 cells mapped to 12 pancreatic cell types, including multiple exocrine subtypes.
View Article and Find Full Text PDFAm J Physiol Cell Physiol
September 2025
Division of Gastroenterology & Hepatology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Chronic diarrhea is a frequent gastrointestinal complication in both type 1 (T1D) and type 2 diabetes (T2D), although the underlying mechanisms differ: T1D is linked to autonomic neuropathy and disrupted transporter regulation, while T2D is often linked to medications and intestinal inflammation. Using streptozotocin-induced mouse models of T1D and T2D, we observed increased luminal fluid in the small intestine of both. Given the role of Na⁺/H⁺ exchanger 3 (NHE3) in fluid absorption and its loss in most diarrheal diseases, we examined NHE3 expression across intestinal segments.
View Article and Find Full Text PDFExp Physiol
September 2025
Department of Hepatobiliary Surgery, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huaian, Jiangsu, China.
Hepatic ischaemia-reperfusion (IR) injury is a serious clinical issue, especially in patients with type 2 diabetes mellitus (T2DM). As mitochondria play a critical role in the regulation of IR-induced liver damage, mitochondria-targeted treatment is of the utmost significance for improving outcomes. The present study explored the mitoprotective role of combined ginsenoside-MC1 (GMC1) and irisin administration in diabetic rats with hepatic IR injury.
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