This NHANES 2011–2018 cross-sectional study of 4,847 participants found that higher DXA-derived vFMI was associated with a higher prevalence of diabetes and some vascular-related outcomes. Log-transformed vFMI showed threshold patterns for diabetes and diabetic nephropathy.

The findings support further evaluation of vFMI in risk research, but they do not establish that visceral fat causes diabetes or complications and cannot replace clinical diagnosis.

The present study investigated the disease burden and associated productivity losses attributable to T2DM among adults, while also forecasting the disease burden through 2050. The study adopted a quantitative approach and drew upon datasets obtained from the Global Burden of Disease (GBD) 2021 database, the World Bank, the United Nations, and the International Labor Organization. Projections based on the BAPC model indicate that the ASDR will rise to 2243.12 per 100,000 population by 2050. The estimated annual productivity loss attributable to T2DM in the region exceeds 220 billion U.S. dollar (USD). Comprehensive and sustainable interventions, including health policies, educational initiatives, and social protection measures, are needed to reduce disparities associated with T2DM.

We are pleased to present a curated collection of our recent cover articles, featuring breakthroughs ranging from enzyme–chemical interaction prediction, genome-scale modeling and novel biosensor development to metabolic engineering of industrially relevant microbial hosts and next-generation gene-editing tools. These studies highlight the field's rapid evolution from fundamental tool discovery to translational industrial applications.

University of Missouri researchers discovered MKV3, the first compound that blocks key copper transport proteins, making bacteria and cancer cells more vulnerable to the toxic effects of copper. The early-stage breakthrough could lead to new treatments for antibiotic-resistant infections and cancer while also providing a powerful tool for studying copper transport across many forms of life.

Pathological cardiac fibrosis is a central hallmark of chronic heart failure, characterized by the maladaptive transformation of quiescent cardiac fibroblasts (CFs) into α-smooth muscle actin (α-SMA)-expressing myofibroblasts. This phenotypic shift drives the excessive accumulation of extracellular matrix proteins, which significantly impairs ventricular compliance and cardiac function. Previous studies have established the unfolded protein response (UPR) as a conserved cellular stress-response pathway involved in restoring endoplasmic reticulum (ER) proteostasis, yet its direct contributions to the fibrotic transcriptional machinery in the heart are not fully elucidated.