Adipokines, Inflammation, and Metabolic Diseases

This study shows that deleting CD44 in preadipocytes promotes adipogenesis by suppressing PPARγ and cell cycle pathways, suggesting CD44 as a therapeutic target for obesity-related metabolic diseases.

This study shows that loss of CTRP10 in female mice leads to obesity without metabolic complications, highlighting a sex-dependent role in metabolic health.

This paper shows that inhibiting BTK in adipose tissue macrophages enhances OxPhos and shifts macrophages to an M2-like state, reducing inflammation and improving metabolic outcomes in obesity.

This study presents transcriptomic and proteomic analyses of obesity and T2D in cynomolgus monkeys, identifying tissue-specific molecular changes and potential therapeutic targets.

The paper identifies molecular and metabolic signatures of cardiometabolic syndrome using extreme phenotype groups and shows changes after bariatric surgery.

This study shows that deleting SLC7A8 in mice protects against diet-induced obesity by reducing lipid accumulation in multiple organs and improving glucose metabolism.

This study shows that reducing hypothalamic somatostatinergic neurons in mice leads to diabetes-like symptoms in multiple tissues without hyperglycemia.

The paper investigates transcriptome changes in human monocytes exposed to arecoline and MNPA, identifying genes linked to diabetes and obesity.

The paper investigates how an omentin gene polymorphism affects adiponectin levels and cardiometabolic health, finding adiponectin mediates this relationship in Asian Indians.

This study uses quantitative proteomics to identify regulators of TNFα-mediated insulin resistance in adipocytes under chronic inflammation.

This study identifies acute-phase cytokines and DNA methylation as regulators of chemerin expression in different cell types.

The paper applies high-dimensional statistical and network visualization techniques to Arab diabetes and obesity data to identify key biomarkers and interactions associated with the diseases.