The prevalence of metabolic dysfunction–associated steatotic liver disease (MASLD), which is increasingly being recognized as a leading cause of chronic liver pathology globally, is increasing. The pathophysiological underpinnings of its progression, which is currently under active investigation, involve oxidative stress. Human adipose tissue, an integral endocrine organ, secretes an array of adipokines that are modulated by dietary patterns and lifestyle choices. These adipokines intricately orchestrate regulatory pathways that impact glucose and lipid metabolism, oxidative stress, and mitochondrial function, thereby influencing the evolution of hepatic steatosis and progression to metabolic dysfunction–associated steatohepatitis (MASH). This review examines recent data, underscoring the critical interplay of oxidative stress, reactive oxygen species, and redox signaling in adipokine-mediated mechanisms. The role of various adipokines in regulating the onset and progression of MASLD/MASH through mitochondrial dysfunction and endoplasmic reticulum stress and the underlying mechanisms are discussed. Due to the emerging correlation between adipokines and the development of MASLD positions, these adipokines are potential targets for the development of innovative therapeutic interventions for MASLD management. A comprehensive understanding of the pathogenesis of MASLD/MASH is instrumental for identifying therapies for MASH.

Liver damage is a primary complication leading to aggravation of diabetes. Therefore, a better understanding of the biological underpinnings of liver damage and the related signalling pathways might lead to the development of novel biomarkers and targeted therapies. While a multitude of transcriptomic data are currently available for diabetes from several parts of the world, almost no such studies have been performed in patients with diabetes after stem cell therapy. This study aimed to improve the understanding of the altered molecular networks in the liver tissue of diabetic rats after stem cell therapy. We compared liver tissues from eight diabetic rats treated with or without adipose-derived stem cells (ADSCs) and identified 1770 upregulated and 362 downregulated transcripts. Selected genes identified by RNA-Seq were subsequently validated using qRT‒PCR. Differentially expressed (2.0-fold change, adj. p < 0.05) transcripts were subjected to Ingenuity Pathway Analysis, which revealed numerous affected signalling pathways and functional categories. Dual specificity phosphatase 1 (DUSP1) mechanistic networks were activated prominently in liver tissue. Additionally, genes related to liver damage, inflammation, and insulin secretion were markedly enriched in liver tissue. Expression of genes indicative of hepatitis, liver steatosis and liver fibrosis was observed in liver tissue. Our data provide novel insight into the biology of liver damage and suggest common alterations in molecular networks during liver damage in diabetic rats and suggest the need for future development of therapeutic interventions targeting these common signalling pathways.