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.

The efficacy of sodium-glucose transporter 2 (SGLT-2) inhibitors for nonalcoholic fatty liver disease (NAFLD) is unclear. Therefore, we conducted a systematic review and meta-analysis to evaluate SGLT-2 inhibitors efficacy for NAFLD treatment. We systematically searched major electronic databases (PubMed, Cochrane Library, Web of Science, Embase) from inception until 11/2023, identifying randomized controlled trials (RCTs) of SGLT-2 inhibitors treatment for patients with NAFLD. The mean differences (MD or SMD) and 95 % confidence intervals (CIs) were calculated via random-effects models. Eleven articles (n = 805 patients with NAFLD) were included in this study. Of these, 408 participants received SGLT-2 inhibitors, while 397 participants were in the control group. SGLT-2 inhibitors significantly reduced liver enzyme levels, including aspartate alanine aminotransferase (ALT) (MD [95 % CI]; -9.31 U/L [-13.41, -5.21], p < 0.00001), aspartate aminotransferase (AST) (MD [95 % CI]; -6.06 U/L [-10.98, -1.15], p = 0.02), and gamma-glutamyltransferase (GGT) (MD [95 % CI]; -11.72 U/L [-15.65, -7.80], p < 0.00001). SGLT-2 inhibitors intervention was also associated with significant reductions in body weight (MD [95 % CI]; -2.72 kg [-3.49, -1.95], p < 0.00001) and BMI (MD [95 % CI]; -1.11 kg/m² [-1.39, -0.82], p < 0.00001) and improvements in glycaemic indices, triglyceride (TG) and high-density lipoprotein cholesterol (HDL-C). However, no significant changes in total cholesterol (TC) or low-density lipoprotein cholesterol (LDL-C) were observed. The meta-analysis revealed a beneficial effect of SGLT-2 inhibitors on liver functions and body weight, BMI, TG, HDL-C, and glucose homeostasis in patients with NAFLD, indicating that SGLT-2 inhibitors might be a clinical therapeutic strategy for these patients, especially individuals with concurrent type 2 diabetes mellitus (T2DM).

Introduction: Allicin is a wide spectrum prebiotic for human health, but whether it can attenuate blood in diabetes patients is rarely reported. In this study, we built a rat model and investigated the effect of allicin on diabetes mellitus type 2 (T2DM). We found that allicin could effectively reduce blood glucose levels, regulate intestinal microbiota, reduce lipid and body weight accumulation, and systemic inflammation in T2DM rats.Methods: The rat model of type 2 diabetes was made by streptozotocin, and different doses of allicin were given orally by gavage. The intestinal contents of diabetes rats were sequenced and analyzed by 16S technology, and the clinical indicators of rats were detected for joint analysis.Results: Allicin can improve the intestinal flora of type 2 diabetes rats, enrich beneficial metabolites, reduce blood glucose, improve blood lipids, reduce systemic inflammation, and improve type 2 diabetes.Discussion: Intestinal microbiome analysis showed that allicin gavage significantly regulated the structure and main components of the intestinal microbiota in T2DM rats. Allicin increased the abundance of probiotic microbes, such as Lactobacillus, Clostridium and Akkermansia, while it reduced pathogenic microbes, such as Enterobacter, Erysipelatoclostridium and Colidextribacter. Allicin gavage increased the abundance of intestinal short-chain fatty acids, such as acetic acid and propionic acid. Correlation analysis showed that the increased gut microbes by allicin gavage were significantly associated with health physiological parameters but negatively related to serum inflammatory factors such as interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-a), and hypersensitive C-reactive protein (hs-CRP). In addition, our study also suggests that allicin may have prebiotic effects on chronic liver injury. This study shows that allicin can regulate various clinical symptoms of T2DM and is a potential therapeutic drug for T2DM.