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Exploring the Interplay among NAFLD, Insulin Resistance, and Metabolic Disorders: Mechanisms, Diagnosis, and Therapeutic Strategies

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: closed (15 May 2024) | Viewed by 1787

Special Issue Editor


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Guest Editor
Department of Neurosciences “Rita Levi Montalcini”, University of Turin, 10126 Turin, Italy
Interests: pharmacology

Special Issue Information

Dear Colleagues,

This Special Issue aims to comprehensively examine the complex relationship between NAFLD, insulin resistance, and metabolic disorders. It addresses the limited number of studies that have explored both NAFLD and insulin resistance simultaneously and aims to bridge the gap in understanding the underlying mechanisms, diagnostic approaches, and potential therapeutic interventions for these interconnected conditions. By expanding the scope beyond the primary focus on NAFLD and insulin resistance, this Special Issue encourages contributions on related metabolic disorders such as obesity, type 2 diabetes, and cardiovascular diseases. The goal is to foster multidisciplinary research collaborations and provide insights into the shared pathophysiological pathways, biomarkers, and novel therapeutic targets.

Dr. Debora Collotta
Guest Editor

Manuscript Submission Information

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Keywords

  • NAFLD
  • non-alcoholic fatty liver disease
  • insulin resistance
  • metabolic disorders
  • obesity
  • type 2 diabetes
  • cardiovascular diseases
  • pathophysiology
  • diagnostic approaches
  • therapeutic intervention

Published Papers (2 papers)

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Research

19 pages, 5144 KiB  
Article
Upregulation of Hepatic Glutathione S-Transferase Alpha 1 Ameliorates Metabolic Dysfunction-Associated Steatosis by Degrading Fatty Acid Binding Protein 1
by Jing Jiang, Hu Li, Mei Tang, Lei Lei, Hong-Ying Li, Biao Dong, Jian-Rui Li, Xue-Kai Wang, Han Sun, Jia-Yu Li, Jing-Chen Xu, Yue Gong, Jian-Dong Jiang and Zong-Gen Peng
Int. J. Mol. Sci. 2024, 25(10), 5086; https://doi.org/10.3390/ijms25105086 - 7 May 2024
Viewed by 270
Abstract
Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common metabolic disease of the liver, characterized by hepatic steatosis in more than 5% of hepatocytes. However, despite the recent approval of the first drug, resmetirom, for the management of metabolic dysfunction-associated steatohepatitis, decades [...] Read more.
Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common metabolic disease of the liver, characterized by hepatic steatosis in more than 5% of hepatocytes. However, despite the recent approval of the first drug, resmetirom, for the management of metabolic dysfunction-associated steatohepatitis, decades of target exploration and hundreds of clinical trials have failed, highlighting the urgent need to find new druggable targets for the discovery of innovative drug candidates against MASLD. Here, we found that glutathione S-transferase alpha 1 (GSTA1) expression was negatively associated with lipid droplet accumulation in vitro and in vivo. Overexpression of GSTA1 significantly attenuated oleic acid-induced steatosis in hepatocytes or high-fat diet-induced steatosis in the mouse liver. The hepatoprotective and anti-inflammatory drug bicyclol also attenuated steatosis by upregulating GSTA1 expression. A detailed mechanism showed that GSTA1 directly interacts with fatty acid binding protein 1 (FABP1) and facilitates the degradation of FABP1, thereby inhibiting intracellular triglyceride synthesis by impeding the uptake and transportation of free fatty acids. Conclusion: GSTA1 may be a good target for the discovery of innovative drug candidates as GSTA1 stabilizers or enhancers against MASLD. Full article
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13 pages, 3801 KiB  
Article
Reduced Lipopolysaccharide-Binding Protein (LBP) Levels Are Associated with Non-Alcoholic Fatty Liver Disease (NAFLD) and Adipose Inflammation in Human Obesity
by Ilaria Barchetta, Flavia Agata Cimini, Federica Sentinelli, Caterina Chiappetta, Claudio Di Cristofano, Gianfranco Silecchia, Frida Leonetti, Marco Giorgio Baroni and Maria Gisella Cavallo
Int. J. Mol. Sci. 2023, 24(24), 17174; https://doi.org/10.3390/ijms242417174 - 6 Dec 2023
Cited by 1 | Viewed by 1234
Abstract
Lipopolysaccharide (LPS) and its binding protein LBP have emerged as potential contributors to the progression from overweight/obesity to overt metabolic diseases and NAFLD. While LPS is known to activate hepatocyte inflammation, thus contributing toward NAFLD development, the role of LBP is more intricate, [...] Read more.
Lipopolysaccharide (LPS) and its binding protein LBP have emerged as potential contributors to the progression from overweight/obesity to overt metabolic diseases and NAFLD. While LPS is known to activate hepatocyte inflammation, thus contributing toward NAFLD development, the role of LBP is more intricate, and recent data have shown that experimental reduction in hepatic LBP promotes NAFLD progression. In this cross-sectional investigation, we evaluated circulating LBP in relation to obesity, NAFLD, visceral adipose tissue (VAT) inflammation, and type 2 diabetes (T2D). We recruited 186 individuals (M/F: 81/105; age: 47 ± 10.4 years; BMI: 35.5 ± 8.6 kg/m2); a subgroup (n = 81) underwent bariatric surgery with intra-operative VAT and liver biopsies. LBP levels were higher in obese individuals than non-obese individuals but were inversely correlated with the parameters of glucose metabolism. Reduced LBP predicted T2D independent of age, sex, and BMI (p < 0.001). LBP levels decreased across more severe stages of hepatosteatosis and lobular inflammation, and were inversely associated with VAT inflammation signatures. In conclusion, LBP levels are increased in obese individuals and are associated with a more favorable metabolic profile and lower NAFLD/NASH prevalence. A possible explanation for these findings is that hepatic LBP production may be triggered by chronic caloric excess and facilitate LPS degradation in the liver, thus protecting these individuals from the metabolic consequences of obesity. Full article
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