ArticleScientific reports2016
Prohibitin-induced, obesity-associated insulin resistance and accompanying low-grade inflammation causes NASH and HCC.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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The trial behind it
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Who cites it
26 citing papers in PubMed, 47 citations in OpenAlex.
- Trial
- Survival after curative hepatectomy for hepatocellular carcinoma in patients with and without MAFLD: a western cohort study.Frontiers in oncology · 2026Article
- mTOR inhibition triggers mitochondrial fragmentation in cardiomyocytes through proteosome-dependent prohibitin degradation and OPA-1 cleavage.Cell communication and signaling : CCS · 2025Article
- Prohibitions in the meta-inflammatory response: a review.Frontiers in molecular biosciences · 2024Review
- Deletion of adipocyte prohibitin 1 exacerbates high-fat diet-induced steatosis but not liver inflammation and fibrosis.Hepatology communications · 2022Article
- Role of the Ghrelin System in Colitis and Hepatitis as Risk Factors for Inflammatory-Related Cancers.International journal of molecular sciences · 2022Review
- KDEL Receptors: Pathophysiological Functions, Therapeutic Options, and Biotechnological Opportunities.Biomedicines · 2022Review
- The chemoprevention of spirulina platensis and garlic against diethylnitrosamine induced liver cancer in rats via amelioration of inflammatory cytokines expression and oxidative stress.Toxicology research · 2022Article
- Prohibitins: A Key Link between Mitochondria and Nervous System Diseases.Oxidative medicine and cellular longevity · 2022Review
- CirculatoryGenes · 2021Article
- Peptide Adjuvant to Invigorate Cytolytic Activity of NK Cells in an Obese Mouse Cancer Model.Pharmaceutics · 2021Article
- Prohibitin S-Nitrosylation Is Required for the Neuroprotective Effect of Nitric Oxide in Neuronal Cultures.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Sex Differences in Nonalcoholic Fatty Liver Disease: State of the Art and Identification of Research Gaps.Hepatology (Baltimore, Md.) · 2019Review
- Signal transducer and activator of transcriptions (STATs)-at the crossroads of obesity-linked non-alcoholic steatohepatitis and hepatocellular carcinoma.Hepatobiliary surgery and nutrition · 2019Article
- Immune-Deficient Pfp/Rag2Cells · 2019Article
- Prohibitin: a prime candidate for a pleiotropic effector that mediates sex differences in obesity, insulin resistance, and metabolic dysregulation.Biology of sex differences · 2019Review
- Prohibitin: A hypothetical target for sex-based new therapeutics for metabolic and immune diseases.Experimental biology and medicine (Maywood, N.J.) · 2019Review
- Obesity-Linked Cancers: Current Knowledge, Challenges and Limitations in Mechanistic Studies and Rodent Models.Cancers · 2018Review
- Mitochondrial role in the neonatal predisposition to developing nonalcoholic fatty liver disease.The Journal of clinical investigation · 2018Review
- Gonadectomy in Mito-Ob mice revealed a sex-dimorphic relationship between prohibitin and sex steroids in adipose tissue biology and glucose homeostasis.Biology of sex differences · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Obesity increases the risk for nonalcoholic steatohepatitis (NASH) and hepatocarcinogenesis. However, the underlying mechanisms involved in the disease process remain unclear. Recently, we have developed a transgenic obese mouse model (Mito-Ob) by prohibitin mediated mitochondrial remodeling in adipocytes. The Mito-Ob mice develop obesity in a sex-neutral manner, but obesity-associated adipose inflammation and metabolic dysregulation in a male sex-specific manner. Here we report that with aging, the male Mito-Ob mice spontaneously develop obesity-linked NASH and hepatocellular carcinoma (HCC). In contrast, the female Mito-Ob mice maintained normal glucose and insulin levels and did not develop NASH and HCC. The anti-inflammatory peptide ghrelin was significantly upregulated in the female mice and down regulated in the male mice compared with respective control mice. In addition, a reduction in the markers of mitochondrial content and function was found in the liver of male Mito-Ob mice with NASH/HCC development. We found that ERK1/2 signaling was significantly upregulated whereas STAT3 signaling was significantly down regulated in the tumors from Mito-Ob mice. These data provide a proof-of-concept that the metabolic and inflammatory status of the adipose tissue and their interplay at the systemic and hepatic level play a central role in the pathogenesis of obesity-linked NASH and HCC.
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