ArticleDiabetologia2011
Osteopontin deficiency protects against obesity-induced hepatic steatosis and attenuates glucose production in mice.
Article in Diabetologia, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 101 citations in OpenAlex.
- Combinatorial targeting of the miR-379/miR-410 cluster normalizes glucose and lipid homeostasis in male models of diabetes and obesity.Nature communications · 2026Article
- The liver-bone axis: an emerging player in disease pathogenesis and therapeutic intervention.Science China. Life sciences · 2026Review
- Osteokines in Nonalcoholic Fatty Liver Disease.Current obesity reports · 2024Review
- Osteopontin: an indispensable component in common liver, pancreatic, and biliary related disease.Journal of cancer research and clinical oncology · 2024Review
- Ursolic acid: A promising therapeutic agent for metabolic dysfunction-associated steatotic liver disease via inhibition of SPP1-induced Th17 cell differentiation: Editorial on "Ursolic acid targets secreted phosphoprotein 1 to regulate Th17 cells against metabolic dysfunction-associated steatotic liver disease".Clinical and molecular hepatology · 2024Article
- Emerging role of liver-bone axis in osteoporosis.Journal of orthopaedic translation · 2024Review
- Amphiregulin from regulatory T cells promotes liver fibrosis and insulin resistance in non-alcoholic steatohepatitis.Immunity · 2024Article
- Patients who received sleeve gastrectomy have lower plasma osteopontin levels than those who did not.Clinics (Sao Paulo, Brazil) · 2024Article
- Article
- Extracellular matrix remodelling in obesity and metabolic disorders.Life metabolism · 2023Article
- New insight of obesity-associated NAFLD: Dysregulated "crosstalk" between multi-organ and the liver?Genes & diseases · 2023Review
- Osteopontin Promotes Macrophage M1 Polarization by Activation of the JAK1/STAT1/HMGB1 Signaling Pathway in Nonalcoholic Fatty Liver Disease.Journal of clinical and translational hepatology · 2023Article
- Lactoferrin, Osteopontin and Lactoferrin-Osteopontin Complex: A Critical Look on Their Role in Perinatal Period and Cardiometabolic Disorders.Nutrients · 2023Review
- Causal effects of non-alcoholic fatty liver disease on osteoporosis: a Mendelian randomization study.Frontiers in endocrinology · 2023Article
- Characteristic gene expression in the liver monocyte-macrophage-DC system is associated with the progression of fibrosis in NASH.Frontiers in immunology · 2023Article
- Osteopontin Exacerbates High-Fat Diet-Induced Metabolic Disorders in a Microbiome-Dependent Manner.mBio · 2022Article
- Article
- MyD88 in hepatic stellate cells promotes the development of alcoholic fatty liver via the AKT pathway.Journal of molecular medicine (Berlin, Germany) · 2022Article
- The Novel-miR-659/Animals : an open access journal from MDPI · 2022Article
- Adipose tissue macrophages in remote modulation of hepatic glucose production.Frontiers in immunology · 2022Review
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Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
Abstract
aims/hypothesisObesity is strongly associated with the development of non-alcoholic fatty liver disease (NAFLD). The cytokine osteopontin (OPN) was recently shown to be involved in obesity-induced adipose tissue inflammation and reduced insulin response. Accumulating evidence links OPN to the pathogenesis of NAFLD. Here we aimed to identify the role of OPN in obesity-associated hepatic steatosis and impaired hepatic glucose metabolism.
methodsWild-type (WT) and Opn (also known as Spp1) knockout (Opn (-/-)) mice were fed a high-fat or low-fat diet to study OPN effects in obesity-driven hepatic alterations.
resultsWe show that genetic OPN deficiency protected from obesity-induced hepatic steatosis, at least in part, by downregulating hepatic triacylglycerol synthesis. Conversely, absence of OPN promoted fat storage in adipose tissue thereby preventing the obesity-induced shift to ectopic fat accumulation in the liver. Euglycaemic-hyperinsulinaemic clamp studies revealed that insulin resistance and excess hepatic glucose production in obesity were significantly attenuated in Opn (-/-) mice. OPN deficiency markedly improved hepatic insulin signalling as shown by enhanced insulin receptor substrate-2 phosphorylation and prevented upregulation of the major hepatic transcription factor Forkhead box O1 and its gluconeogenic target genes. In addition, obesity-driven hepatic inflammation and macrophage accumulation was blocked by OPN deficiency. CONCLUSIONS/
interpretationOur data strongly emphasise OPN as mediator of obesity-associated hepatic alterations including steatosis, inflammation, insulin resistance and excess gluconeogenesis. Targeting OPN action could therefore provide a novel therapeutic strategy to prevent obesity-related complications such as NAFLD and type 2 diabetes.
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