Resistin induces insulin resistance, but does not affect glucose output in rat-derived hepatocytes
| Autor: | Jie Qiu, Hong-qi Fan, Feng Liu, Bin Wang, Tao Yang, Rong-hua Chen, Mei Guo, Nan Gu, Li Fei, Chun-Mei Zhang, Xiao-qing Pan, Xirong Guo, Min Zhang |
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| Rok vydání: | 2008 |
| Předmět: |
medicine.medical_specialty
medicine.medical_treatment Suppressor of Cytokine Signaling Proteins Cell Line Insulin Antagonists Insulin resistance Insulin receptor substrate Internal medicine medicine Animals Resistin Pharmacology (medical) SOCS3 Glycogen synthase Protein kinase B Pharmacology biology business.industry Insulin nutritional and metabolic diseases General Medicine medicine.disease Rats Insulin receptor Glucose Endocrinology Suppressor of Cytokine Signaling 3 Protein Hepatocytes Insulin Receptor Substrate Proteins biology.protein RNA Insulin Resistance business Glycogen hormones hormone substitutes and hormone antagonists Oligoribonucleotides Antisense |
| Zdroj: | Acta Pharmacologica Sinica. 29:98-104 |
| ISSN: | 1745-7254 1671-4083 |
| DOI: | 10.1111/j.1745-7254.2008.00709.x |
| Popis: | Aim: The aim of the present study was to observe the effects of resistin on insulin sensitivity and glucose output in rat-derived hepatocytes. Methods: The rat hepatoma cell line H4IIE was cultured and stimulated with resistin; supernant glucose and glycogen content were detected. The insulin receptor substrate (IRS)-1 and IRS-2, protein kinase B/Akt, glycogen synthase kinase-3b (GSK-3b), the suppressor of cytokine signaling 3 (SOCS-3) protein content, as well as the phosphorylation status were assessed by Western blotting. Specific antisense oligodeoxynucleotides directed against SOCS-3 were used to knockdown SOCS-3. Results: Resistin induced insulin resistance, but did not affect glucose output in rat hepatoma cell line H4IIE. Resistin attenuated multiple effects of insulin, including insulin-stimulated glycogen synthesis and phosphorylation of IRS, protein kinase B/Akt, as well as GSK-3b. Resistin treatment markedly induced the gene and protein expression of SOCS-3, a known inhibitor of insulin signaling. Furthermore, a specific antisense oligodeoxynucleotide directed against SOCS-3 treatment prevented resistin from antagonizing insulin action. Conclusion: The major function of resistin on liver is to induce insulin resistance. SOCS-3 induction may contribute to the resistin-mediated inhibition of insulin signaling in H4IIE hepatocytes. |
| Databáze: | OpenAIRE |
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