ArticleDiabetologia2003
Insulin down-regulates resistin mRNA through the synthesis of protein(s) that could accelerate the degradation of resistin mRNA in 3T3-L1 adipocytes.
Article in Diabetologia, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 48 citations in OpenAlex.
- High insulin and leptin increase resistin and inflammatory cytokine production from human mononuclear cells.BioMed research international · 2013Trial
- Association ofDiabetes, metabolic syndrome and obesity : targets and therapy · 2020Article
- Insulin and Insulin Receptors in Adipose Tissue Development.International journal of molecular sciences · 2019Review
- Shift work is associated with metabolic syndrome in male steel workers-the role of resistin and WBC count-related metabolic derangements.Diabetology & metabolic syndrome · 2017Article
- Association of circulating resistin with metabolic risk factors in Indian females having metabolic syndrome.Toxicology international · 2011Article
- Breast milk hormones and regulation of glucose homeostasis.International journal of pediatrics · 2011Article
- Serum adiponectin and resistin levels in patients with polycystic ovarian syndrome and their clinical implications.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2010Article
- Cord blood resistin and adiponectin in term newborns of diabetic mothers.Archives of medical science : AMS · 2010Article
- Peripheral mononuclear cell resistin mRNA expression is increased in type 2 diabetic women.Mediators of inflammation · 2008Article
- Regulation of human resistin gene expression in cell systems: an important role of stimulatory protein 1 interaction with a common promoter polymorphic site.Diabetologia · 2005Article
- Regulatory sequence responsible for insulin destabilization of cytochrome P450 2B1 (CYP2B1) mRNA.The Biochemical journal · 2005Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisResistin is a peptide secreted by adipocytes and recognized as a hormone that could link obesity to insulin resistance. This study was designed to examine the effect and mechanism(s) of insulin on resistin expression in 3T3-L1 adipocytes.
methodsDifferentiated 3T3-L1 adipocytes were stimulated with insulin and resistin mRNA expression was examined by Northern blot analysis. In some experiments, the insulin signal was blocked by several chemical inhibitors or overexpression of a dominant negative form (Deltap85) of the p85 subunit of phosphatidylinositol 3-kinase (PI 3-kinase).
resultsInsulin treatment caused a reduction of resistin mRNA in time-dependent and dose-dependent manners in 3T3-L1 adipocytes. Pre-treatment with PD98059, an inhibitor of extracellular signal-regulated kinase 1/2 (ERK1/2) pathway, or SB203580, an inhibitor of p38 mitogen-activated protein-kinase (p38 MAP-kinase) pathway, did not influence insulin-induced reduction of resistin mRNA. Inhibition of PI 3-kinase by LY294002 or Deltap85 also failed to block insulin-induced reduction of resistin mRNA. Cycloheximide, a protein synthesis inhibitor, completely blocked insulin-induced reduction of resistin mRNA. Actinomycin D, a RNA synthesis inhibitor, also blocked insulin-induced reduction of resistin mRNA, and the decreasing rate of resistin mRNA in cells treated with insulin alone was faster than that with actinomycin D. CONCLUSION/
interpretationInsulin downregulates resistin mRNA via PI 3-kinase, ERK or p38 MAP-kinase independent pathways in 3T3-L1 adipocytes. The downregulation mechanism of resistin mRNA by insulin would be an indirect event through the synthesis of novel protein(s) that could accelerate the degradation of resistin mRNA.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.