ArticleScientific reports2016
Acute knockdown of the insulin receptor or its substrates Irs1 and 2 in 3T3-L1 adipocytes suppresses adiponectin production.
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 12 papers.
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Who cites it
12 citing papers in PubMed, 31 citations in OpenAlex.
- Epigenetic and transcriptional control of adipocyte function by centenarian-associated SIRT6 N308K/A313S mutant.Clinical epigenetics · 2024Article
- Defective Visceral Adipose Tissue Adaptation in Gestational Diabetes Mellitus.The Journal of clinical endocrinology and metabolism · 2024Article
- Exploring the multifaceted role of obesity in breast cancer progression.Frontiers in cell and developmental biology · 2024Review
- Adiponectin Resistance in Obesity: Adiponectin Leptin/Insulin Interaction.Advances in experimental medicine and biology · 2024Review
- miR-33a Inhibits the Differentiation of Bovine Preadipocytes through the IRS2-Akt Pathway.Genes · 2023Article
- Smooth Muscle Insulin Receptor Deletion Causes Voiding Dysfunction: A Mechanism for Diabetic Bladder Dysfunction.Diabetes · 2022Article
- 3,3',4,5'-Tetramethoxy-trans-stilbene Improves Insulin Resistance by Activating the IRS/PI3K/Akt Pathway and Inhibiting Oxidative Stress.Current issues in molecular biology · 2022Article
- Comparison of transcriptome between high- and low-marbling fineness in longissimus thoracis muscle of Korean cattle.Animal bioscience · 2022Article
- Zyflamend, a unique herbal blend, induces cell death and inhibits adipogenesis through the coordinated regulation of PKA and JNK.Adipocyte · 2020Article
- Integrative genomics reveal a role for MCPIP1 in adipogenesis and adipocyte metabolism.Cellular and molecular life sciences : CMLS · 2020Article
- Multifaceted Physiological Roles of Adiponectin in Inflammation and Diseases.International journal of molecular sciences · 2020Review
- SGBS cells as a model of human adipocyte browning: A comprehensive comparative study with primary human white subcutaneous adipocytes.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Loss of function of the insulin receptor (INSR) in humans produces severe insulin resistance. Unlike "common" insulin resistance, this is associated with elevated plasma levels of the insulin-sensitising, adipose-derived protein adiponectin. The underlying mechanism for this paradox is unclear, and it is at odds with the acute stimulation of adiponectin secretion reported on insulin treatment of cultured adipocytes. Given recent evidence for ligand-independent actions of the INSR, we used a lentiviral system to knock down Insr or its substrates Irs1 and Irs2 conditionally in 3T3-L1 murine preadipocytes/adipocytes to assess whether acute loss of their expression has different consequences to withdrawal of insulin. Efficient knockdown of either Insr or Irs1/2 was achieved by conditional shRNA expression, severely attenuating insulin-stimulated AKT phosphorylation and glucose uptake. Dual knockdown of Irs1 and Irs2 but not Insr in preadipocytes impaired differentiation to adipocytes. Acute knockdown of Insr or both Irs1 and Irs2 in adipocytes increased Adipoq mRNA expression but reduced adiponectin secretion, assessed by immunoassay. Knockdown sustained for 14 days also reduced immunoassay-detected adiponectin secretion, and moreover induced delipidation of the cells. These findings argue against a distinct effect of Insr deficiency to promote adiponectin secretion as the explanation for paradoxical insulin receptoropathy-related hyperadiponectinaemia.
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