ArticleDiabetologia2004
Direct demonstration of lipid sequestration as a mechanism by which rosiglitazone prevents fatty-acid-induced insulin resistance in the rat: comparison with metformin.
Article in Diabetologia, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
43 citing papers in PubMed, 137 citations in OpenAlex.
- Therapeutic targeting of local metabolic dysfunction in secondary lymphedema: mechanisms and opportunities.Frontiers in physiology · 2026Review
- PFKFB3 protein in adipose tissue contributes to whole body glucose homeostasis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- The Role of Acyl-CoA Synthetase 1 in Bioactive Lipid Accumulation and the Development of Hepatic Insulin Resistance.Nutrients · 2024Article
- Insulin-stimulated adipocytes secrete lactate to promote endothelial fatty acid uptake and transport.Journal of cell science · 2022Article
- PFKFB3-dependent glucose metabolism regulates 3T3-L1 adipocyte development.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Article
- Type 2 Innate Lymphoid Cells: Protectors in Type 2 Diabetes.Frontiers in immunology · 2021Review
- Anti-inflammatory mechanisms of the vascular smooth muscle PPARγ.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2021Review
- Impact of PCSK9 on CTRP9-Induced Metabolic Effects in Adult Rat Cardiomyocytes.Frontiers in physiology · 2021Article
- Cited4 is a sex-biased mediator of the antidiabetic glitazone response in adipocyte progenitors.EMBO molecular medicine · 2018Article
- Screening for PPAR Non-Agonist Ligands Followed by Characterization of a Hit, AM-879, with Additional No-Adipogenic and cdk5-Mediated Phosphorylation Inhibition Properties.Frontiers in endocrinology · 2018Article
- Re-highlighting the action of PPARγ in treating metabolic diseases.F1000Research · 2018Review
- RORα controls hepatic lipid homeostasis via negative regulation of PPARγ transcriptional network.Nature communications · 2017Article
- Stimulatory Effects of Cinnamon Extract (Cinnamomum cassia) during the Initiation Stage of 3T3-L1 Adipocyte Differentiation.Foods (Basel, Switzerland) · 2016Article
- Epigenomic and transcriptional control of insulin resistance.Journal of internal medicine · 2016Review
- Nuclear Mechanisms of Insulin Resistance.Trends in cell biology · 2016Review
- Insulin resistance as a physiological defense against metabolic stress: implications for the management of subsets of type 2 diabetes.Diabetes · 2015Review
- Revisiting PPARγ as a target for the treatment of metabolic disorders.BMB reports · 2014Review
- Thiazolidinediones and the promise of insulin sensitization in type 2 diabetes.Cell metabolism · 2014Review
- Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisThiazolidinediones can enhance clearance of whole-body non-esterified fatty acids and protect against the insulin resistance that develops during an acute lipid load. The present study used [(3)H]-R-bromopalmitate to compare the effects of the thiazolidinedione, rosiglitazone, and the biguanide, metformin, on insulin action and the tissue-specific fate of non-esterified fatty acids in rats during lipid infusion.
methodsNormal rats were treated with rosiglitazone or metformin for 7 days. Triglyceride/heparin (to elevate non-esterified fatty acids) or glycerol (control) were then infused for 5 h, with a hyperinsulinaemic clamp being performed between the 3rd and 5th hours.
resultsRosiglitazone and metformin prevented fatty-acid-induced insulin resistance (reduced clamp glucose infusion rate). Both drugs improved insulin-mediated suppression of hepatic glucose output but only rosiglitazone enhanced systemic non-esterified fatty acid clearance (plateau plasma non-esterified fatty acids reduced by 40%). Despite this decrease in plateau plasma non-esterified fatty acids, rosiglitazone increased fatty acid uptake (two-fold) into adipose tissue and reduced fatty acid uptake into liver (by 40%) and muscle (by 30%), as well as reducing liver long-chain fatty acyl CoA accumulation (by 30%). Both rosiglitazone and metformin increased liver AMP-activated protein kinase activity, a possible mediator of the protective effects on insulin action, but in contrast to rosiglitazone, metformin had no significant effect on non-esterified fatty acid kinetics or relative tissue fatty acid uptake. CONCLUSIONS/
interpretationThese results directly demonstrate the "lipid steal" mechanism, by which thiazolidinediones help prevent fatty-acid-induced insulin resistance. The contrasting mechanisms of action of rosiglitazone and metformin could be beneficial when both drugs are used in combination to treat insulin resistance.
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