ArticlePPAR research2013
The PPAR α / γ Agonist, Tesaglitazar, Improves Insulin Mediated Switching of Tissue Glucose and Free Fatty Acid Utilization In Vivo in the Obese Zucker Rat.
Article in PPAR research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Peroxisome proliferator-activated receptors as targets to treat metabolic diseases: Focus on the adipose tissue, liver, and pancreas.World journal of gastroenterology · 2023Review
- Review
- Involvement of circulating factors in the transmission of paternal experiences through the germline.The EMBO journal · 2020Article
- The Glitazars Paradox: Cardiotoxicity of the Metabolically Beneficial Dual PPARα and PPARγ Activation.Journal of cardiovascular pharmacology · 2020Review
- PPARγ and PPARα synergize to induce robust browning of white fat in vivo.Molecular metabolism · 2020Article
- NPYMolecular metabolism · 2020Article
- Dual peroxisome-proliferator-activated-receptor-α/γ activation inhibits SIRT1-PGC1α axis and causes cardiac dysfunction.JCI insight · 2019Article
- Effects of Dual Peroxisome Proliferator-Activated ReceptorsPPAR research · 2019Article
- Metabolic Flexibility as an Adaptation to Energy Resources and Requirements in Health and Disease.Endocrine reviews · 2018Review
- Article
- Nicotinic acid timed to feeding reverses tissue lipid accumulation and improves glucose control in obese Zucker rats[S].Journal of lipid research · 2017Article
- Activation of β3-adrenoceptors increases in vivo free fatty acid uptake and utilization in brown but not white fat depots in high-fat-fed rats.American journal of physiology. Endocrinology and metabolism · 2016Article
- Dosing profile profoundly influences nicotinic acid's ability to improve metabolic control in rats.Journal of lipid research · 2015Article
- Peroxisome proliferator-activated receptors α and γ are linked with alcohol consumption in mice and withdrawal and dependence in humans.Alcoholism, clinical and experimental research · 2015Article
- Pharmacological PPARα activation markedly alters plasma turnover of the amino acids glycine, serine and arginine in the rat.PloS one · 2014Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
metabolic flexibility was assessed in male zucker ratslean controls, obese controls, and obese rats treated with the dual peroxisome proliferator activated receptor (PPAR) α/γ agonist, tesaglitazar, 3 μ mol/kg/day for 3 weeks. Whole body glucose disposal rate (R d ) and hepatic glucose output (HGO) were assessed under basal fasting and hyperinsulinemic isoglycemic clamp conditions using [3,(3)H]glucose. Indices of tissue specific glucose utilization (R g ') were measured at basal, physiological, and supraphysiological levels of insulinemia using 2-deoxy-D-[2,6-(3)H]glucose. Finally, whole body and tissue specific FFA and glucose utilization and metabolic fate were evaluated under basal and hyperinsulinemic conditions using a combination of [U-(13)C]glucose, 2-deoxy-D-[U-(14)C]glucose, [U-(14)C]palmitate, and [9,10-(3)H]-(R)-bromopalmitate. Tesaglitazar improved whole body insulin action by greater suppression of HGO and stimulation of R d compared to obese controls. This involved increased insulin stimulation of R g ' in fat and skeletal muscle as well as increased glycogen synthesis. Tesaglitazar dramatically improved insulin mediated suppression of plasma FFA level, whole body turnover (R fa ), and muscle, liver, and fat utilization. At basal insulin levels, tesaglitazar failed to lower HGO or R fa compared to obese controls. In conclusion, the results demonstrate that tesaglitazar has a remarkable ability to improve insulin mediated control of glucose and FFA fluxes in obese Zucker rats.
Identifiers
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Registered trials
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