The lipid peroxidation end-product and oxidant 4-hydroxynonenal induces insulin resistance in rat slow-twitch skeletal muscle. (February 2014)

• Record Type: Journal Article
• Authors: Prasannarong, Mujalin; Santos, Fernando R.; Hooshmand, Payam; Hooshmand, Paria; Giovannini, Franchesca J.; Henriksen, Erik J.
• Is Part Of: Archives of physiology and biochemistry. Volume 120:Number 1(2014)
• Page Start: 22
• Page End: 28
• Publication Date: 2014-02
• Subjects: Physiology -- Periodicals; Biochemistry -- Periodicals; Biophysics -- Periodicals; Biochemistry; Physiology; 571
• DOI: 10.3109/13813455.2013.834937
• Languages: English
• ISSNs: 1381-3455

Abstract

<abstract> <title>Abstract</title> <p> <italic>Context</italic>: The lipid peroxidation end-product and oxidant 4-hydroxynonenal (4-HNE) impairs cell function. However, the impact of 4-HNE on the glucose transport system in mammalian slow-twitch skeletal muscle is not known. <italic>Objective</italic>: We assessed the effects of 4-HNE on insulin signalling and glucose transport activity in slow-twitch muscle by incubating soleus strips from lean Zucker rats with 4-HNE (50 µM) in the absence or presence of insulin (5 mU/ml) for up to 6 hr. <italic>Results</italic>: Insulin-stimulated glucose transport activity was significantly (<italic>p</italic> &lt; 0.05) decreased by 4-HNE at 2 hr. AS160 Thr⁶⁴² phosphorylation was decreased at 2 hr, whereas Akt Ser⁴⁷³ phosphorylation and IRS-1 protein expression were not substantially changed until 4 hr. IRS-2 protein expression was slightly decreased only at 6 hr. <italic>Conclusions</italic>: The lipid peroxidation end-product and oxidant 4-HNE induces insulin resistance of glucose transport activity in rat slow-twitch skeletal muscle, initially associated with impaired phosphorylation of AS160.</p> </abstract>