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Delaying of insulin signal transduction in skeletal muscle cells by selenium compounds.

Abstract：

:Supranutritional selenium (Se) intake and high serum Se levels have been associated epidemiologically with increased risk for type 2 diabetes, suggesting adverse effects of dietary Se compounds and/or antioxidant selenoenzymes on the sensitivity of target tissues for insulin. Here, we compared the capability of inorganic (sodium selenite and sodium selenate) and organic (selenomethionine and methylseleninic acid (MSeA)) Se compounds to interfere with insulin signaling in rat L6 myotubes, differentiated skeletal muscle cells. When applied at doses of 1 μM, only selenite and MSeA were capable of delaying insulin-induced phosphorylation of protein kinase B (Akt) and attenuating insulin-induced phosphorylation of forkhead box class O transcription factors FoxO1a and FoxO3. Insulin-stimulated glucose uptake was lowered by selenite and MSeA as well. Even though all tested Se compounds strongly stimulated expression/activity of the cellular selenoproteins glutathione peroxidase 1 and selenoprotein W, selenite and MSeA were the most efficiently utilized Se donors. Moreover, at doses of 1 μM, only selenite and MSeA had a significant inhibitory effect on generation of intracellular reactive oxygen species (ROS). These results suggest that the Se(IV) compounds selenite and MSeA may impair the insulin sensitivity of myocytes by influencing cellular redox homeostasis.

journal_name

J Inorg Biochem

journal_title

Journal of inorganic biochemistry

authors

Pinto A,Speckmann B,Heisler M,Sies H,Steinbrenner H

doi

10.1016/j.jinorgbio.2011.03.010

subject

Has Abstract

pub_date

2011-06-01 00:00:00

pages

812-20

issue

6

eissn

0162-0134

issn

1873-3344

pii

S0162-0134(11)00061-4

journal_volume

105

pub_type

杂志文章

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