ONO Masafumi    Department   School of Medicine(Tokyo Women's Medical University Adachi Medical Center), School of Medicine    Position
Article types	Original article
Language	English
Peer review	Peer reviewed
Title	Lack of 17β-estradiol reduces sensitivity to insulin in the liver and muscle of male mice.
Journal	Formal name：Heliyon Abbreviation：Heliyon ISSN code：24058440/24058440
Domestic / Foregin	Foregin
Volume, Issue, Page	4(9),pp.e00772
Author and coauthor	Toda Katsumi, Toda Akiko, Ono Masafumi, Saibara Toshiji
Publication date	2018/09
Summary	The importance of estrogens for glucose homeostasis has been demonstrated by clinical, pharmacological, and experimental studies. Male mice lacking the aromatase gene (ArKO mice), which encodes an enzyme involved in estrogen synthesis, develop glucose- and insulin-intolerance. However, it remains unclear whether insulin signaling is actually impaired in the liver and muscle of ArKO mice. We examined the effects of estrogen-deficiency on insulin signaling by quantifying phosphorylation levels of protein kinase B (Akt) in the liver and muscle and by examining the expression levels of insulin-target genes in the liver. Insulin administration enhanced phosphorylation levels of Akt in the liver and muscle of wild-type (WT) mice, ArKO mice, and ArKO mice supplemented with 17β-estradiol (E2), but insulin was less effective in ArKO mice. Gene expression analysis revealed that alterations induced by insulin in WT liver were also observed in ArKO liver, but the degree of altered expression in a subset of genes was smaller in ArKO mice than in WT mice. E2 supplementation improved the insulin responses of some genes in ArKO mice. Thus, these findings suggest that insulin signaling in the liver and muscle of ArKO mice is less efficient than in WT mice, which contributes to whole-body glucose intolerance in ArKO mice.
DOI	10.1016/j.heliyon.2018.e00772
PMID	30211334