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The role of oestrogens in the adaptation of islets to insulin resistance
Author(s) -
Nadal Angel,
AlonsoMagdalena Paloma,
Soriano Sergi,
Ropero Ana B.,
Quesada Ivan
Publication year - 2009
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2009.177188
Subject(s) - endocrinology , medicine , insulin resistance , insulin , hormone , biology , adipose tissue , prolactin , receptor , insulin oscillation , downregulation and upregulation , biochemistry , gene
Pregnancy is characterized by peripheral insulin resistance, which is developed in parallel with a plasma increase of maternal hormones; these include prolactin, placental lactogens, progesterone and oestradiol among others. Maternal insulin resistance is counteracted by the adaptation of the islets of Langerhans to the higher insulin demand. If this adjustment is not produced, gestational diabetes may be developed. The adaptation process of islets is characterized by an increase of insulin biosynthesis, an enhanced glucose‐stimulated insulin secretion (GSIS) and an increase of β–cell mass. It is not completely understood why, in some individuals, β–cell mass and function fail to adapt to the metabolic demands of pregnancy, yet a disruption of the β–cell response to maternal hormones may play a key part. The role of the maternal hormone 17β‐oestradiol (E2) in this adaptation process has been largely unknown. However, in recent years, it has been demonstrated that E2 acts directly on β–cells to increase insulin biosynthesis and to enhance GSIS through different molecular mechanisms. E2 does not increase β–cell proliferation but it is involved in β–cell survival. Classical oestrogen receptors ERα and ERβ, as well as the G protein‐coupled oestrogen receptor (GPER) seem to be involved in these adaptation changes. In addition, as the main production of E2 in post‐menopausal women comes from the adipose tissue, E2 may act as a messenger between adipocytes and islets in obesity.