2016年5月10日(火)に筑波大学「ヒューマンバイオロジー学位プログラム」が主催となり，World Science Leader’s Seminarを開催いたします。
World Science Leader’s Seminarは，サイエンスの世界で活躍されている方々にお越しいただき，トップレベルの知識と技術をご指導いただく貴重な機会です。
今回の講演者はDr. Jingbo Pi (Professor, School of Public Health, China Medical University, Shenyang, China)です。
どなたでも参加可能ですので，ふるってご参加ください。尚，本セミナーは英語で行われます。
■開催日時：2016年５月10日(火) 16:45 -17:45
■会 場 ：健康医科学イノベーション棟105
アクセス：
筑波大学筑波キャンパスへは「筑波キャンパスへの交通アクセス」をご覧ください。
利用停留所（関東鉄道バス）：筑波大学中央行き又は筑波大学循環バス「追越学生宿舎前」
■ゲストスピーカー：Dr. Jingbo Pi (Professor, School of Public Health, China Medical University, Shenyang, China)
■セミナータイトル：Involvement of CNC-bZIP protein NRF1 in arsenic¬induced impairments in adipogenesis and adipose function
■主催：筑波大学 ヒューマンバイオロジー学位プログラム
■セミナー概要：
Environmental arsenic exposure is a worldwide public health problem. Chronic exposure to high levels of inorganic arsenic (iAs) is associated with many human ailments including cancer, skin disorders, vascular diseases and type 2 diabetes (T2D). White adipose tissue (WAT) is an active organ that stores and releases energy, maintains glucose homeostasis, and secretes a variety of factors that influence appetite, insulin sensitivity, and inflammation. Disturbance of adipogenesis and WAT function is associated with insulin resistance, which plays an early pathogenic role in the development of T2D. iAs and its trivalent methylated metabolites inhibit adipogenesis and impair WAT function. However, the underlying mechanism remains elusive. In the present study we found that iAs, during the early stage of adipogenesis, significantly induces the protein expression of the long isoforms of Nuclear factor E2-related factor 1 (L-NRF1), a primary transcription factor regulating adaptive antioxidant response and proteasome homeostasis. Moreover, L-NRF1 negatively regulates the expression of PPARγ, a regulator of terminal adipogenic differentiation and adipose function. In contrast, short isoforms of NRF1 (S-NRF1) derived from alternative splicing and/or posttranslational modification play fundamental roles in promoting adipogenesis. Phenotypic analysis of fat-specific Nrf1-knockout mice showed that S-NRF1 are essential in the development of WAT. It appears that iAs-induced L-NRF1 disturbs the normal function of S-NRF1 leading to the effects of arsenic on adipogenesis and insulin sensitivity. Our studies highlight the importance of NRF1 in WAT and provide insight into the effects of iAs exposure on WAT development and function and on the mechanism(s) of iAs-induced T2D.
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