title: Triiodothyronine induces UCP-1 expression and mitochondrial biogenesis in human adipocytes.
abstract: Uncoupling protein (UCP)-1 expressed in brown adipose tissue plays an important role in thermogenesis. Recent data suggest that brown-like adipocytes in white adipose tissue (WAT) and skeletal muscle play a crucial role in the regulation of body weight. Understanding of the mechanism underlying the increase in UCP-1 expression level in these organs should, therefore, provide an approach to managing obesity. The thyroid hormone (TH) has profound effects on mitochondrial biogenesis and promotes the mRNA expression of UCP in skeletal muscle and brown adipose tissue. However, the action of TH on the induction of brown-like adipocytes in WAT has not been elucidated. Thus we investigate whether TH could regulate UCP-1 expression in WAT using multipotent cells isolated from human adipose tissue. In this study, triiodothyronine (T(3)) treatment induced UCP-1 expression and mitochondrial biogenesis, accompanied by the induction of the CCAAT/enhancer binding protein, peroxisome proliferator-activated receptor-γ coactivator-1α, and nuclear respiratory factor-1 in differentiated human multipotent adipose-derived stem cells. The effects of T(3) on UCP-1 induction were dependent on TH receptor-β. Moreover, T(3) treatment increased oxygen consumption rate. These findings indicate that T(3) is an active modulator, which induces energy utilization in white adipocytes through the regulation of UCP-1 expression and mitochondrial biogenesis. Our findings provide evidence that T(3) serves as a bipotential mediator of mitochondrial biogenesis.
authors.affiliation: Laboratory of Molecular Function of Food, Division of Food Science and Biotechnology, Graduate School of Agriculture, Kyoto University, Japan.
authors.forename: Joo-Young
authors.initials: JY
authors.lastname: Lee
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Takahashi
authors.forename: Midori
authors.initials: M
authors.lastname: Yasubuchi
authors.forename: Young-Il
authors.initials: YI
authors.lastname: Kim
authors.forename: Hikari
authors.initials: H
authors.lastname: Hashizaki
authors.forename: Min-Ji
authors.initials: MJ
authors.lastname: Kim
authors.forename: Tomoya
authors.initials: T
authors.lastname: Sakamoto
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Goto
authors.forename: Teruo
authors.initials: T
authors.lastname: Kawada
mesh_terms: D017667:Adipocytes / Q000166:cytology* / Q000187:drug effects* / Q000378:metabolism*; D002001:Adipose Tissue, Brown / Q000166:cytology / Q000378:metabolism; D052436:Adipose Tissue, White / Q000166:cytology / Q000378:metabolism; D000818:Animals; D002454:Cell Differentiation / Q000187:drug effects; D005227:Fatty Acids / Q000378:metabolism; D006801:Humans; D007473:Ion Channels / Q000235:genetics / Q000378:metabolism*; D008928:Mitochondria / Q000235:genetics / Q000378:metabolism*; D024101:Mitochondrial Proteins / Q000235:genetics / Q000378:metabolism*; D039902:Multipotent Stem Cells / Q000166:cytology / Q000187:drug effects / Q000502:physiology; D010084:Oxidation-Reduction; D010101:Oxygen Consumption / Q000187:drug effects; D034741:RNA, Small Interfering / Q000235:genetics / Q000378:metabolism; D022722:Thermogenesis / Q000502:physiology; D037042:Thyroid Hormone Receptors beta / Q000235:genetics / Q000378:metabolism; D014284:Triiodothyronine / Q000494:pharmacology*; D000071256:Uncoupling Protein 1
chemical_list: D005227:Fatty Acids; D007473:Ion Channels; D024101:Mitochondrial Proteins; D034741:RNA, Small Interfering; D037042:Thyroid Hormone Receptors beta; C000604371:UCP1 protein, human; D000071256:Uncoupling Protein 1; D014284:Triiodothyronine