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The Small Polyphenolic Molecule Kaempferol Increases Cellular Energy Expenditure and Thyroid Hormone Activation

安普克 生物化学 化学 内分泌学 内科学 脱碘酶 生物 细胞生物学 蛋白激酶A 激素 激酶 三碘甲状腺素 医学
作者
Wagner Seixas da‐Silva,John W. Harney,Brian W. Kim,Jing Li,Suzy D.C. Bianco,Alessandra Crescenzi,Marcelo A. Christoffolete,Stephen A. Huang,Antônio C. Bianco
出处
期刊:Diabetes [American Diabetes Association]
卷期号:56 (3): 767-776 被引量:141
标识
DOI:10.2337/db06-1488
摘要

Disturbances in energy homeostasis can result in obesity and other metabolic diseases. Here we report a metabolic pathway present in normal human skeletal muscle myoblasts that is activated by the small polyphenolic molecule kaempferol (KPF). Treatment with KPF leads to an ∼30% increase in skeletal myocyte oxygen consumption. The mechanism involves a several-fold increase in cyclic AMP (cAMP) generation and protein kinase A activation, and the effect of KPF can be mimicked via treatment with dibutyryl cAMP. Microarray and real-time PCR studies identified a set of metabolically relevant genes influenced by KPF including peroxisome proliferator–activated receptor γ coactivator-1α, carnitine palmitoyl transferase-1, mitochondrial transcription factor 1, citrate synthase, and uncoupling protein-3, although KPF itself is not a direct mitochondrial uncoupler. The cAMP-responsive gene for type 2 iodothyronine deiodinase (D2), an intracellular enzyme that activates thyroid hormone (T3) for the nucleus, is approximately threefold upregulated by KPF; furthermore, the activity half-life for D2 is dramatically and selectively increased as well. The net effect is an ∼10-fold stimulation of D2 activity as measured in cell sonicates, with a concurrent increase of ∼2.6-fold in the rate of T3 production, which persists even 24 h after KPF has been removed from the system. The effects of KPF on D2 are independent of sirtuin activation and only weakly reproduced by other small polyphenolic molecules such as quercetin and fisetin. These data document a novel mechanism by which a xenobiotic-activated pathway can regulate metabolically important genes as well as thyroid hormone activation and thus may influence metabolic control in humans.
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