Cold exposure induces cellular responses, including subcellular molecule expression and transport responses, similar to those stimulated by insulin in 3T3-L1 (L1) adipocytes. The transport response is induced in L1 adipocytes treated with translation inhibitors. We examined the level
of phospho-Thr-172 AMPK (an active form of AMPK, a known energy-state sensor) in L1 adipocytes exposed to different temperatures of 4–37°C or stressors, including chemical inhibitors and activators. The phospho-AMPK level increased in cold-exposed cells and their subcellular fractions
and decreased after rewarming and serum depletion. The phospho-molecule was also induced by anisomycin, which induces protein kinase activation and translation inhibition; mithramycin A, an inhibitor of transcription factor binding; and ionic compounds, which stimulate molecular signaling
and alter several gene expression. These results indicate that temperature responses are mimicked by metabolic stressors through phospho-molecule alteration. Our results provide possible clues for clarifying the mechanisms underlying cold responses in L1 adipocytes.
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AMP-ACTIVATED PROTEIN KINASE;
Document Type: Research Article
May 1, 2010
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CryoLetters is a bimonthly international journal for low temperature sciences, including cryobiology, cryopreservation or vitrification of cells and tissues, chemical and physical aspects of freezing and drying, and studies involving ecology of cold environments, and cold adaptation
The journal publishes original research reports, authoritative reviews, technical developments and commissioned book reviews of studies of the effects produced by low temperatures on a wide variety of scientific and technical processes, or those involving low temperature techniques in the investigation of physical, chemical, biological and ecological problems.