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Updated: Jun 25, 2026

Measuring the Rate of Lipolysis in Ex Vivo Murine Adipose Tissue and Primary Preadipocytes Differentiated In Vitro
Published on: March 17, 2023
Involvement of Ca(2+) in globular adiponectin-induced reactive oxygen species
Sumio Akifusa1, Noriaki Kamio, Yoshihiro Shimazaki
1Department of Preventive Dentistry, Kyushu University, Higashi-ku, Fukuoka, Japan. akifusa@dent.kyushu-u.ac.jp
Abstract:
Globular adiponectin (gAd) induces the generation of reactive oxygen species (ROS) and nitric oxide (NO) in the murine macrophage cell line RAW 264. We investigated the role of Ca(2+) in gAd-induced ROS and NO generation. Pretreatment with BAPTA-AM, a selective chelator of intracellular Ca(2+) ([Ca(2+)](i)), partially reduced gAd-induced generation of ROS and NO in gAd-treated RAW 264 cells. The lowest [Ca(2+)](i) occurred 30min after gAd treatment, after which [Ca(2+)](i) increased continually and exceeded the initial level. The mitochondrial Ca(2+) ([Ca(2+)](m)) detected by Rhod-2 fluorescence started to increase at 6h after gAd treatment. Pretreatment with a NAD(P)H oxidase inhibitor, diphenyleneiodonium, prevented the reduction of [Ca(2+)](i) in the early phase after gAd treatment. Calcium depletion by BAPTA-AM had no effect on the gAd-induced [Ca(2+)](m) oscillation. The administration of a specific calmodulin inhibitor, calmidazolium, significantly suppressed gAd-induced ROS and NO generation and NOS activity.
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