Sulforaphane induced adipolysis via hormone sensitive lipase activation, regulated by AMPK signaling pathway

► Sulforaphane activated the hormone sensitive lipase (HSL). ► The AMPK signaling was regulated by sulforaphane. ► Sulforaphane activated HSL activity via inactivation of AMPK signaling. ► Sulforaphane stimulated lipolysis by regulating AMPK signaling in differentiated adipocytes. Sulforaphane, an a...

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Published in:Biochemical and biophysical research communications 2012-10, Vol.426 (4), p.492-497
Main Authors: Lee, Ju-Hee, Moon, Myung-Hee, Jeong, Jae-Kyo, Park, Yang-Gyu, Lee, You-Jin, Seol, Jae-Won, Park, Sang-Youel
Format: Article
Language:English
Subjects:
3T3-L1 Cells
Adipocytes - drug effects
Adipocytes - metabolism
Adipogenesis - drug effects
Adipolysis
AMP-Activated Protein Kinases - metabolism
AMPK
Animals
Anti-Obesity Agents - pharmacology
HSL
Isothiocyanates
Lipolysis - drug effects
Mice
Phosphorylation
Serine - metabolism
Signal Transduction - drug effects
Sterol Esterase - biosynthesis
Sulforaphane
Thiocyanates - pharmacology
Threonine - metabolism
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Summary:► Sulforaphane activated the hormone sensitive lipase (HSL). ► The AMPK signaling was regulated by sulforaphane. ► Sulforaphane activated HSL activity via inactivation of AMPK signaling. ► Sulforaphane stimulated lipolysis by regulating AMPK signaling in differentiated adipocytes. Sulforaphane, an aliphatic isothiocyanate derived from cruciferous vegetables, is known for its antidiabetic properties. The effects of sulforaphane on lipid metabolism in adipocytes are not clearly understood. Here, we investigated whether sulforaphane stimulates lipolysis. Mature adipocytes were incubated with sulforaphane for 24h and analyzed using a lipolysis assay which quantified glycerol released into the medium. We investigated gene expression of hormone-sensitive lipase (HSL), and levels of HSL phosphorylation and AMP-activated protein kinase on sulforaphane-mediated lipolysis in adipocytes. Sulforaphane promoted lipolysis and increased both HSL gene expression and HSL activation. Sulforaphane suppressed AMPK phosphorylation at Thr-172 in a dose-dependent manner, which was associated with a decrease in HSL phosphorylation at Ser-565, enhancing the phosphorylation of HSL Ser-563. Taken together, these results suggest that sulforaphane promotes lipolysis via hormone sensitive lipase activation mediated by decreasing AMPK signal activation in adipocytes.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2012.08.107