Extra-adrenal glucocorticoids contribute to the postprandial increase of circulating leptin in mice
Yuka Tomabechi, Takeshi Tsuruta, Shinichi Saito, Martin Wabitsch, Kei Sonoyama
Graduate School of Environmental and Life Science
Academic Field of Environmental and Life Science
Leptin, an adipokine secreted by white adipocytes, is known for its function in regulating food intake and energy expenditure, but the mechanisms regulating its circulating levels is not fully understood. Our previous findings suggest that as yet unidentified humoral factors released from enterocytes are involved. The present study tested glucocorticoids (GCs) as candidate factors. Supplementation of corticosterone and cortisol promoted leptin production in murine adipocytes from the 3T3-L1 cell strain and human adipocytes from the Simpson Golabi–Behmel syndrome (SGBS) cell strain, respectively. These changes were observed in the absence but not presence of the GC-receptor antagonist mifepristone. The cortisol concentration in conditioned medium (CM) of human enterocyte-like Caco-2 cells was increased by phorbol-12-myristate 13-acetate and decreased by metyrapone. When SGBS adipocytes were cultured in these CMs, leptin production was positively associated with cortisol concentrations. During a 2-h refeeding after fasting, plasma leptin levels continued to increase in sham-operated mice, transiently increased at 60 min in adrenalectomized mice, and were unchanged in mifepristone-administered mice. These results suggest that extra-adrenal GCs contribute to the GC-receptor signaling-dependent increase of postprandial circulating leptin, whereas further studies will be required to determine whether enterocytes participate in the GCs-mediated increase of postprandial circulating leptin.
Journal of Cell Communication and Signaling
Adipocyte
Enterocyte
Glucocorticoid
Dive into the research topics of 'Extra-adrenal glucocorticoids contribute to the postprandial increase of circulating leptin in mice'. Together they form a unique fingerprint.
Leptin Chemical Compounds 100%
Glucocorticoid Chemical Compounds 75%
Glucocorticoids Medicine & Life Sciences 53%
Cortisol Chemical Compounds 37%
Enterocytes Medicine & Life Sciences 34%
Simpson-Golabi-Behmel syndrome Medicine & Life Sciences 34%
Adipocytes Medicine & Life Sciences 27%
Hydrocortisone Medicine & Life Sciences 25%
Tomabechi, Y., Tsuruta, T., Saito, S., Wabitsch, M., & Sonoyama, K. (2018). Extra-adrenal glucocorticoids contribute to the postprandial increase of circulating leptin in mice. Journal of Cell Communication and Signaling, 12(2), 433-439. https://doi.org/10.1007/s12079-017-0403-9
Extra-adrenal glucocorticoids contribute to the postprandial increase of circulating leptin in mice. / Tomabechi, Yuka; Tsuruta, Takeshi; Saito, Shinichi et al.
In: Journal of Cell Communication and Signaling, Vol. 12, No. 2, 01.06.2018, p. 433-439.
Tomabechi, Y, Tsuruta, T, Saito, S, Wabitsch, M & Sonoyama, K 2018, 'Extra-adrenal glucocorticoids contribute to the postprandial increase of circulating leptin in mice', Journal of Cell Communication and Signaling, vol. 12, no. 2, pp. 433-439. https://doi.org/10.1007/s12079-017-0403-9
Tomabechi Y, Tsuruta T, Saito S, Wabitsch M, Sonoyama K. Extra-adrenal glucocorticoids contribute to the postprandial increase of circulating leptin in mice. Journal of Cell Communication and Signaling. 2018 Jun 1;12(2):433-439. doi: 10.1007/s12079-017-0403-9
Tomabechi, Yuka ; Tsuruta, Takeshi ; Saito, Shinichi et al. / Extra-adrenal glucocorticoids contribute to the postprandial increase of circulating leptin in mice. In: Journal of Cell Communication and Signaling. 2018 ; Vol. 12, No. 2. pp. 433-439.
@article{8d90be342df1491b9b3c536b16f0d0fe,
title = "Extra-adrenal glucocorticoids contribute to the postprandial increase of circulating leptin in mice",
abstract = "Leptin, an adipokine secreted by white adipocytes, is known for its function in regulating food intake and energy expenditure, but the mechanisms regulating its circulating levels is not fully understood. Our previous findings suggest that as yet unidentified humoral factors released from enterocytes are involved. The present study tested glucocorticoids (GCs) as candidate factors. Supplementation of corticosterone and cortisol promoted leptin production in murine adipocytes from the 3T3-L1 cell strain and human adipocytes from the Simpson Golabi–Behmel syndrome (SGBS) cell strain, respectively. These changes were observed in the absence but not presence of the GC-receptor antagonist mifepristone. The cortisol concentration in conditioned medium (CM) of human enterocyte-like Caco-2 cells was increased by phorbol-12-myristate 13-acetate and decreased by metyrapone. When SGBS adipocytes were cultured in these CMs, leptin production was positively associated with cortisol concentrations. During a 2-h refeeding after fasting, plasma leptin levels continued to increase in sham-operated mice, transiently increased at 60 min in adrenalectomized mice, and were unchanged in mifepristone-administered mice. These results suggest that extra-adrenal GCs contribute to the GC-receptor signaling-dependent increase of postprandial circulating leptin, whereas further studies will be required to determine whether enterocytes participate in the GCs-mediated increase of postprandial circulating leptin.",
keywords = "Adipocyte, Enterocyte, Glucocorticoid, Leptin",
author = "Yuka Tomabechi and Takeshi Tsuruta and Shinichi Saito and Martin Wabitsch and Kei Sonoyama",
note = "Funding Information: Acknowledgments This study was supported in part by the Regional Innovation Strategy Support Program of the MEXT, and by the Center of Innovation Program Trial, Japan Science and Technology Agency. Publisher Copyright: {\textcopyright} 2017, The International CCN Society.",
journal = "Journal of Cell Communication and Signaling",
publisher = "Springer Netherlands",
T1 - Extra-adrenal glucocorticoids contribute to the postprandial increase of circulating leptin in mice
AU - Tomabechi, Yuka
AU - Tsuruta, Takeshi
AU - Saito, Shinichi
AU - Wabitsch, Martin
AU - Sonoyama, Kei
N1 - Funding Information: Acknowledgments This study was supported in part by the Regional Innovation Strategy Support Program of the MEXT, and by the Center of Innovation Program Trial, Japan Science and Technology Agency. Publisher Copyright: © 2017, The International CCN Society.
N2 - Leptin, an adipokine secreted by white adipocytes, is known for its function in regulating food intake and energy expenditure, but the mechanisms regulating its circulating levels is not fully understood. Our previous findings suggest that as yet unidentified humoral factors released from enterocytes are involved. The present study tested glucocorticoids (GCs) as candidate factors. Supplementation of corticosterone and cortisol promoted leptin production in murine adipocytes from the 3T3-L1 cell strain and human adipocytes from the Simpson Golabi–Behmel syndrome (SGBS) cell strain, respectively. These changes were observed in the absence but not presence of the GC-receptor antagonist mifepristone. The cortisol concentration in conditioned medium (CM) of human enterocyte-like Caco-2 cells was increased by phorbol-12-myristate 13-acetate and decreased by metyrapone. When SGBS adipocytes were cultured in these CMs, leptin production was positively associated with cortisol concentrations. During a 2-h refeeding after fasting, plasma leptin levels continued to increase in sham-operated mice, transiently increased at 60 min in adrenalectomized mice, and were unchanged in mifepristone-administered mice. These results suggest that extra-adrenal GCs contribute to the GC-receptor signaling-dependent increase of postprandial circulating leptin, whereas further studies will be required to determine whether enterocytes participate in the GCs-mediated increase of postprandial circulating leptin.
AB - Leptin, an adipokine secreted by white adipocytes, is known for its function in regulating food intake and energy expenditure, but the mechanisms regulating its circulating levels is not fully understood. Our previous findings suggest that as yet unidentified humoral factors released from enterocytes are involved. The present study tested glucocorticoids (GCs) as candidate factors. Supplementation of corticosterone and cortisol promoted leptin production in murine adipocytes from the 3T3-L1 cell strain and human adipocytes from the Simpson Golabi–Behmel syndrome (SGBS) cell strain, respectively. These changes were observed in the absence but not presence of the GC-receptor antagonist mifepristone. The cortisol concentration in conditioned medium (CM) of human enterocyte-like Caco-2 cells was increased by phorbol-12-myristate 13-acetate and decreased by metyrapone. When SGBS adipocytes were cultured in these CMs, leptin production was positively associated with cortisol concentrations. During a 2-h refeeding after fasting, plasma leptin levels continued to increase in sham-operated mice, transiently increased at 60 min in adrenalectomized mice, and were unchanged in mifepristone-administered mice. These results suggest that extra-adrenal GCs contribute to the GC-receptor signaling-dependent increase of postprandial circulating leptin, whereas further studies will be required to determine whether enterocytes participate in the GCs-mediated increase of postprandial circulating leptin.
KW - Adipocyte
KW - Enterocyte
KW - Glucocorticoid
KW - Leptin
JO - Journal of Cell Communication and Signaling
JF - Journal of Cell Communication and Signaling