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.
| Original language | English |
|---|---|
| Pages (from-to) | 1-7 |
| Number of pages | 7 |
| Journal | Journal of Cell Communication and Signaling |
| DOIs | |
| Publication status | Accepted/In press - Jul 25 2017 |
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Keywords
- Adipocyte
- Enterocyte
- Glucocorticoid
- Leptin
ASJC Scopus subject areas
- Biochemistry
- Molecular Biology
- Cell Biology
Cite this
Extra-adrenal glucocorticoids contribute to the postprandial increase of circulating leptin in mice. / Tomabechi, Yuka; Tsuruta, Takeshi; Saito, Shinichi; Wabitsch, Martin; Sonoyama, Kei.
In: Journal of Cell Communication and Signaling, 25.07.2017, p. 1-7.Research output: Contribution to journal › Article
}
TY - JOUR
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
PY - 2017/7/25
Y1 - 2017/7/25
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
UR - http://www.scopus.com/inward/record.url?scp=85025830465&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85025830465&partnerID=8YFLogxK
U2 - 10.1007/s12079-017-0403-9
DO - 10.1007/s12079-017-0403-9
M3 - Article
SP - 1
EP - 7
JO - Journal of Cell Communication and Signaling
JF - Journal of Cell Communication and Signaling
SN - 1873-9601
ER -