Abstract
Gastric inhibitory polypeptide (GIP) is an incretin and directly promotes fat accumulation in adipocytes. Inhibition of GIP signaling prevents onset of obesity and increases fat oxidation in peripheral tissues under high-fat diet (HFD), but the mechanism is unknown. In the present study, we investigated the effects of inhibition of GIP signaling on adiponectin levels after 3 weeks of HFD by comparing wild-type (WT) mice and GIP receptor-deficient (Gipr-/-) mice. In HFD-fed Gipr-/- mice, fat oxidation was significantly increased and adiponectin mRNA levels in white adipose tissue and plasma adiponectin levels were significantly increased compared to those in HFD-fed WT mice. In addition, the PPARα mRNA level was increased and the ACC mRNA level was decreased in skeletal muscle of HFD-fed Gipr-/- mice compared with those in HFD-fed WT mice. These results indicate that inhibition of GIP signaling increases adiponectin levels, resulting in increased fat oxidation in peripheral tissues under HFD.
| Original language | English |
|---|---|
| Pages (from-to) | 21-25 |
| Number of pages | 5 |
| Journal | Biochemical and Biophysical Research Communications |
| Volume | 376 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - Nov 7 2008 |
| Externally published | Yes |
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All Science Journal Classification (ASJC) codes
- Biochemistry
- Biophysics
- Molecular Biology
Cite this
Inhibition of GIP signaling modulates adiponectin levels under high-fat diet in mice. / Naitoh, Rei; Miyawaki, Kazumasa; Harada, Norio; Mizunoya, Wataru; Toyoda, Kentaro; Fushiki, Tohru; Yamada, Yuichiro; Seino, Yutaka; Inagaki, Nobuya.
In: Biochemical and Biophysical Research Communications, Vol. 376, No. 1, 07.11.2008, p. 21-25.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Inhibition of GIP signaling modulates adiponectin levels under high-fat diet in mice
AU - Naitoh, Rei
AU - Miyawaki, Kazumasa
AU - Harada, Norio
AU - Mizunoya, Wataru
AU - Toyoda, Kentaro
AU - Fushiki, Tohru
AU - Yamada, Yuichiro
AU - Seino, Yutaka
AU - Inagaki, Nobuya
PY - 2008/11/7
Y1 - 2008/11/7
N2 - Gastric inhibitory polypeptide (GIP) is an incretin and directly promotes fat accumulation in adipocytes. Inhibition of GIP signaling prevents onset of obesity and increases fat oxidation in peripheral tissues under high-fat diet (HFD), but the mechanism is unknown. In the present study, we investigated the effects of inhibition of GIP signaling on adiponectin levels after 3 weeks of HFD by comparing wild-type (WT) mice and GIP receptor-deficient (Gipr-/-) mice. In HFD-fed Gipr-/- mice, fat oxidation was significantly increased and adiponectin mRNA levels in white adipose tissue and plasma adiponectin levels were significantly increased compared to those in HFD-fed WT mice. In addition, the PPARα mRNA level was increased and the ACC mRNA level was decreased in skeletal muscle of HFD-fed Gipr-/- mice compared with those in HFD-fed WT mice. These results indicate that inhibition of GIP signaling increases adiponectin levels, resulting in increased fat oxidation in peripheral tissues under HFD.
AB - Gastric inhibitory polypeptide (GIP) is an incretin and directly promotes fat accumulation in adipocytes. Inhibition of GIP signaling prevents onset of obesity and increases fat oxidation in peripheral tissues under high-fat diet (HFD), but the mechanism is unknown. In the present study, we investigated the effects of inhibition of GIP signaling on adiponectin levels after 3 weeks of HFD by comparing wild-type (WT) mice and GIP receptor-deficient (Gipr-/-) mice. In HFD-fed Gipr-/- mice, fat oxidation was significantly increased and adiponectin mRNA levels in white adipose tissue and plasma adiponectin levels were significantly increased compared to those in HFD-fed WT mice. In addition, the PPARα mRNA level was increased and the ACC mRNA level was decreased in skeletal muscle of HFD-fed Gipr-/- mice compared with those in HFD-fed WT mice. These results indicate that inhibition of GIP signaling increases adiponectin levels, resulting in increased fat oxidation in peripheral tissues under HFD.
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U2 - 10.1016/j.bbrc.2008.08.052
DO - 10.1016/j.bbrc.2008.08.052
M3 - Article
VL - 376
SP - 21
EP - 25
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
SN - 0006-291X
IS - 1
ER -