Increased expression of the adipokine genes resistin and fasting-induced adipose factor in hypoxic/ischaemic mouse brain

被引:41
作者
Wiesner, Glen
Brown, Russell E.
Robertson, George S.
Imran, Syed A.
Ur, Ehud
Wilkinson, Michael
机构
[1] Dalhousie Univ, Dept Obstet & Gynaecol, IWK Hlth Ctr, Fac Med, Halifax, NS B3K 6R8, Canada
[2] Dalhousie Univ, Dept Psychiat, Fac Med, Halifax, NS B3K 6R8, Canada
[3] Dalhousie Univ, Dept Pharmacol, Fac Med, Halifax, NS B3K 6R8, Canada
[4] Dalhousie Univ, Dept Physiol & Biophys, Fac Med, Halifax, NS B3K 6R8, Canada
[5] Dalhousie Univ, Div Endocrinol & Metab, Fac Med, Halifax, NS B3K 6R8, Canada
[6] Baker Med Res Inst, Human Neurotransmitter Lab, Melbourne, Vic, Australia
关键词
fasting-induced adipose factor; hypoxia; ischaemia; lipopolysaccharide; resistin;
D O I
10.1097/01.wnr.0000224776.12647.ba
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Adipose tissue is the primary source of the adipokines resistin and fasting-induced adipose factor (FIAF). We reported that the brain is also a site of adipokine expression, although their function there is unknown. Peripheral resistin and fasting-induced adipose factor are reported to be inflammatory markers, and we hypothesized that they would be induced in the brain by hypoxia/ischaemia. We show that neonatal hypoxia/ischaemia rapidly increased flaf mRNA in the injured cortex and hippocampus at 2 and 7 days after hypoxia/ischaemia. In contrast, resistin (retn) mRNA was increased in the cortex only at 21 days after hypoxia/ischaemia. As a lipopolysaccharide-induced inflammatory response did not increase brain fiaf and retn mRNA levels, we conclude that brain injury may be responsible for the novel hypoxia/ischaemia-induced changes in adipokine gene expression. In summary, our results indicate that brain injury, or an inflammatory stimulus, regulates the central expression of two genes normally considered to be adipose tissue-specific. These observations add to our previous evidence that the brain is an important site of adipokine gene expression.
引用
收藏
页码:1195 / 1198
页数:4
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