A pilot investigation of visceral fat adiposity and gene expression profile in peripheral blood cells.
A pilot investigation of visceral fat adiposity and gene expression profile in peripheral blood cells.
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DOI:
10.1371/journal.pone.0047377
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发表时间:
2012
期刊:
影响因子:
3.7
通讯作者:
Shimomura I
中科院分区:
文献类型:
--
作者:
Yamaoka M;Maeda N;Nakamura S;Kashine S;Nakagawa Y;Hiuge-Shimizu A;Okita K;Imagawa A;Matsuzawa Y;Matsubara K;Funahashi T;Shimomura I
Evidence suggests that visceral fat accumulation plays a central role in the development of metabolic syndrome. Excess visceral fat causes local chronic low-grade inflammation and dysregulation of adipocytokines, which contribute in the pathogenesis of the metabolic syndrome. These changes may affect the gene expression in peripheral blood cells. This study for the first time examined the association between visceral fat adiposity and gene expression profile in peripheral blood cells. The gene expression profile was analyzed in peripheral blood cells from 28 obese subjects by microarray analysis. Reverse transcription-polymerase chain reaction (RT-PCR) was performed using peripheral blood cells from 57 obese subjects. Obesity was defined as body mass index (BMI) greater than 25 kg/m2 according to the Japanese criteria, and the estimated visceral fat area (eVFA) was measured by abdominal bioelectrical impedance. Analysis of gene expression profile was carried out with Agilent whole human genome 4×44 K oligo-DNA microarray. The expression of several genes related to circadian rhythm, inflammation, and oxidative stress correlated significantly with visceral fat accumulation. Period homolog 1 (PER1) mRNA level in blood cells correlated negatively with visceral fat adiposity. Stepwise multiple regression analysis identified eVFA as a significant determinant of PER1 expression. In conclusion, visceral fat adiposity correlated with the expression of genes related to circadian rhythm and inflammation in peripheral blood cells.
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DOI:
10.1126/science.1195027
发表时间:
2010-12-03
期刊:
Science (New York, N.Y.)
影响因子:
--
作者:
Bass J;Takahashi JS
通讯作者:
Takahashi JS
影响因子:
2.8
作者:
Dallmann R;Weaver DR
通讯作者:
Weaver DR
影响因子:
3.3
作者:
Matsuzawa, Y;Nakamura, T;Nagai, M
通讯作者:
Nagai, M
影响因子:
56.9
作者:
Turek, FW;Joshu, C;Bass, J
通讯作者:
Bass, J
DOI:
10.1016/j.bbrc.2007.01.063
发表时间:
2007-03-23
影响因子:
3.1
作者:
Fukuya, Hiroyuki;Emoto, Noriaki;Yokoyama, Mitsuhiro
通讯作者:
Yokoyama, Mitsuhiro