title: A pilot investigation of visceral fat adiposity and gene expression profile in peripheral blood cells.
abstract: 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/m(2) 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.
authors.affiliation: Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
authors.forename: Masaya
authors.initials: M
authors.lastname: Yamaoka
authors.forename: Norikazu
authors.initials: N
authors.lastname: Maeda
authors.forename: Seiji
authors.initials: S
authors.lastname: Nakamura
authors.forename: Susumu
authors.initials: S
authors.lastname: Kashine
authors.forename: Yasuhiko
authors.initials: Y
authors.lastname: Nakagawa
authors.forename: Aki
authors.initials: A
authors.lastname: Hiuge-Shimizu
authors.forename: Kohei
authors.initials: K
authors.lastname: Okita
authors.forename: Akihisa
authors.initials: A
authors.lastname: Imagawa
authors.forename: Yuji
authors.initials: Y
authors.lastname: Matsuzawa
authors.forename: Ken-ichi
authors.initials: K
authors.lastname: Matsubara
authors.forename: Tohru
authors.initials: T
authors.lastname: Funahashi
authors.forename: Iichiro
authors.initials: I
authors.lastname: Shimomura
mesh_terms: D050154:Adiposity / Q000235:genetics*; D000328:Adult; D000368:Aged; D001773:Blood Cells / Q000378:metabolism; D015992:Body Mass Index; D005260:Female; D006801:Humans; D050152:Intra-Abdominal Fat / Q000378:metabolism*; D008297:Male; D024821:Metabolic Syndrome / Q000235:genetics / Q000378:metabolism; D008875:Middle Aged; D056950:Period Circadian Proteins / Q000235:genetics; D059467:Transcriptome
chemical_list: C539022:PER1 protein, human; D056950:Period Circadian Proteins