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Fat depot‐specific expression of H OX C 9 and H OX C 10 may contribute to adverse fat distribution and related metabolic traits
Author(s) -
Brune Jakob E.,
Kern Matthias,
Kunath Anne,
Flehmig Gesine,
Schön Michael R.,
Lohmann Tobias,
Dressler Miriam,
Dietrich Arne,
Fasshauer Mathias,
Kovacs Peter,
Stumvoll Michael,
Blüher Matthias,
Klöting Nora
Publication year - 2016
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1002/oby.21317
Subject(s) - adipose tissue , medicine , endocrinology , obesity , homeobox , stromal cell , stromal vascular fraction , messenger rna , biology , gene expression , gene , genetics
Objective Independent previous studies in both rodents and humans suggest a role of developmental genes in the origin of obesity and body fat distribution. Here, the hypothesis that human adipose tissue (AT) expression of the developmental genes homeobox transcription factors C9 ( HOXC9 ) and C10 ( HOXC10 ) is fat depot‐specific and related to obesity‐related traits was tested. Methods In 636 individuals, HOXC9 and HOXC10 mRNA expression was investigated in paired abdominal subcutaneous (SC) and omental AT samples in relation to a wide range of age, BMI, fat distribution, and metabolic parameters and in subfractions of isolated adipocytes and cells of the stromal vascular fraction (SVF). Results HOXC9 and HOXC10 mRNA expression is significantly higher in SC compared to omental AT. HOXC9 and HOXC10 mRNA expression significantly correlates with body fat mass, even after adjustment for age and gender. In smaller subgroups (depending on the availability of data), fat depot‐related significant gender‐ and BMI‐independent associations between HOXC9 and HOXC10 gene expression and parameters of glucose metabolism and AT biology were found (e.g., adipocyte size). Conclusions Taken together, these data suggest that HOXC9 and HOXC10 may play an important role in the development of obesity, adverse fat distribution, and subsequent alterations in whole‐body metabolism and AT function.