Metabolic obesity, adipose inflammation and elevated breast aromatase in women with normal body mass index Academic Article uri icon


MeSH Major

  • Breast Neoplasms
  • Patient Participation
  • Practice Guidelines as Topic
  • Precision Medicine


  • Obesity is associated with breast white adipose tissue (WAT) inflammation, elevated levels of the estrogen biosynthetic enzyme, aromatase, and systemic changes that have been linked to the pathogenesis of breast cancer. Here, we determined whether metabolic obesity, including changes in breast biology and systemic effects, occurs in a subset of women with normal body mass index (BMI). Breast WAT and fasting blood were collected from 72 women with normal BMI (<25 kg/m(2)) undergoing mastectomy for breast cancer risk reduction or treatment. WAT inflammation was defined by the presence of crown-like structures of the breast (CLS-B) which are composed of dead or dying adipocytes surrounded by macrophages. Severity of inflammation was measured as CLS-B/cm(2) The primary objective was to determine whether breast WAT inflammation is associated with aromatase expression and activity. Secondary objectives included assessment of circulating factors and breast adipocyte size. Breast WAT inflammation was present in 39% of women. Median BMI was 23.0 kg/m(2) (range, 18.4-24.9 kg/m(2)) in women with breast WAT inflammation versus 21.8 kg/m(2) (range, 17.3-24.6 kg/m(2)) in those without inflammation (P = 0.04). Breast WAT inflammation was associated with elevated aromatase expression and activity, which increased with severity of inflammation (P < 0.05). Breast WAT inflammation correlated with larger adipocytes (P = 0.01) and higher circulating levels of C-reactive protein, leptin, insulin, and triglycerides (P ≤ 0.05). A subclinical inflammatory state associated with elevated aromatase in the breast, adipocyte hypertrophy, and systemic metabolic dysfunction occurs in some normal BMI women and may contribute to the pathogenesis of breast cancer. Cancer Prev Res; 10(4); 235-43. ©2017 AACRSee related article by Berger, p. 223-25.

publication date

  • April 2017



  • Academic Article



  • eng

PubMed Central ID

  • PMC5380584

Digital Object Identifier (DOI)

  • 10.1158/1940-6207.CAPR-16-0314

PubMed ID

  • 28270386

Additional Document Info

start page

  • 235

end page

  • 243


  • 10


  • 4