The integrative role of leptin, oestrogen and the insulin family in obesity-associated breast cancer: potential effects of exercise

Obes Rev. 2015 Jun;16(6):473-87. doi: 10.1111/obr.12281. Epub 2015 Apr 15.


Obesity is an established risk factor for postmenopausal breast cancer. The mechanisms through which obesity influences the development and progression of breast cancer are not fully elucidated; however, several factors such as increased oestrogen, concentrations of various members of the insulin family and inflammation that are associated with adiposity are purported to be important factors in this relationship. Emerging research has also begun to focus on the role of adipokines, (i.e. adipocyte secreted factors), in breast cancer. Leptin secretion is directly related to adiposity and is believed to promote breast cancer directly and independently, as well as through involvement with the oestrogen and insulin signalling pathways. As leptin is secreted from white adipose tissue, any intervention that reduces adiposity may be favourable. However, it is also important to consider that energy expenditure through exercise, independent of fat loss, may improve leptin regulation. The purpose of this narrative review was to explore the role of leptin in breast cancer development and progression, identify key interactions with oestrogen and the insulin family, and distinguish the potential effects of exercise on these interactions.

Keywords: Adipokines; IGF-1; body composition; energy expenditure.

Publication types

  • Review

MeSH terms

  • Adiposity
  • Animals
  • Breast Neoplasms / epidemiology
  • Breast Neoplasms / etiology
  • Breast Neoplasms / metabolism
  • Breast Neoplasms / prevention & control*
  • Energy Metabolism
  • Estrogens / blood
  • Estrogens / metabolism*
  • Exercise*
  • Female
  • Humans
  • Insulin / blood
  • Insulin / metabolism*
  • Insulin Secretion
  • Leptin / blood
  • Leptin / metabolism*
  • Models, Biological*
  • Molecular Sequence Data
  • Obesity / blood
  • Obesity / metabolism
  • Obesity / physiopathology
  • Obesity / therapy*
  • Risk Factors
  • Signal Transduction


  • Estrogens
  • Insulin
  • Leptin