Obesity, body fat distribution and breast cancer

Lovegrove, Julie A.

doi:10.1079/nrr200245

Cited by 15 publications

(15 citation statements)

References 138 publications

(227 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…There are several plausible biological mechanisms why body fat distribution might be a predictor of breast cancer risk. The first mechanism is that central obesity is associated with hyperinsulinaemia and insulin resistance [41,42]. A meta-analysis showed that type II diabetes is associated with increased risk of breast cancer [43], supporting this theory.…”

Section: Discussionmentioning

confidence: 99%

“…Another proposed mechnasim is that body fat distribution is related to hormone levels. Visceral adiposity is associated with decreased sex hormone binding globulin (SHBG) and thus unbound, bioavailable oestrogen and testosterone levels may be increased in women with central obesity [41,44–46]. The third proposed mechanism is that obesity affects breast cancer risk through inflammation and aromatase axis.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Body fat distribution and breast cancer risk: findings from the Nigerian breast cancer study

Ogundiran

Huo

Adenipekun

et al. 2012

Cancer Causes Control

View full text Add to dashboard Cite

Purpose The relationship between overall obesity and breast cancer risk has been well recognized, but the role of central obesity in breast cancer development is uncertain. Methods Between 1998 and 2009, 1233 invasive breast cancer cases and 1101 community controls were recruited into the Nigerian Breast Cancer Study at Ibadan, Nigeria. Logistic regressions were used to calculate multivariate odds ratio (OR) and 95% confidence intervals (CI), adjusting for age, body mass index (BMI), and other known risk factors for breast cancer. Results The OR for the highest quartile group of waist circumference relative to the lowest was 2.39 (95% CI: 1.59–3.60; P-trend<0.001). Comparing women with waist-hip ratio (WHR) in the lowest quartile group, the OR for women in the highest quartile category was 2.15 (95% CI: 1.61–2.85; P-trend<0.001). An inverse association was observed between hip circumference and breast cancer, with an OR of 0.36 for the highest quartile (95% CI: 0.24–0.55; P-trend<0.001). The effects of these three measures existed in both pre- and post-menopausal women. Of note, we found a significant interaction between WHR and BMI (P-interaction=0.016): the OR comparing the highest to lowest WHR quartile was 2.81 (95% CI: 1.90–4.16) for women with BMI<25 kg/m2 and 1.70 (95% CI: 1.11–2.61) for women with BMI ≥25 kg/m2. Conclusions These results suggest that central adiposity, measured by waist circumference and waist-hip ratio, was an important risk factor for breast cancer in Nigerian women, and the effect of central adiposity was strong in normal weight women.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Body fat distribution and breast cancer risk: findings from the Nigerian breast cancer study

Ogundiran

Huo

Adenipekun

et al. 2012

Cancer Causes Control

View full text Add to dashboard Cite

show abstract

“…It is difficult to compare results of these studies with each other and with ours because in some cases mice were homozygous for the neu gene or it was not indicated whether they were homozygous or heterozygous for neu. Serum factors, including estrogen, insulin, and/or IGF-I levels, are considered to be mediators of obesity's effect on postmenopausal breast cancer risk (36). One of our goals is to develop animal models to identify mechanisms to explain the body weight/breast cancer relationship.…”

Section: Discussionmentioning

confidence: 99%

Diet-Induced Obesity and Mammary Tumor Development in MMTV-neu Female Mice

Cleary

Grande

Juneja

et al. 2004

Nutrition and Cancer

View full text Add to dashboard Cite

Obesity is a risk factor for postmenopausal breast cancer and is associated with shortened latency and/or increased mammary tumor (MT) incidence in animals. Elevated body weight is usually associated with hormone-responsive tumors. In agreement with these data we previously showed that latency of hormone-responsive MTs in MMTV-TGF-alpha mice with diet-induced obesity was significantly shortened. Here, we used the same protocol to determine the impact of diet-induced obesity on estrogen receptor-negative MT development in MMTV-neu (strain 202) mice. Mice were fed a low-fat diet (n=20) or a high-fat diet (n=54) from 10 wk of age. Body weight at 19 wk of age was used to assign high-fat mice to obesity-prone, overweight, and obesity-resistant groups. Mice were euthanized due to MT size or at 85 wk of age. Final body weights of obesity-prone mice were heaviest, and those of obesity-resistant and low-fat groups were similar. Fat pad weights were heaviest in obesity-prone mice followed by overweight and obesity-resistant groups, and lightest in low-fat mice. Serum IGF-I levels were similar for low-fat and high-fat mice, whereas leptin was higher in high-fat mice (P <0.0001). MT latency, incidence, metastasis, and burden were similar for all groups. These findings support that obesity is not a risk factor for development of estrogen-negative breast cancer.

show abstract

“…45 Recently, interest has focused on leptin as a possible growth factor for mammary tumorigenesis. Leptin receptors are expressed in human breast tumors and breast cancer cell lines and the addition of leptin increases cell proliferation.…”

Section: Discussionmentioning

confidence: 99%

Effect of high fat diet on body weight and mammary tumor latency in MMTV-TGF-α mice

2004

View full text Add to dashboard Cite

OBJECTIVE:The role of high fat diets in breast cancer/mammary tumor (MT) development is controversial. This may be partially attributable to variable effects of high fat diets on body weight. Here, we used a moderately high fat diet (32.5% fat calories) expected to cause obesity in most mice, but predicted to result in some mice remaining in the weight range of mice fed the low fat diet (11% fat calories). This provided the opportunity to compare mice fed the high fat diet exhibiting different body weights and mice of similar weight consuming high vs low fat diets. EXPERIMENTAL METHODS: Transgenic MMTV-TGF-a mice, a model of postmenopausal breast cancer, consumed a low fat diet, that is, chow-fed (n ¼ 25) or a moderately high fat diet from 10 weeks of age (n ¼ 51). Body weight at 34 weeks of age was used to assign high fat diet mice to obesity-prone4overweight4obesity-resistant groups (n ¼ 17) (Po0.0001). Mice were euthanized when MTs developed or at 85 weeks of age. RESULTS: Final body weights were highest in obesity-prone4overweight 4obesity-resistant ¼ chow-fed mice. Fat pads and fat pad:carcass were heaviest in obesity-prone followed by overweight mice. However, obesity-resistant mice had fat pad weights and fat pad:carcass three-fold greater than chow-fed mice. All groups had MT incidences between 72 and 82%. Obesity-prone mice exhibited the shortest MT latency (Po0.0001), but obesity-resistant mice had significantly shorter latency than chow-fed mice. CONCLUSIONS: Consumption of a high fat diet increased adiposity and shortened MT latency in relation to its effect on body weight. These results indicate a complex role of dietary fat level on mammary tumorigenesis.

show abstract

Obesity, body fat distribution and breast cancer

Cited by 15 publications

References 138 publications

Body fat distribution and breast cancer risk: findings from the Nigerian breast cancer study

Body fat distribution and breast cancer risk: findings from the Nigerian breast cancer study

Diet-Induced Obesity and Mammary Tumor Development in MMTV-neu Female Mice

Effect of high fat diet on body weight and mammary tumor latency in MMTV-TGF-α mice

Contact Info

Product

Resources

About