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A surprising link between the energetics of ovariectomy-induced weight gain and mammary tumor progression in obese rats.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	MacLean, Paul S. Giles, Erin D. Johnson, Ginger C. McDaniel, Shauntae M. Fleming-Elder, Brooke K. Gilman, Kaite A. Andrianakos, Anna G. Jackman, Matthew R. Shroyer, Kenneth R. Schedin, Pepper J.
Description	Country affiliation: United States Author Affiliation: MacLean PS ( Center for Human Nutrition, University of Colorado Denver, Aurora, Colorado, USA. paul.maclean@ucdenver.edu)
Abstract	Obesity increases the risk for postmenopausal breast cancer. We have modeled this metabolic context using female Wistar rats that differ in their polygenic predisposition for obesity under conditions of high-fat feeding and limited physical activity. At 52 days of age, rats were injected with 1-methyl-1-nitrosourea (MNU, 50 mg/kg) and placed in an obesogenic environment. At 19 weeks of age, the rats were separated into lean, mid-weight, and obese rats, based upon their weight gained during this time. The rats were ovariectomized (OVX) at approximately 24 weeks of age and the change in tumor multiplicity and burden, weight gain, energy intake, tumor estrogen receptor (ER) status, and humoral metabolite and cytokine profiles were examined. The survival and growth of tumors increased in obese rats in response to OVX. OVX induced a high rate of weight gain during post-OVX weeks 1-3, compared to SHAM-operated controls. During this time, feed efficiency (mg gain/kcal intake) was lower in obese rats, and this reduced storage efficiency of ingested fuels predicted the OVX-induced changes in tumor multiplicity (r = -0.64, P < 0.001) and burden (r = -0.57, P < 0.001). Tumors from obese rats contained more cells that expressed ERalpha, and post-OVX plasma from rats with the lowest feed efficiency had lower interleukin (IL)-2 and IL-4 levels. Our observations suggest a novel link between obesity and mammary tumor promotion that involves impaired fuel metabolism during OVX-induced weight gain. The metabolically inflexible state of obesity and its inability to appropriately respond to the OVX-induced energy imbalance provides a plausible explanation for this relationship and the emergence of obesity's impact on breast cancer risk after menopause.
File Format	HTM / HTML
ISSN	19307381
e-ISSN	1930739X
DOI	10.1038/oby.2009.307
Journal	Obesity
Issue Number	4
Volume Number	18
Language	English
Publisher	Wiley-Blackwell
Publisher Date	2010-04-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Endocrinology Breast Neoplasms Pathology Energy Metabolism Estrogen Receptor Alpha Metabolism Estrogens Deficiency Obesity Complications Ovary Physiology Weight Gain Alkylating Agents Animals Blood Chemically Induced Dietary Fats Administration & Dosage Disease Models, Animal Disease Progression Energy Intake Interleukin-2 Interleukin-4 Menopause Methylnitrosourea Ovariectomy Rats, Wistar Sedentary Lifestyle Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Nutrition and Dietetics Endocrinology, Diabetes and Metabolism Endocrinology

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Excess weight gain accelerates 1-methyl-1-nitrosourea-induced mammary carcinogenesis in a rat model of premenopausal breast cancer.

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Scopolin Prevents Adipocyte Differentiation in 3T3-L1 Preadipocytes and Weight Gain in an Ovariectomy-Induced Obese Mouse Model

A surprising link between the energetics of ovariectomy-induced weight gain and mammary tumor progression in obese rats.

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