Interactions Between Food Energy Consumption Tumor Growth And Angiogenesis

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A strong positive correlation between energy intake and the incidence or growth of tumors has been reported in virtually every animal model system evaluated (6,10,40,41). Many studies have shown that an imposed restriction of total food intake or energy inhibits tumorigenesis (Fig. 1; 12). In addition, groups of mice or rats with free access to food, which is typical in most rodent studies, also show a striking positive correlation between self-selected energy intake and risk of cancer (Fig. 2; 40,42,43). Recent examination of data derived from the National Toxicology Program shows that chemicals reducing body weight, and presumably reducing self-selected energy intake, are associated with a lower cancer risk (44). Subsequent studies show that energy intake can have a profound influence upon the sensitivity of the bioassays used to identify health risks from environmental chemicals and define regulatory policy (45).

Readers of cancer therapy literature, including studies of antiangiogenic agents, must carefully evaluate the data, try to ascertain if the drug or therapeutic intervention alters food intake and body weight, and determine if energy intake has confounded the interpretation of the data. If food consumption is altered by the growth of a tumor, or changed by the anticancer treatments employed, it may be difficult to disentangle the results of the

Energy Intake (kcal/day)

  1. 1. The effects of high-fat or low-fat diets fed at controlled levels of energy intake on spontaneous mammary carcinoma in C'3H micc (12). Both dietary fat intake and energy intake exhibit significant effects on tumorigencsis.
  2. 1. The effects of high-fat or low-fat diets fed at controlled levels of energy intake on spontaneous mammary carcinoma in C'3H micc (12). Both dietary fat intake and energy intake exhibit significant effects on tumorigencsis.

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ftnergy intake ( kcitl / day )

  1. 2. The effects of self-selected energy intake on risk of developing breast cancer in female Sprague-Dawley rats previously exposed to the mammary carcinogen 7,12-dimethylbenz(a)anthracene. The frequency distribution shows the number of rats self-selecting a specific average daily energy intake. Regression analysis generated the curve illustrating the odds of exhibiting a breast tumor over the range of self-selected energy intake. The odds of having a tumor was increased by approx 10% for each 1-kcal increase in self-selected energy intake (43).
  2. It is highly desirable to monitor the effects of anticancer agents on food consumption and body weight of the experimental animals. In some cases, pair-feeding and other methods of compensating for treatment-induced differences in energy intake can be used to assist the investigator in understanding the results of studies in which food intake is a covariable of treatment.

Thus far, few studies have focused on the role of energy intake and tumor vascular biology. A recent report showed that the transplantable Englebreth-Holm-Swarm (EHS) sarcoma (46), grown in young mice fed reduced-energy intake, contained fewer blood vessels and increased matrix, compared to those fed ad libitum (47). These observations are supported by the authors' recent unpublished experiments. The authors have completed a series of studies employing total diet or energy restriction with a variety of rodent tumor models, and assessed tumor growth and its relationship to microvessel density, based on factor VIII staining. These studies show that energy or diet restriction significantly reduces microvessel density in several transplantable tumor models, including murine MB49 bladder cancer, RT2 rat glioma, Dunning R3327H rat prostate cancer, and LNCaP human prostate carcinoma grown in nude mice (48).

Since the inhibition of tumor growth by energy restriction appears to be associated with a reduction in microvessel density, one can begin to speculate on the potential mechanisms involved. The endocrine system plays a significant role in the integration of nutritional status with the coordinated function of tissues and organs in mammals. Possible mediators of changes in tumor angiogenesis during dietary restriction are several hormones and growth factors that show changes with energy balance, and have been linked to angiogenesis.

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