Insulin-Like Growth Factor I (IGF-I) and IGF Binding Protein-1 Modulate Prostate Cancer Cell Growth and Apoptosis: Possible Mediators for the Effects of Diet and Exercise on Cancer Cell Survival

Epidemiological studies suggest a positive association between nutrient intake, hyperinsulinemia and risk of Benign prostatic hyperplasis (BPH). This study tests the hypothesis that a low-fat, highfiber diet and daily exercise would lower serum insulin and reduce the growth of serum-stimulated primary prostate epithelial cells in culture. Serum samples were obtained from eight overweight men before and after the Pritikin residential, 2-week diet and exercise intervention and from seven men who were long-term followers of the low-fat, high-fiber diet and regular exercise lifestyle. The serum was used to stimulate primary prostate epithelial cells in culture. Growth was measured after 48 and 96 h and apoptosis after 96 h. At 48 h there was no significant difference in growth within the Pre, 2-week or Long-Term groups. At 96 h growth was significantly reduced in the 2-week (13%) and in the Long-Term (14%) groups compared to the Pre data. At 96 h, apoptosis was not significantly different among the three groups. Fasting insulin was reduced by 30% in the 2-week group and by 52% in the Long-Term group compared to the Pre data. Testosterone was unchanged in the 2-week group. The results of this study indicate that a low-fat, high-fiber diet and daily exercise lowers insulin and reduces growth of prostate primary epithelial cells and suggests that lifestyle may be an important factor in the development or progression of BPH. Future prospective trials should address the effects of this lifestyle modification on BPH symptomatology and progression.

Section: Discussionmentioning

confidence: 70%

Section: Discussionmentioning

confidence: 81%

Effect of diet and exercise intervention on the growth of prostate epithelial cells

Barnard

Kobayashi

Aronson

2008

“…Specifically, aerobic exercise lowers serum levels of several metabolic and sex steroid hormones hypothesized to stimulate PC, including insulin-like growth factor-1 (IGF-1), fasting insulin, leptin and testosterone. [59][60][61][62][63] Chronic exercise is a potent stimulator of endogenous antioxidant protection pathways. [64][65][66][67] Exercise may also improve innate immune function and surveillance.…”

Section: Proposed Molecular Mechanismsmentioning

confidence: 99%

“…61,62 Furthermore, serum from men who exercised reduced the growth rate and induced apoptosis in LNCaP cells in vitro significantly more than serum from a control group of men who did not exercise. 59,61,62 In addition to modulation through metabolic pathways, there are other molecular avenues, such as antioxidants and immune function, through which exercise could possibly exert an effect on PC biology. Specifically, chronic exercise has been shown to modify endogenous antioxidant protection pathways by decreasing lipid peroxidation and reducing reactive oxygen species (ROS).…”

Section: Proposed Molecular Mechanismsmentioning

confidence: 99%

Exercise therapy across the prostate cancer continuum

Antonelli

Freedland

Jones

2009

Exercise has been increasingly investigated as an adjunct therapy for cancer patients. The purpose of this paper is to comprehensively review the literature regarding exercise as a therapeutic adjunct for prostate cancer (PC). Several studies in patients with PC have shown quality of life improvements associated with exercise. Although no study has established the effect of exercise as a monotherapy for PC, the molecular mechanisms responsible for the potential association between exercise and PC are being elucidated. Given the low-risk, high-reward nature of these studies, further investigations are needed to better define the function of exercise along the PC continuum.

“…35 In addition, dietary fat reduction may impact serum insulin-like growth factor levels in the serum. 36 Certainly, a more thorough understanding of the possible association between dietary fat and prostate cancer risk requires further inquiry.…”

Section: Dietary Fatmentioning

confidence: 99%

Impact of diet on prostate cancer: a review

Sonn

Aronson

Litwin

2005

134

Epidemiological studies suggest that environmental factors may mediate the transformation of latent prostate cancer into clinically apparent tumors and that diet appears to influence this progression. Close correlations between average per capita fat intake and prostate cancer mortality internationally generated interest in underlying mechanisms for this link, such as through serum levels of androgens, free radicals, proinflammatory fatty acid metabolites, or insulin-like growth factor. Much interest currently lies in the potential of HMG-CoA reductase inhibitors (statins) to play a chemopreventative role in prostate cancer. Lycopene, a potent antioxidant found in tomatoes, may exert a protective effect in the prostate. Selenium and vitamin E have also been shown to decrease the risk of prostate cancer in some men. Calcium may support vitamin D-related antiproliferative effects in prostate cancer. Certain soy proteins, common in the Asian diet, have been shown to inhibit prostate cancer cell growth. Finally, green tea may also have a chemopreventive effect by inducing apoptosis. Despite confounding factors present in clinical studies assessing the effect of diet on cancer risk, the data remain compelling that a variety of nutrients may prevent the development and progression of prostate cancer.