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In a randomized trial in prostate cancer patients, dietary protein restriction modifies markers of leptin and insulin signaling in plasma extracellular vesicles.
Eitan, E, Tosti, V, Suire, CN, Cava, E, Berkowitz, S, Bertozzi, B, Raefsky, SM, Veronese, N, Spangler, R, Spelta, F, et al
Aging cell. 2017;16(6):1430-1433
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Plain language summary
Obesity and insulin resistance are associated with accelerated aging and increased risk of many age-related diseases. The risk of many cancers, including prostate cancer, increases with age and being overweight further increases the risk. The aim of the study is to investigate the inhibition of tumour growth through the effect of protein restriction diets and hence, levels of circulating amino acids. The participants of the study were men (n=38) with prostate cancer awaiting prostatectomy surgery. Most of the subjects were overweight with a BMI of 30.45 ± 5.8. They were randomly assigned to either a control diet or a protein restricted diet. In comparison to the control diet, results show that protein restriction increased the levels of receptors (a protein molecule that receives chemical signals from outside a cell) responsible of leptin, the hormone that controls hunger. The results also show that protein restriction can improve the body’s sensitivity to the effects of the insulin in neurons (a nerve cell specialised to transmit information throughout the body). Authors conclude that protein restriction can counteract major age-related diseases.
Abstract
Obesity, metabolic syndrome, and hyperleptinemia are associated with aging and age-associated diseases including prostate cancer. One experimental approach to inhibit tumor growth is to reduce dietary protein intake and hence levels of circulating amino acids. Dietary protein restriction (PR) increases insulin sensitivity and suppresses prostate cancer cell tumor growth in animal models, providing a rationale for clinical trials. We sought to demonstrate that biomarkers derived from plasma extracellular vesicles (EVs) reflect systemic leptin and insulin signaling and respond to dietary interventions. We studied plasma samples from men with prostate cancer awaiting prostatectomy who participated in a randomized trial of one month of PR or control diet. We found increased levels of leptin receptor in the PR group in total plasma EVs and in a subpopulation of plasma EVs expressing the neuronal marker L1CAM. Protein restriction also shifted the phosphorylation status of the insulin receptor signal transducer protein IRS1 in L1CAM+ EVs in a manner suggestive of improved insulin sensitivity. Dietary PR modifies indicators of leptin and insulin signaling in circulating EVs. These findings are consistent with improved insulin and leptin sensitivity in response to PR and open a new window for following physiologic responses to dietary interventions in humans.
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Magnesium and anabolic hormones in older men.
Maggio, M, Ceda, GP, Lauretani, F, Cattabiani, C, Avantaggiato, E, Morganti, S, Ablondi, F, Bandinelli, S, Dominguez, LJ, Barbagallo, M, et al
International journal of andrology. 2011;34(6 Pt 2):e594-600
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Abstract
Optimal nutritional and hormonal statuses are determinants of successful ageing. The age associated decline in anabolic hormones such as testosterone and insulin-like growth factor 1 (IGF-1) is a strong predictor of metabolic syndrome, diabetes and mortality in older men. Studies have shown that magnesium intake affects the secretion of total IGF-1 and increase testosterone bioactivity. This observation suggests that magnesium can be a modulator of the anabolic/catabolic equilibrium disrupted in the elderly people. However, the relationship between magnesium and anabolic hormones in men has not been investigated. We evaluated 399 ≥65-year-old men of CHIANTI in a study population representative of two municipalities of Tuscany (Italy) with complete data on testosterone, total IGF-1, sex hormone binding globulin (SHBG), dehydroepiandrosterone sulphate (DHEAS) and serum magnesium levels. Linear regression models were used to test the relationship between magnesium and testosterone and IGF-1. Mean age of the population was 74.18 ± 6.43 (years ± SD, age range 65.2-92.4). After adjusting for age, magnesium was positively associated with total testosterone (β ± SE, 34.9 ± 10.3; p = 0.001) and with total IGF-1 (β ± SE, 15.9 ± 4.8; p = 0.001). After further adjustment for body mass index (BMI), log (IL-6), log (DHEAS), log (SHBG), log (insulin), total IGF-1, grip strength, Parkinson's disease and chronic heart failure, the relationship between magnesium and total testosterone remained strong and highly significant (β ± SE, 48.72 ± 12.61; p = 0.001). In the multivariate analysis adjusted for age, BMI, log (IL-6), liver function, energy intake, log (insulin), log (DHEAS), selenium, magnesium levels were also still significantly associated with IGF-1 (β ± SE, 16.43 ± 4.90; p = 0.001) and remained significant after adjusting for total testosterone (β ± SE, 14.4 ± 4.9; p = 0.01). In a cohort of older men, magnesium levels are strongly and independently associated with the anabolic hormones testosterone and IGF-1.