Maternal protein malnutrition: effects on prostate development and adult disease

Abstract

Well-controlled intrauterine development is an essential condition for many aspects of normal adult physiology and health. This process is disrupted by poor maternal nutrition status during pregnancy. Indeed, physiological adaptations occur in the fetus to ensure nutrient supply to the most vital organs at the expense of the others, leading to irreversible consequences in tissue formation and differentiation. Evidence indicates that maternal undernutrition in early life promotes changes in key hormones, such as glucocorticoids, growth hormones, insulin-like growth factors, estrogens and androgens, during fetal development. These alterations can directly or indirectly affect hormone release, hormone receptor expression/distribution, cellular function or tissue organization, and impair tissue growth, differentiation and maturation to exert profound long-term effects on the offspring. Within the male reproductive system, maternal protein malnutrition alters development, structure, and function of the gonads, testes and prostate gland. Consequently, these changes impair the reproductive capacity of the male offspring. Further, permanent alterations in the prostate gland occur at the molecular and cellular level and thereby affect the onset of late life diseases such as prostatitis, hyperplasia and even prostate cancer. This review assembles current thoughts on the concepts and mechanisms behind the developmental origins of health and disease as they relate to protein malnutrition, and highlights the effects of maternal protein malnutrition on rat prostate development and homeostasis. Such insights on developmental trajectories of adult-onset prostate disease may help provide a foundation for future studies in this field.

Gestational exposure to the great Chinese famine: early life undernutrition impact on prostatic hyperplasia in adulthood

“…Another study in rural Bangladesh showed that young adults with gestational exposure to famine have higher risk of hyperglycemic than those unexposed ( 11 ). In addition, animal studies also found that maternal protein malnutrition delayed the prostate’s ( 12 ) and epididymal’s ( 13 ) development, growth, and maturation, which suggests that a link between early life nutrition status and the development of BPH may also exist ( 14 ). We, therefore, hypothesized that malnutrition exposure in the fetal stage can also increase the risk of BPH in midlife adults.…”

Maternal Protein Restriction Alters the Expression of Proteins Related to the Structure and Functioning of the Rat Offspring Epididymis in an Age-Dependent Manner

“…Hormonal signaling changes during sensitive periods of development may alter the development of specific fetal tissues, lead to long-lasting changes in tissue sensitivity to hormones or even change hormone secretion ( Godfrey and Barker, 2000 ; Console et al, 2001 ; Peixoto-Silva et al, 2011 ; Rinaldi et al, 2018 ). Rats subjected to maternal protein restriction during intrauterine development show changes in testosterone, estradiol and aldosterone concentration that result in significant impacts on organs and functions of the genital system ( Zambrano et al, 2005 ; Colombelli et al, 2017 ; Santos et al, 2018 ; Cavariani et al, 2019 ).…”