Abstract
The consumption of cow’s milk is a part of the basic nutritional habits of Western industrialized countries. Recent epidemiological studies associate the intake of cow’s milk with an increased risk of diseases, which are associated with overactivated mechanistic target of rapamycin complex 1 (mTORC1) signaling. This review presents current epidemiological and translational evidence linking milk consumption to the regulation of mTORC1, the master-switch for eukaryotic cell growth. Epidemiological studies confirm a correlation between cow’s milk consumption and birthweight, body mass index, onset of menarche, linear growth during childhood, acne vulgaris, type 2 diabetes mellitus, prostate cancer, breast cancer, hepatocellular carcinoma, diffuse large B-cell lymphoma, neurodegenerative diseases, and all-cause mortality. Thus, long-term persistent consumption of cow’s milk increases the risk of mTORC1-driven diseases of civilization. Milk is a highly conserved, lactation genome-controlled signaling system that functions as a maternal-neonatal relay for optimized species-specific activation of mTORC1, the nexus for regulation of eukaryotic cell growth, and control of autophagy. A deeper understanding of milk´s impact on mTORC1 signaling is of critical importance for the prevention of common diseases of civilization.
Highlights
The health-related effects of cow milk consumption by humans has been the focus of recent epidemiological research [1,2]
Milk provides a variety of macronutrients that relay the appropriate, species-specific activation of mechanistic target of rapamycin complex 1 (mTORC1) [7]: (1) amino acids that induce growth factor signals (GH; insulin, IGF-1); (2) a well-balanced array of amino acids that communicate with amino acids sensors that activate mTORC1; (3) milk lipids, especially palmitic acid, which activates mTORC1; and (4) lactose and its hydrolysis products glucose and galactose that provide cellular energy and promote mTORC1 activation
As mammals rely on milk for the promotion of postnatal growth, the effectors provided by the lactation genome on the donor site and the milk sensors of the milk recipient have to interact in a synergistic fashion to fulfill milks biological function: the activation of mTORC1, the primary cell-autonomous nutrient sensor for growth and maturation in mammals [131]
Summary
The health-related effects of cow milk consumption by humans has been the focus of recent epidemiological research [1,2]. There is accumulating evidence that milk, the secretory product of mammary glands promoting growth and anabolism of newborn mammals, is not a simple food, but a signaling system activating the nutrient- and growth factor-sensitive kinase mechanistic target of rapamycin complex 1 (mTORC1) [6,7]. Recent evidence has suggested that microbial fermentation of milk attenuates milk-mediated mTORC1 signaling, extensively reviewed elsewhere [9]. It is the intention of this review to present epidemiological and translational evidence that links milk consumption to mTORC1-driven pathologies and diseases of civilization. Milks effects on mTORC1 signaling beginning from fetal growth, childhood, puberty, adolescence, and senescence will be presented
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