1. Introduction
Body growth depends on the transport of a variety of nutrients between tissues and their subsequent retention inside cells. In mammals, maternal nutrient transfer via the placenta and umbilical cord in the fetus controls fetal growth, whereas the supply from mothers to nursing babies via milk, regulates infant growth [1]. The importance of milk as a major nutrient source to infants is well established; however, the effect of milk consumption on growth is still under debate.
Milk contains highly concentrated nutrients including proteins and minerals such as calcium, potassium, and phosphorus [2]. Milk also contains regulators of body growth by stimulating secretion of endocrine hormones in infants [3]. In addition, dietary consumption of cow's milk increases blood concentration of insulin-like growth factor 1 (IGF-1), an important factor in body growth during development [4].
Phosphate is the second most abundant mineral nutrient in the mammalian body, and the regulation of phosphate metabolism has both clinical and biological significance [5], [6] and [7]. Phosphate imbalance can lead to a wide range of disorders; for example, excessive phosphorus intake causes hypocalcemia and hyperphosphatemia. However, the effect of dietary insufficiency is unclear. We recently reported that dietary phosphorus insufficiency affected the ability of milk to promote infant growth in mice, particularly causing bony malformation [8]. Because the crucial role of milk in infant growth is still controversial, mother mice fed a low-phosphorus diet (LPD) appears to be a good model for analyzing the milk function. Here, we explored the molecular mechanism underlying infant growth via milk in mice.