Abstract

The uptake of phosphate (Pi) into cells and its assimilation into cellular material are essential features of metabolism. In ruminants, secretion of Pi via the parotid saliva and the subsequent reabsorption in the small intestine are essential aspects of the massive recycling of Pi. Pi serves both as a buffer against the volatile fatty acids produced in the rumen by microbial fermentation, and as a nutrient for the rumen microorganisms. Dietary Pi deficiency in ruminants has been shown to lead to reduced rumen microbial protein synthesis, reduced growth rate, disturbances in reproduction and lactation, and reduced bone mineralization. Pi deficiency is the predominant mineral imbalance affecting ruminants in many parts of the world [1—3]. Ruminants consuming roughage diets such as hay, straw and grass usually excrete little Pi in the urine and are more dependent on the gut rather than the kidney for major adjustments in Pi-homeostasis. Fecal Pi is the main excretory pathway for Pi; this is derived mainly from saliva [4, 5]. This situation is in contrast to that seen in non-ruminants, as well as pre-ruminants, where the kidney is the major control site for maintenance of plasma phosphate. In ruminants fed concentrate diets, however, significant Pi is excreted by the kidneys. The reason for this is unclear, although it has been suggested that this is due to alterations in salivary flow rate. A reduction in the salivary flow rate in ruminants fed concentrate diets results in a high plasma Pi and excess Pi is excreted via the kidneys. The physical nature of the diet is shown to be the major factor influencing the salivary flow rate and hence producing a renal response [5]. This paper describes the mechanisms and properties of Pi transport systems in ovine intestine, parotid gland and kidney. The approaches towards structural identity of these transporters will be discussed. The accumulated information is to serve as a baseline for further studies to identify the structure of these transporters. Such studies will facilitate a better understanding of the molecular mechanisms which underlie the control of Pi homeostasis in ruminants.

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