Abstract
A high phosphorus (HP) diet causes disorders of renal function, bone metabolism, and vascular function. We previously demonstrated that DNA microarray analysis is an appropriate method to comprehensively evaluate the effects of a HP diet on kidney dysfunction such as calcification, fibrillization, and inflammation. We reported that type IIb sodium-dependent phosphate transporter is significantly up-regulated in this context. In the present study, we performed DNA microarray analysis to investigate the effects of a HP diet on the liver, which plays a pivotal role in energy metabolism. DNA microarray analysis was performed with total RNA isolated from the livers of rats fed a control diet (containing 0.3% phosphorus) or a HP diet (containing 1.2% phosphorus). Gene Ontology analysis of differentially expressed genes (DEGs) revealed that the HP diet induced down-regulation of genes involved in hepatic amino acid catabolism and lipogenesis, while genes related to fatty acid β-oxidation process were up-regulated. Although genes related to fatty acid biosynthesis were down-regulated in HP diet-fed rats, genes important for the elongation and desaturation reactions of omega-3 and -6 fatty acids were up-regulated. Concentrations of hepatic arachidonic acid and eicosapentaenoic acid were increased in HP diet-fed rats. These essential fatty acids activate peroxisome proliferator-activated receptor alpha (PPARα), a transcription factor for fatty acid β-oxidation. Evaluation of the upstream regulators of DEGs using Ingenuity Pathway Analysis indicated that PPARα was activated in the livers of HP diet-fed rats. Furthermore, the serum concentration of fibroblast growth factor 21, a hormone secreted from the liver that promotes fatty acid utilization in adipose tissue as a PPARα target gene, was higher (p = 0.054) in HP diet-fed rats than in control diet-fed rats. These data suggest that a HP diet enhances energy expenditure through the utilization of free fatty acids released via lipolysis of white adipose tissue.
Highlights
Phosphorus is a vital mineral in many biological processes and exists in the form of inorganic phosphates in the body
The effects of the high phosphorus (HP) diet on food intake, body weight, serum phosphorus concentration, and phosphorus balance were identical to those previously reported [13], because the animals used in the present study were the same as those used in the previous study
There were no significant differences between rats fed the HP diet and those fed the control diet in terms of the serum concentrations of lipids, total cholesterol (T-CHO), esterified cholesterol (E-CHO), triacylglycerol (TG), phospholipid (PL), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), non-esterified fatty acid (NEFA), and total ketone body (T-KB) (S2 Fig)
Summary
Phosphorus is a vital mineral in many biological processes and exists in the form of inorganic phosphates in the body. Phosphorus is abundant in many foods as natural phosphorus and phosphate-containing food additives. Dietary phosphorus intake is about 2–3-fold higher [1,2,3] than the recommended level (700 mg/d) [4]. Intake of phosphorus from phosphate additives has gradually increased over the past several decades owing to lifestyle changes [5,6,7]. Administration of a high phosphorus (HP) diet causes disorders of renal function, bone metabolism, and vascular cell function [8,9,10]. Recent reports suggest that HP diets accelerate aging [11, 12]
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