Imi Yukiko, Yabiki Norie, Abuduli Maerjianghan, Masuda Masashi, Yamanaka-Okumura Hisami, Taketani Yutaka
Department of Clinical Nutrition and Food Management, Institute of Biomedical Sciences, Tokushima University Graduate School, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japan.
J Clin Biochem Nutr. 2018 Nov;63(3):181-191. doi: 10.3164/jcbn.17-141. Epub 2018 Jul 11.
Excessive phosphate intake has been positively associated with renal and vascular dysfunction, conversely negatively associated with body fat accumulation. We investigated the effect of a high-phosphate diet on the expression of lipid metabolic genes in white adipose tissue and liver. Male 8-week-old Sprague-Dawley rats were fed a control diet containing 0.6% phosphate or a high-phosphate diet containing 1.5% phosphate for 4 weeks. In comparison to the control group, the HP group showed a significantly lower body fat mass and fasting plasma insulin level alongside decreased lipogenic and increased lipolytic gene expression in visceral fat. Additionally, the expression of genes involved in hepatic lipogenesis, hepatic glycogenesis, and triglyceride accumulation decreased in the high-phosphate group. Exogenous phosphate, parathyroid hormone, and fibroblast growth factor 23 did not directly affect the expression of lipolytic or lipogenic genes in 3T3-L1 adipocytes and HepG2 hepatocytes. Thus, the high-phosphate diet suppressed the activity of white adipose tissue by increasing lipolytic gene expression and decreasing lipogenic gene expression. These effects could have been caused by the lowered fasting plasma insulin level that occurred in response to the high-phosphate diet, but were not directly caused by the increases in plasma phosphate or phosphaturic hormones.
过量的磷摄入与肾脏和血管功能障碍呈正相关，相反，与体脂积累呈负相关。我们研究了高磷饮食对白色脂肪组织和肝脏中脂质代谢基因表达的影响。将8周龄雄性斯普拉格-道利大鼠喂食含0.6%磷的对照饮食或含1.5%磷的高磷饮食4周。与对照组相比，高磷组的体脂量和空腹血浆胰岛素水平显著降低，同时内脏脂肪中脂肪生成基因表达降低，脂肪分解基因表达增加。此外，高磷组中参与肝脏脂肪生成、肝糖原生成和甘油三酯积累的基因表达下降。外源性磷、甲状旁腺激素和成纤维细胞生长因子23对3T3-L1脂肪细胞和HepG2肝细胞中脂肪分解或脂肪生成基因的表达没有直接影响。因此，高磷饮食通过增加脂肪分解基因表达和降低脂肪生成基因表达来抑制白色脂肪组织的活性。这些影响可能是由高磷饮食导致的空腹血浆胰岛素水平降低引起的，但不是由血浆磷或排磷激素的增加直接导致的。
