Parathyroid glands exhibit reduced parenchymatic chief cells and increased extracellular collagen as a response to a long-term low-phosphorus diet in pigs.

猪长期低磷饮食会导致甲状旁腺实质主细胞减少和细胞外胶原蛋白增加

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作者:Oster Michael, Reyer Henry, Hadlich Frieder, Ponsuksili Siriluck, Wolf Petra, Wimmers Klaus, Keiler Jonas
Parathyroid glands (PTG) are essential in maintaining mineral homeostasis, particularly in regulating blood calcium (Ca) and phosphorus (P) levels. The endocrine regulation via parathyroid hormone (PTH) is a prerequisite for the efficient utilization of dietary P. The PTG contain lobules of PTH-producing chief cells surrounded by extracellular collagen. It is hypothesized that the areal proportions of chief cells and extracellular collagen in PTG are dependent on dietary P intake. Based on PTG gene expression patterns, a total of 18 crossbred pigs balanced for sex and litter were fed one of three long-term diets with low (n = 6), medium (n = 6), or high P levels (n = 6) from weaning at d 28 until slaughter at d 120. Total dietary P levels of low, medium, and high P groups were 5.20, 6.48 and 7.80 g/kg diet for grower, respectively, and 4.12, 5.50 and 6.96 g/kg diet for fattener, respectively. The effects of P supply were analyzed for their impact on the microscopic structure of porcine PTG using microphotographs following Azan trichrome staining verified by immunohistochemistry of PTH, calcium-sensing receptor (CaSR), collagen type I (COL1), and collagen type III (COL3) and related to gene expression data. Histological stainings of PTG showed significantly reduced areas of PTG chief cells (P < 0.001) and increased extracellular collagen (P < 0.001) in animals fed low dietary P compared to control and high P diets. The long-term adaptation to a low P diet indicates a PTG reorganization and suggests that the lobular structure, along with the extracellular matrix, may play a role in the complex processes of mineral homeostasis. Mechanistically, this could be a component of a physiologic and possibly reversible response following long-term P intake, which has implications for PTG regulation and, consequently, PTH control.

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