甲状旁腺激素(PTH)是一种内分泌肽，仅在甲状旁腺中存在，而甲状旁腺激素相关蛋白(PTHrP)在多种组织和器官中表达，并发挥内分泌、旁分泌和自分泌作用。PTH和PTHrP具有相似的同源性，在N-末端共享相同的13个氨基酸残基，并与相同类型1 PTH受体(PTH1R)结合，调节钙稳态。甲状旁腺功能亢进可导致PTH异常增加，而恶性肿瘤细胞可以大量产生PTHrP。除了增加骨吸收和高钙血症外，最新研究证据表明PTH和PTHrP过量可能导致蛋白-能量消耗过量、营养不良和虚弱。通过与PTH1R结合，激活白色脂肪组织中的环磷酸腺苷单磷酸(cAMP)-依赖性蛋白激酶A，PTH和PTHrP可以刺激热能基因的表达，导致脂肪组织布朗化。这种变化导致静息能量消耗的增加、肌肉和脂肪质量的减少和体重减轻。这些发现为甲状旁腺功能亢进和肌无力之间以及癌症和虚弱之间已建立的长期关联关系提供了机制链。本综述的目的是对实验研究和临床研究中关于PTH和PTHrP在蛋白-能量营养不良中的作用的新证据进行总结。© 2023作者（们）。由IMR Press出版。

Parathyroid hormone (PTH) is an endocrine peptide found exclusively in the parathyroid glands, whereas parathyroid hormone-related protein (PTHrP) is expressed in a wide range of tissues and organs and exerts endocrine, paracrine, and autocrine actions. PTH and PTHrP have a similar homology, sharing the initial 13 amino acid residues at the N-terminus and binding to the same type 1 PTH receptor (PTH1R), which regulates calcium homeostasis. An abnormal increase in PTH production can occur in primary and secondary hyperparathyroidism, whereas PTHrP can be produced in large quantities by malignant cancer cells from solid organs. In addition to increased bone resorption and hypercalcemia, recent evidence suggests that excess PTH and PTHrP can result in protein-energy wasting, malnutrition, and cachexia. Through binding to PTH1R and activation of cyclic adenosine monophosphate (cAMP)-dependent protein kinase A in white adipose tissue, PTH and PTHrP can stimulate the expression of thermogenic genes causing adipose tissue browning. This change results in an increase in resting energy expenditure, loss of muscle and fat mass, and weight loss. These findings provide a mechanistic link for the long-established relationship between hyperparathyroidism and myopathy, as well as cancer and cachexia. The purpose of this review is to provide a summary of the emerging evidence from both experimental and clinical studies on the role of PTH and PTHrP in protein-energy malnutrition.© 2023 The Author(s). Published by IMR Press.