The Emerging Role of Nutritional Vitamin D in Secondary Hyperparathyroidism in CKD
In chronic kidney disease (CKD), hyperphosphatemia induces fibroblast growth factor-23 (FGF-23) expression that disturbs renal 1,25-dihydroxy vitamin D (1,25D) synthesis; thereby increasing parathyroid hormone (PTH) production. FGF-23 acts on the parathyroid gland (PTG) to increase 1α-hydroxylase ac...
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| Veröffentlicht in: | Nutrients 2018-12, Vol.10 (12), p.1890 |
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| creator | Lu, Chien-Lin Yeih, Dong-Feng Hou, Yi-Chou Jow, Guey-Mei Li, Zong-Yu Liu, Wen-Chih Zheng, Cai-Mei Lin, Yuh-Feng Shyu, Jia-Fwu Chen, Remy Huang, Chung-Yu Lu, Kuo-Cheng |
| description | In chronic kidney disease (CKD), hyperphosphatemia induces fibroblast growth factor-23 (FGF-23) expression that disturbs renal 1,25-dihydroxy vitamin D (1,25D) synthesis; thereby increasing parathyroid hormone (PTH) production. FGF-23 acts on the parathyroid gland (PTG) to increase 1α-hydroxylase activity and results in increase intra-gland 1,25D production that attenuates PTH secretion efficiently if sufficient 25D are available. Interesting, calcimimetics can further increase PTG 1α-hydroxylase activity that emphasizes the demand for nutritional vitamin D (NVD) under high PTH status. In addition, the changes in hydroxylase enzyme activity highlight the greater parathyroid 25-hydroxyvitmain D (25D) requirement in secondary hyperparathyroidism (SHPT); the higher proportion of oxyphil cells as hyperplastic parathyroid progression; lower cytosolic vitamin D binding protein (DBP) content in the oxyphil cell; and calcitriol promote vitamin D degradation are all possible reasons supports nutritional vitamin D (NVD; e.g., Cholecalciferol) supplement is crucial in SHPT. Clinically, NVD can effectively restore serum 25D concentration and prevent the further increase in PTH level. Therefore, NVD might have the benefit of alleviating the development of SHPT in early CKD and further lowering PTH in moderate to severe SHPT in dialysis patients. |
| doi_str_mv | 10.3390/nu10121890 |
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FGF-23 acts on the parathyroid gland (PTG) to increase 1α-hydroxylase activity and results in increase intra-gland 1,25D production that attenuates PTH secretion efficiently if sufficient 25D are available. Interesting, calcimimetics can further increase PTG 1α-hydroxylase activity that emphasizes the demand for nutritional vitamin D (NVD) under high PTH status. In addition, the changes in hydroxylase enzyme activity highlight the greater parathyroid 25-hydroxyvitmain D (25D) requirement in secondary hyperparathyroidism (SHPT); the higher proportion of oxyphil cells as hyperplastic parathyroid progression; lower cytosolic vitamin D binding protein (DBP) content in the oxyphil cell; and calcitriol promote vitamin D degradation are all possible reasons supports nutritional vitamin D (NVD; e.g., Cholecalciferol) supplement is crucial in SHPT. Clinically, NVD can effectively restore serum 25D concentration and prevent the further increase in PTH level. Therefore, NVD might have the benefit of alleviating the development of SHPT in early CKD and further lowering PTH in moderate to severe SHPT in dialysis patients.</description><identifier>ISSN: 2072-6643</identifier><identifier>EISSN: 2072-6643</identifier><identifier>DOI: 10.3390/nu10121890</identifier><identifier>PMID: 30513912</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>blood serum ; Calciferol ; Calcification ; Calcitriol ; cholecalciferol ; Dialysis ; Enzymatic activity ; Enzyme activity ; Enzymes ; Fibroblast growth factor 23 ; fibroblasts ; Gene expression ; Growth factors ; Hemodialysis ; Homeostasis ; Hydroxylase ; Hyperparathyroidism ; Hyperphosphatemia ; Hyperplasia ; Hypocalcemia ; Kidney diseases ; Metabolism ; Mortality ; Parathyroid ; Parathyroid gland ; Parathyroid hormone ; Pathophysiology ; patients ; Population ; Review ; secretion ; Vitamin D ; vitamin D-binding protein ; Vitamin deficiency</subject><ispartof>Nutrients, 2018-12, Vol.10 (12), p.1890</ispartof><rights>2018 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2018 by the authors. 2018</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c439t-9cf848b32b6f9a72c33db16664e5210b30feff872c0e2d574efe82b701c88a0f3</citedby><cites>FETCH-LOGICAL-c439t-9cf848b32b6f9a72c33db16664e5210b30feff872c0e2d574efe82b701c88a0f3</cites><orcidid>0000-0001-7861-5054 ; 0000-0003-0370-3951 ; 0000-0002-9452-5179</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6316278/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6316278/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30513912$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lu, Chien-Lin</creatorcontrib><creatorcontrib>Yeih, Dong-Feng</creatorcontrib><creatorcontrib>Hou, Yi-Chou</creatorcontrib><creatorcontrib>Jow, Guey-Mei</creatorcontrib><creatorcontrib>Li, Zong-Yu</creatorcontrib><creatorcontrib>Liu, Wen-Chih</creatorcontrib><creatorcontrib>Zheng, Cai-Mei</creatorcontrib><creatorcontrib>Lin, Yuh-Feng</creatorcontrib><creatorcontrib>Shyu, Jia-Fwu</creatorcontrib><creatorcontrib>Chen, Remy</creatorcontrib><creatorcontrib>Huang, Chung-Yu</creatorcontrib><creatorcontrib>Lu, Kuo-Cheng</creatorcontrib><title>The Emerging Role of Nutritional Vitamin D in Secondary Hyperparathyroidism in CKD</title><title>Nutrients</title><addtitle>Nutrients</addtitle><description>In chronic kidney disease (CKD), hyperphosphatemia induces fibroblast growth factor-23 (FGF-23) expression that disturbs renal 1,25-dihydroxy vitamin D (1,25D) synthesis; thereby increasing parathyroid hormone (PTH) production. FGF-23 acts on the parathyroid gland (PTG) to increase 1α-hydroxylase activity and results in increase intra-gland 1,25D production that attenuates PTH secretion efficiently if sufficient 25D are available. Interesting, calcimimetics can further increase PTG 1α-hydroxylase activity that emphasizes the demand for nutritional vitamin D (NVD) under high PTH status. In addition, the changes in hydroxylase enzyme activity highlight the greater parathyroid 25-hydroxyvitmain D (25D) requirement in secondary hyperparathyroidism (SHPT); the higher proportion of oxyphil cells as hyperplastic parathyroid progression; lower cytosolic vitamin D binding protein (DBP) content in the oxyphil cell; and calcitriol promote vitamin D degradation are all possible reasons supports nutritional vitamin D (NVD; e.g., Cholecalciferol) supplement is crucial in SHPT. Clinically, NVD can effectively restore serum 25D concentration and prevent the further increase in PTH level. 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thereby increasing parathyroid hormone (PTH) production. FGF-23 acts on the parathyroid gland (PTG) to increase 1α-hydroxylase activity and results in increase intra-gland 1,25D production that attenuates PTH secretion efficiently if sufficient 25D are available. Interesting, calcimimetics can further increase PTG 1α-hydroxylase activity that emphasizes the demand for nutritional vitamin D (NVD) under high PTH status. In addition, the changes in hydroxylase enzyme activity highlight the greater parathyroid 25-hydroxyvitmain D (25D) requirement in secondary hyperparathyroidism (SHPT); the higher proportion of oxyphil cells as hyperplastic parathyroid progression; lower cytosolic vitamin D binding protein (DBP) content in the oxyphil cell; and calcitriol promote vitamin D degradation are all possible reasons supports nutritional vitamin D (NVD; e.g., Cholecalciferol) supplement is crucial in SHPT. Clinically, NVD can effectively restore serum 25D concentration and prevent the further increase in PTH level. Therefore, NVD might have the benefit of alleviating the development of SHPT in early CKD and further lowering PTH in moderate to severe SHPT in dialysis patients.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>30513912</pmid><doi>10.3390/nu10121890</doi><orcidid>https://orcid.org/0000-0001-7861-5054</orcidid><orcidid>https://orcid.org/0000-0003-0370-3951</orcidid><orcidid>https://orcid.org/0000-0002-9452-5179</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | blood serum Calciferol Calcification Calcitriol cholecalciferol Dialysis Enzymatic activity Enzyme activity Enzymes Fibroblast growth factor 23 fibroblasts Gene expression Growth factors Hemodialysis Homeostasis Hydroxylase Hyperparathyroidism Hyperphosphatemia Hyperplasia Hypocalcemia Kidney diseases Metabolism Mortality Parathyroid Parathyroid gland Parathyroid hormone Pathophysiology patients Population Review secretion Vitamin D vitamin D-binding protein Vitamin deficiency |
| title | The Emerging Role of Nutritional Vitamin D in Secondary Hyperparathyroidism in CKD |
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