Regulation of Calcium Metabolism

1976 ◽  
Vol 13 (1-6) ◽  
pp. 518-539 ◽  
Author(s):  
R. G. G. Russell
Keyword(s):  
Growth Hormone ◽  
Calcium Metabolism ◽  
Gonadal Steroids ◽  
Renal Handling ◽  
Renal Metabolism ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
Clinical Disorders ◽  
The Relationship

This paper reviews the regulation of calcium metabolism in man. The body's calcium economy is determined by the relationship between the intestinal absorption of calcium, the renal handling of calcium, and by the movements of calcium in and out of the skeleton. These processes are influenced by many factors, the most important of which are parathyroid hormone and the hormones derived from the renal metabolism of vitamin D, notably 1,25-dihydroxyvitamin D8. The role of endogenous calcitonin in man is still controversial, but there are several other hormones which have some influence on calcium metabolism, including thyroid hormone, growth hormone, and the adrenal and gonadal steroids. Clinical disorders of calcium metabolism and their treatment are discussed in terms of the disturbances in normal physiology they represent.

The role of cyadox and recombinant growth hormone (rGH) on the promotion of growth through epigenetics

2020 ◽  
Author(s):  
Aimei Liu ◽  
Feng Zhu ◽  
Xiaohui Zhu ◽  
Yulian Wang ◽  
Awais Ihsan ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Chromatin Structure ◽  
Dna Methyltransferases ◽  
Promoter Regions ◽  
Recombinant Growth Hormone ◽  
Animal Growth ◽  
Growth Promoting ◽  
The Relationship ◽  
Accessible Chromatin

Abstract Background: Cyadox is an effective growth-promoting antibiotic, which is similar to the role of recombinant growth hormone (rGH). Current studies have shown that cyadox can promote animal growth through altering intestinal microflora, improving protein utilization and increasing protein synthesis. Increasing evidence suggests that epigenetics are also closely related to growth. However, the potential role of epigenetics in the cyadox for growth has not been explored. Results: Here, we used recombinant growth hormone (rGH) and cyadox to study the relationship between growth and changes in epigenetics including DNA methylation, histone modification and chromatin structure. Bisulfite DNA sequencing (BSP) assay suggested that cyadox and rGH treatments increased IGF-1 expression partially by hypomethylation at CpG sites within the promoter region of IGF-1, which was regulated by DNA methyltransferases (DNMTs). We also observed an enrichment of H3K4me3 and H3K27ac at the promoter regions of IGF-1 by ChIP-qPCR assay, which contributed to an increase in IGF-1 transcription. In addition, immunofluorometric assay displayed cellular accessible chromatin structure following the treatment of cyadox and rGH, facilitating the combination of transcription factors and DNA and thus enhancing gene transcription. Conclusions: Taken together, our findings indicated that cyadox and rGH promote cell growth partially through epigenetic changes, providing a prospect for the development of animal growth-promoting drugs in the future.

scholarly journals Mechanistic study of the cause of decreased blood 1,25-Dihydroxyvitamin D in sepsis

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Chih-Huang Li ◽  
Xiaolei Tang ◽  
Samiksha Wasnik ◽  
Xiaohua Wang ◽  
Jintao Zhang ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Vitamin D ◽  
Growth Factor ◽  
Kidney Failure ◽  
Mechanistic Study ◽  
Blood Levels ◽  
Biological Functions ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
Fgf 23

Abstract Background Vitamin D deficiency, determined by blood levels of 25-hydroxyvitamin D [25(OH) D, i.e. the major vitamin D form in blood], has been shown to associate with all-cause mortalities. We recently demonstrated that blood levels of 1,25-dihydroxyvitamin D [1,25(OH)2D, i.e. the active vitamin D] were significantly lower in non-survivors compared to survivors among sepsis patients. Unexpectedly, despite the well documented roles of 1,25(OH)2D in multiple biological functions such as regulation of immune responses, stimulation of antimicrobials, and maintenance of barrier function, 1,25(OH)2D supplementation failed to improve disease outcomes. These previous findings suggest that, in addition to 1,25(OH)2D deficiency, disorders leading to the 1,25(OH)2D deficiency also contribute to mortality among sepsis patients. Therefore, this study investigated the mechanisms leading to sepsis-associated 1,25(OH)2D deficiency. Methods We studied mechanisms known to regulate kidney 25-hydroxylvitamin D 1α-hydroxylase which physiologically catalyzes the conversion of 25(OH) D into 1,25(OH)2D. Such mechanisms included parathyroid hormone (PTH), insulin-like growth factor 1 (IGF-1), fibroblast growth factor 23 (FGF-23), and kidney function. Results We demonstrated in both human subjects and mice that sepsis-associated 1,25(OH)2D deficiency could not be overcome by increased production of PTH which stimulates 1α-hydroxylase. Further studies showed that this failure of PTH to maintain blood 1,25(OH)2D levels was associated with decreased blood levels of IGF-1, increased blood levels of FGF-23, and kidney failure. Since the increase in blood levels of FGF-23 is known to associate with kidney failure, we further investigated the mechanisms leading to sepsis-induced decrease in blood levels of IGF-1. Our data showed that blood levels of growth hormone, which stimulates IGF-1 production in liver, were increased but could not overcome the IGF-1 deficiency. Additionally, we found that the inability of growth hormone to restore the IGF-1 deficiency was associated with suppressed expression and signaling of growth hormone receptor in liver. Conclusions Because FGF-23 and IGF-1 have multiple biological functions besides their role in regulating kidney 1α-hydroxylase, our data suggest that FGF-23 and IGF-1 are warranted for further investigation as potential agents for the correction of 1,25(OH)2D deficiency and for the improvement of survival among sepsis patients.

scholarly journals The Role of 1,25-Dihydroxyvitamin D in the Inhibition of Bone Formation Induced by Skeletal Unloading*

Endocrinology ◽  
1986 ◽  
Vol 118 (3) ◽  
pp. 948-954 ◽  
Author(s):  
BERNARD P. HALLORAN ◽  
DANIEL D. BIKLE ◽  
THOMAS J. WRONSKI ◽  
RUTH K. GLOBUS ◽  
MARILYN J. LEVENS ◽  
...  
Keyword(s):  
Bone Formation ◽  
Skeletal Unloading ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D

Role of Insulin in the Increase in Serum 1,25- Dihydroxyvitamin D Concentrations in Response Phosphorus Deprivation in Streptozotocin-Induced Diabetic Rats

Endocrinology ◽  
1986 ◽  
Vol 118 (4) ◽  
pp. 1440-1444 ◽  
Author(s):  
TOSHIO MATSUMOTO ◽  
YUMIKO KAWANOBE ◽  
IKUKO EZAWA ◽  
NAOHIKO SHIBUYA ◽  
KEISHI HATA ◽  
...  
Keyword(s):  
Diabetic Rats ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
Phosphorus Deprivation

THE ROLE OF VITAMIN D IN THE PATHOGENESIS OF THE ARTERIAL HYPERTENSION

2020 ◽  
Vol 65 (1) ◽  
pp. 5-10
Author(s):  
N. L. Lystsova ◽  
Tatiana Ivanovna Petelina ◽  
L. I. Gapon ◽  
K. S. Avdeeva ◽  
S. G. Bucova ◽  
...  
Keyword(s):  
Vitamin D ◽  
Arterial Hypertension ◽  
Vitamin D Deficiency ◽  
Calcium Metabolism ◽  
Hormonal Status ◽  
Age Changes ◽  
Numerous Data ◽  
Mechanisms Of Development ◽  
The Relationship

In recent years, accumulated numerous data on the pathogenetic links of the formation of arterial hypertension. A number of studies have shown that vitamin D deficiency, associated with age, changes in sex hormonal status, increased tone of the renin-angiotensin-aldosterone system, endothelial dysfunction, and calcium metabolism, can be one of the mechanisms of development and progression of arterial hypertension. The purpose of the review was to summarize the results of the original domestic and foreign studies, prospective observations and meta-analyzes on the relationship between vitamin D deficiency and arterial hypertension.

scholarly journals Clinical Significance of FGF-23 in Patients with CKD

2011 ◽  
Vol 2011 ◽  
pp. 1-5 ◽  
Author(s):  
Domenico Russo ◽  
Yuri Battaglia
Keyword(s):  
Ventricular Hypertrophy ◽  
Vascular Dysfunction ◽  
Left Ventricular ◽  
Vitamin D Metabolism ◽  
Fgf Receptor ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
Phosphate Retention ◽  
Fgf 23

FGF23 is a bone-derived hormone that plays an important role in the regulation of phosphate and 1,25-dihydroxy vitamin D metabolism. FGF23 principally acts in the kidney to induce urinary phosphate excretion and suppress 1,25-dihydroxyvitamin D synthesis in the presence of FGF receptor 1 (FGFR1) and its coreceptor Klotho. In patients with chronic kidney disease (CKD), circulating FGF23 levels are progressively increased to compensate for persistent phosphate retention, but this results in reduced renal production of 1,25-dihydroxyvitamin D and leads to hypersecretion of parathyroid hormone. Furthermore, FGF23 is associated with vascular dysfunction, atherosclerosis, and left ventricular hypertrophy. This paper summarizes the role of FGF23 in the pathogenesis of mineral, bone, and cadiovascular disorders in CKD.

scholarly journals The Relationship between Growth Hormone Kinetics and Sarcopenia in Postmenopausal Women: The Role of Fat Mass and Leptin1

1998 ◽  
Vol 83 (5) ◽  
pp. 1502-1506
Author(s):  
Ronenn Roubenoff ◽  
Laura C. Rall ◽  
Johannes D. Veldhuis ◽  
Joseph J. Kehayias ◽  
Clifford Rosen ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Postmenopausal Women ◽  
Fat Mass ◽  
The Relationship

Side-chain oxidation of vitamin D3 in mouse kidney mitochondria: effect of the Hyp mutation and 1,25-dihydroxyvitamin D3 treatment

1987 ◽  
Vol 65 (10) ◽  
pp. 853-859 ◽  
Author(s):  
Glenville Jones ◽  
Agatha Yip ◽  
Harriet S. Tenenhouse
Keyword(s):  
Enzyme Activity ◽  
Mouse Kidney ◽  
Side Chain ◽  
Mitochondrial Enzyme ◽  
Renal Metabolism ◽  
Chain Oxidation ◽  
Hydroxyvitamin D ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
25 Hydroxyvitamin D

Side-chain oxidation of vitamin D is an important degradative pathway. In the present study we compared the enzymes involved in side-chain oxidation in normal and Hyp mouse kidney. Homogenates of normal mouse kidney catalyze the conversion of 25-hydroxyvitamin D3 to 24,25-dihydroxyvitamin D3, 24-oxo-25-hydroxyvitamin D3, and 24-oxo-23,25-dihydroxyvitamin D3. After subcellular fractionation, total side-chain oxidative activity, estimated by the sum of the three products synthesized per milligram protein under initial rate conditions, coincided with the mitochondrial enzyme marker succinate–cytochrome-c reductase. Treatment of normal mice with 1,25-dihydroxyvitamin D3 (1.5 ng/g) resulted in an eightfold increase in mitochondrial enzyme activity, with no change in apparent Km but a significant rise in Vmax. With 24,25-dihydroxyvitamin D3 as the substrate, normal renal mitochondria produced 24-oxo-25-hydroxyvitamin D3 and 24-oxo-23,25-dihydroxyvitamin D3, and the synthesis of these metabolites could be increased sixfold by pretreatment with 1,25-dihydroxyvitamin D3. In the Hyp mouse, the side-chain oxidation pathway showed similar subcellular distribution of enzyme activity. However, product formation from 25-hydroxyvitamin D3 and 24,25-dihydroxyvitamin D3 was twofold greater in mutant than in normal mitochondria. Furthermore, 1,25-dihydroxyvitamin D3 pretreatment of Hyp mice resulted in a 3.4-fold increase over basal metabolism of both 25-hydroxyvitamin D3 and 24,25-dihydroxyvitamin D3. These results demonstrate that (i) kidneys from normal and Hyp mice possess basal and 1,25-dihydroxyvitamin D3 inducible enzyme system(s) in the mitochondrial fraction, which catalyze the side-chain oxidation of 25-hydroxyvitamin D3 and 24,25-dihydroxyvitamin D3, and (ii) the Hyp mutation appears to perturb the renal metabolism of both substrates only in the basal state.

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