Vitamin D Deficiency

I think that these articles support my theory that if you consume cholecalciferol every day, you will suppress the production of calcitriol in your body.

Feedback regulation of 25-hydroxycholecalciferol metabolism by vitamin D3 - PubMed

1. In vitamin D-deficient chicks both vitamin D3 and 1alpha-hydroxycholecalciferol markedly decrease renal 1-hydroxylase activity and induce 24-hydroxylase activity. 2. Actinomycin D abolishes both effects. 3. These results are consistent with feedback regulation of vitamin D3 metabolism by a...
pubmed.ncbi.nlm.nih.gov

Regulation and its refractoriness of 25-hydroxyvitamin D3 metabolism in vitamin D deficiency - PubMed

The time course of change in plasma calcium levels and renal metabolism of 25-hydroxyvitamin D3 [25(OH)D3] was investigated in chicks maintained on a vitamin D-deficient diet for 4 weeks. Plasma calcium concentrations dropped sharply between the 7th and 14th day of the feeding period. Renal...
pubmed.ncbi.nlm.nih.gov

The Regulation of Vitamin D Metabolism - Nature

VITAMIN D is hydroxylated in the liver to 25-hydroxychole-calciferol (25-HCC)1, and this relatively inactive metabolite is further hydroxylated in the kidney to 1,25-dihydroxychole-calciferol (1,25-DHCC)2 (Fig. 1), the most active form, or to 24,25-dihydroxycholecalciferol (24,25-DHCC)3, a less...
www.nature.com

Vitamin D metabolism in pregnant rabbits: differences between the maternal and fetal response to administration of large amounts of vitamin D3 - PubMed

Maternal and fetal metabolism of vitamin D was examined in term pregnant rabbits fed a normal diet and in those supplemented with a large amount of vitamin D3. Term pregnant rabbits (27--30 days of gestation) fed the normal diet showed lower levels of plasma calcium, 25-hydroxyvitamin D3...
pubmed.ncbi.nlm.nih.gov


 
I managed to find one study where they followed cholecalciferol all the way down to calcitriol. It's done on cows and it was a big dose. But it's still interesting what they found. Unlike everything else that went first up and then down, calcitriol went up, then down, then up again.

Metabolism of orally administered [3H]ergocalciferol and [3H]cholecalciferol by dairy calves - PubMed

Concentrations of ergocalciferol, cholecalciferol, and their metabolites in plasma were determined after a single oral dose of [3H]ergocalciferol or [3H]cholecalciferol was given to 95- to 105-kg Jersey bull calves. One group (three calves) was given 365 muCi of [3H]ergocalciferol (1.2 Ci/mmol)...
pubmed.ncbi.nlm.nih.gov

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High fat diet increases the production of calcitriol.

As a fat-soluble vitamin, vitamin D3 relies on fat to perform its biological function, affecting lipid metabolism and innate immunity. This study used different percentages of lipid and vitamin D3 diets to evaluate the synergistic effects on the growth, lipid metabolism and immunity of juvenile Eriocheir sinensis (5.83 ± 0.01 g) for 56 days, including low lipid (LL, 1.5%) and normal lipid (NL, 7.5%) and three levels of vitamin D3: low (LVD, 0 IU/kg), medium (MVD, 9000 IU/kg) and high (HVD, 27,000, IU/kg). The synergistic effect of lipid and vitamin D3 was not significant on growth but significant on ash content, total protein, hepatopancreas lipid content, hemolymph 1α,25-hydroxy vitamin D3 [1α,25(OH)2D3] content, hepatopancreas lipolysis and synthesis genes. Crabs fed normal lipid (7.5%) and medium vitamin D3 (9000 IU/kg) had the highest hepatopancreas index, hemolymph 1α,25(OH)2D3 content, antibacterial ability, immune-related genes and hepatopancreatic lipid synthesis genes expression, but down-regulated the lipolysis genes expression. In contrast, crabs fed diets with low lipid percentage (1.5%) had low growth performance, hemolymph 1α,25(OH)2D3, mRNA levels of lipid synthesis genes, antibacterial ability and immune-related gene expression. At the 1.5% lipid level, excessive or insufficient vitamin D3 supplementation led to the obstruction of ash and protein deposition, reduced growth and molting, aggravated the reduction in antioxidant capacity, hindered antimicrobial peptide gene expression and reduced innate immunity, and resulted in abnormal lipid accumulation and the risk of oxidative stress. This study suggests that diets' lipid and vitamin D3 percentage can enhance antioxidant capacity, lipid metabolism and innate immunity in E. sinensis. A low lipid diet can cause growth retardation, reduce antioxidant capacity and innate immunity, and enhance lipid metabolism disorder.

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Low serum 25(OH)D concentrations have been reported in obese humans. Inadequate sun exposure and impaired hepatic 25-hydroxylation have been suggested as possible reasons for obesity-associated vitamin D deficiency; however, the underlying mechanism has not been elucidated. We investigated the effects of high fat diet-induced obesity on vitamin D status and vitamin D metabolizing enzyme expression. Male C57BL mice (4 weeks old) were fed control diet containing 10% energy from fat (control group) or high fat diet containing 45% energy from fat (obese group) for 18 weeks. There were no differences in serum 25(OH)D concentrations between two groups, while serum 1,25(OH)2D concentrations were significantly higher in obese mice. Hepatic mRNA levels of 25-hydroxylases (Cyp2r1, Cyp27a1, and Cyp2j3) were lower in the obese group (31, 30, and 48% lower, respectively). Renal 1α-hydroxylase (Cyp27b1) mRNA levels were higher and 24-hydroxylase (Cyp24) mRNA levels were lower in the obese group. Serum 1,25(OH)2D concentrations correlated positively with renal Cyp27b1 expression levels and negatively with renal Cyp24 expression levels. Serum PTH concentrations were higher in obese mice. In visceral adipose tissue, Cyp27a1, Cyp2j3, and vitamin D receptor mRNA levels were higher in obese mice. Overall, vitamin D metabolizing enzyme expression was influenced by high fat diet-induced obesity, which might partly explain the mechanisms of the altered vitamin D endocrine system associated with obesity. Higher serum PTH and 1,25(OH)2D concentrations in obese mice suggest abnormal regulation of serum 1,25(OH)2D concentrations due to hyperparathyroidism, which might have contributed to lower hepatic 25-hydroxylase mRNA levels.

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Bicarbonate also increases the production of calcitriol.

 
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