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Related Experiment Video

Updated: Jun 23, 2026

Assessing Lysosomal Alkalinization in the Intestine of Live Caenorhabditis elegans

Assessing Lysosomal Alkalinization in the Intestine of Live Caenorhabditis elegans

Published on: April 13, 2018

Vitamin D and aging.

Pentti Tuohimaa¹

¹Medical School, 33014 University of Tampere, Finland. pentti.tuohimaa@uta.fi

The Journal of Steroid Biochemistry and Molecular Biology

|May 16, 2009

Summary

This summary is machine-generated.

Vitamin D

Related Experiment Videos

Last Updated: Jun 23, 2026

Assessing Lysosomal Alkalinization in the Intestine of Live Caenorhabditis elegans

Assessing Lysosomal Alkalinization in the Intestine of Live Caenorhabditis elegans

Published on: April 13, 2018

Area of Science:

Endocrinology and Aging Research
Mineral Metabolism and Vitamin D Signaling

Background:

Genetically modified mouse models (FGF23-/-, Klotho-/-, VDR-/-, CYP27B1-/-) exhibit premature aging phenotypes linked to altered vitamin D and mineral homeostasis.
Both hypervitaminosis D and vitamin D deficiency/resistance contribute to accelerated aging, suggesting a complex U-shaped relationship.

Purpose of the Study:

To investigate the role of vitamin D in aging and age-related diseases.
To explore the potential of calcidiol as a key circulating hormone in determining vitamin D's biological output.
To examine the association between vitamin D, aging, cancer, and other chronic diseases.

Main Methods:

Analysis of phenotypes in genetically modified mice with altered vitamin D and mineral metabolism.
Review of existing studies on vitamin D action, aging, and cancer.
Examination of signaling pathways (IGF-1, FGF-23, p53, NF-kappaB, TERT) influenced by vitamin D.

Main Results:

Premature aging phenotypes in mice are reversible by normalizing vitamin D or mineral homeostasis, indicating hypervitaminosis D as a potential cause.
Vitamin D receptor (VDR) and CYP27B1 deficient mice show aging phenotypes resistant to dietary mineral correction, suggesting VDR or calcidiol dependency.
Calcidiol, due to its higher serum concentration and uptake, may be more directly associated with aging-related diseases than calcitriol.

Conclusions:

Aging exhibits a U-shaped dependency on vitamin D, implying an optimal concentration for delaying aging.
Calcidiol may be a crucial circulating hormone influencing aging and chronic disease risk.
Further research is needed to determine optimal calcidiol levels for preventing aging-associated diseases like osteoporosis, hypertension, and diabetes.