Eur. J. Entomol. 116: 16-32, 2019 | DOI: 10.14411/eje.2019.003

Vitamin D1 versus ecdysteroids: Growth effects on cell regeneration and malignant growth in insects are similar to those in humansPoint of view

Karel SLÁMA
Laboratory of Insect Physiology, Evropská 674, 16000 Praha 6, Czech Republic; e-mail: karel.slama34@gmail.com

Polyhydroxylated derivatives of 6-keto,7-dehydrocholesterol (ecdysteroids) are common constituents of various plants. In 1965, they were accidentally discovered in the search for the insect moulting hormone. These biologically important natural compounds are neither insect hormones nor inducers of insect ecdysis. Due to their strong anabolic, vitamin D-like effects in insects, domestic animals and humans, I propose the use of the arbitrary term vitamin D1. The present paper describes the effects of vitamin D1 on the growth and regeneration of excised epidermal cells of the tobacco hornworm, Manduca sexta (Sphingidae). The periods of programmed cell death and cell proliferation (histolysis and histogenesis, respectively) exactly coincide in insects with endogenous peaks of increased concentration of vitamin D1. Epidermal cells communicate with each other, creating a mutually integrated tissue, connected by mechanical, chemical, electrical, ionic or other so far incompletely known factors. After natural cell death, or after the artificial removal of some epidermal cells, the neighbouring cells that lose communication integrity, begin to divide mitotically to replace the disconnected part. Cell divisions are arrested as soon as the integrity of the living tissue is established. During insect ontogeny, the application of juvenile hormone causes regenerating epidermal cells to repeat the previous morphogenetic programme (i.e., development of patches of larval tissue on the body of a pupa, or metathetely). Conversely, the application of vitamin D1 (20-hydroxyecdysone) caused the regenerating cells to prematurely execute a future morphogenetic programme (i.e., development of patches of pupal tissue on the body of a larva, or prothetely). Among the key features of insect regeneration, is the arrest of cell divisions when tissues resume living cell-to-cell integrity. This prevents the formation of aberrant groups of cells, or tumours. It is well established that the main physiological systems of insects (e.g., circulatory, respiratory, neuro-endocrine) are structurally and functionally similar to corresponding systems in humans. Thus the basic principles of cell regeneration and the role of vitamin D1 in insects may also be valid for humans. The common vitamins D2 (ergocalciferol) or D3 (cholecalciferol), are exclusively lipid soluble secosterols, which require activation by UV irradiation and hydroxylation in the liver. By contrast, the neglected vitamin D1 is a natural derivative of polyhydroxylated 7-dehydrocholesterol of predominantly plant origin, which is both partly a water and partly a lipid soluble vitamin. It neither requires UV irradiation, nor hydroxylation due to 6 or 7 already built-in hydroxylic groups. Like other vitamins, it enters insect or human bodies in plant food or is produced by intestinal symbionts. Vitamin D1 causes strong anabolic, vitamin D-like effects in domestic animals and in humans. I am convinced that avitaminosis associated with a deficiency of vitamin D1 in human blood may be responsible for certain hitherto incurable human diseases, especially those related to impaired nerve functions and somatic growth, aberrant cell regeneration or formation of malignant tumours.

Keywords: Insects, ecdysteroids, vitamin D, 20-hydroxyecdysone, cell regeneration, living tissue integrity, insect/human similarity, malignant growth, tumours, D1 avitaminosis, rachitis

Received: August 1, 2018; Revised: October 10, 2018; Accepted: October 10, 2018; Published online: January 11, 2019  Show citation

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SLÁMA, K. (2019). Vitamin D1 versus ecdysteroids: Growth effects on cell regeneration and malignant growth in insects are similar to those in humans. EJE116, Article 16-32. https://doi.org/10.14411/eje.2019.003
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