Insufficient levels of vitamin D have been demonstrated by many
authors as a risk factor for autistic patients, however, the
causality has not been reliably elucidated. In the present study,
levels of calcidiol were determined in group of autistic children
and compared with age matched healthy children as controls.
Suboptimal levels of calcidiol in more than 60 % of both autistic
patients as well as of control group were found. No significant
differences in vitamin D between autistic children and healthy
controls were observed.
In women with chronic autoimmune thyroiditis and vitamin D deficiency we have found reference levels of relevant metabolichormonal parameters except for parathormone and total calcium. Three months supplementation with vitamin D (4300 IU/day, cholekalciferol) did not lead to significant changes of investigated hormonal parameters, while the levels of parathormone and calcium reached normal levels. However, a correlation analysis revealed marked changes in mutual relations. First, an inverse correlation of vitamin D with parathormone, insulin secretion (C peptide, insulin) and its efficiency (HOMA IR) disappeared. Relationships of vitamin D to hepatic insulin resistance (insulin/C peptide), to DHEA (both negative), and to DHEAS/DHEA ratio (positive) were newly found. Second, a positive correlation of CRP with insulin secretion remained, while its relation to insulin efficiency (HOMA IR, insulin/ C peptide) was newly observed. Analogical positive correlations appeared also among anti TPO and insulinemia, insulin/C peptide, HOMA IR, and anti Tg to C peptide. A relationship of the CRP with anti TPO became significant (+). Third, out of glucose metabolism parameters only insulin/C peptide and glycemia did not correlate with vitamin D during its deficiency, while after supplementation insulin/ C peptide alone correlated positively with both DHEAS and DHEA, and negatively with vitamin D., K. Vondra, R. Bílek, P. Matucha, M. Salátová, M. Vosátková, L. Stárka, R. Hampl., and Obsahuje bibliografii
We examined the upregulation of ET-1/ETBR/eNOS signaling in renoprotective effect of vitamin D in kidney fibrosis model in mice using unilateral ureteral obstruction (UUO). One group was treated with intraperitoneal injection of 0.125 mg/kg of Calcitriol (UUO+VD). Vascular remodeling was quantified based on lumen area and lumen/wall area ratio (LWAR) of intrarenal arteries using Sirius Red staining. ET-1, ETBR, eNOS, CD31 and VEGF mRNA expressions were quantified using qRT-PCR. Focusing on endothelin-1 (ET-1) signaling in endothelial cells (EC), siRNA of ET-1 was performed in human umbilical vein endothelial cells (HUVEC) for reducing ET-1 expression. Then HUVECs were treated with and without 100 nM Calcitriol treatment in hypoxic and normoxic conditions to elucidate ET-1/eNOS signaling. Our in vivo study revealed vascular remodeling and renal ischemia attenuation after Calcitriol treatment. Vascular remodeling was attenuated in the UUO+VD group as shown by increasing lumen areas and LWAR in intrarenal arteries. These findings were associated with significant higher CD31 and VEGF mRNA expression compared to the UUO group. Vitamin D treatment also increased ET-1, ETBR and eNOS mRNA expressions. Our in vitro study demonstrated Calcitriol induced ET-1 and eNOS mRNA expressions upregulation in HUVEC under normoxic and hypoxic condition. Meanwhile, siRNA for ET-1 inhibited the upregulation of eNOS mRNA expression after Calcitriol treatment. Vitamin D ameliorates kidney fibrosis through attenuating vascular remodeling and ischemia with upregulating ET-1/ETBR and eNOS expression., N. Arfian, M. H. H. Kusuma, N. Anggorowati, D. B. Nugroho, A. Jeffilano, Y. Suzuki, K. Ikeda, N. Emoto., and Seznam literatury
Vitamin D had been for a long time investigated for its effects on bone metabolism. Recently has been observed that the incidence of some neurodevelopmental disorders (including autism) increases hand in hand with vitamin D deficiency. Indeed, vitamin D was reported to modulate the biosynthesis of neurotransmitters and neurotrophic factors; moreover, its receptor was found in the central nervous system. Vitamin D deficiency was therefore assessed as a risk factor for autism, however the biological mechanism has not yet been revealed. In our review we focused on potential connections among vitamin D, steroids and autism. Potential mechanisms of vitamin D action are also discussed., L. Máčová, M. Bičíková, D. Ostatníková, M. Hill, L. Stárka., and Obsahuje bibliografii
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 artifi cial 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 defi ciency 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.
Vitamin D3 is well-known as a major regulator of calcium and
phosphorus homeostasis. A growing body of evidence highlights
its crucial role in the regulation of reproductive processes in
females. The role of vitamin D3 in the female reproductive tract
has been extensively investigated because its receptor is
abundant in reproductive organs, including ovary. Importantly,
besides expression of vitamin D3 receptor, the ovary is an
extrarenal site of vitamin D3 metabolism. The influence of vitamin
D3 on follicular development and ovarian steroidogenesis has
been investigated. Furthermore, vitamin D3 deficiency has also
been associated with polycystic ovary syndrome, premature
ovarian failure and ovarian cancer. The objective of this review is
to summarize our knowledge about the contribution of vitamin D3
to physiological and pathological processes within the ovary.
Suplementace přiměřenými dávkami vitaminů a stopových prvků je zcela nezbytná k prevenci rozvoje karenčních stavů. Nepřiměřený přívod může vést k závažným jevům (poruchy metabolismu, poškození volnými radikály, zpomalená reparace tkání atd.). Odpovídající příjem vitaminů je nutný jak u běžné populace, tak u rizikových skupin (děti, starší věkové skupiny) a u vážně nemocných, hospitalizovaných pacientů se zvýšenou spotřebou proteinů a energie. Všechny mikronutrientý (s výjimkou některých ve vodě rozpustných vitaminů) mohou být při vysokém příjmu toxické a neměly by být užívány bez indikace., Provision of adequate amounts of vitamins and trace elements is indispensable for prevention of clinical deficiency states and simultaneously inadequate supply may lead to the important effects (metabolic disturbances, free radical damage, insufficient repair of tissue etc.). Adequate intake of vitamins and trace elements is necessary in general healthy population as well as in groups at the risk (elderly individuals, children) and in seriously ill patients in hospital with increased requirements for protein and energy. All essential micronutrients (except of the some water soluble vitamins) could be toxic at high levels of intake and patients or healthy subjects should not take nutrient supplements unless they are clinically indicated., Zdeněk Zadák, Lit: 8, and Souhrn: eng