Vitamin D:
Gespeichert in:
| Format: | Buch |
|---|---|
| Sprache: | English |
| Veröffentlicht: |
Philadelphia [u.a.]
Saunders
2012
|
| Schriftenreihe: | Rheumatic disease clinics of North America
38,1 |
| Schlagworte: | |
| Online-Zugang: | Inhaltsverzeichnis |
| Beschreibung: | XIV, 242 S. Ill., graph. Darst. |
| ISBN: | 9781455739318 |
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| adam_text | Vitamin D
Contents
Preface
xiii
Sol Epstein
Vitamin D: Metabolism
1
Sylvia
Christakos,
Dare V. Ajibade, Puneet Dhawan, Adam J. Fechner, and
Leila J.
Mady
The biologically active metabolite of vitamin D,
1
,25(OH)2D3, affects min¬
eral homeostasis and has numerous other diverse physiologic functions
including effects on growth of cancer cells and protection against certain
immune disorders. This article reviews the role of vitamin
D hydroxylases
in
providing a tightly regulated supply of
1
,25(OH)2D3. The role of
extrarenai
1
a(OH)ase in placenta and
macrophages
is also discussed, as well as reg¬
ulation of vitamin
D
hydroxylases in aging and chronic kidney disease. Un¬
derstanding specific factors involved in regulating the hydroxylases may
lead to the design of drugs that can selectively modulate the hydroxylases.
The ability to alter levels of these enzymes would have therapeutic poten¬
tial for the treatment of various diseases, including bone loss disorders and
certain immune diseases.
The Vitamin
D
Receptor: New Paradigms for the Regulation of Gene Expression
by 1,25-Dihydroxyvitamin D3
13
J. Wesley Pike and Mark B. Meyer
The actions of the vitamin
D
hormone
1
,25-dihydroxyvitamin D3
(1
¿Ј^ОН^ВД
are mediated by the vitamin
D
receptor (VDR), a ligand-activated transcription
factor that functions to control gene expression. After ligand activation, the
VDR binds directly to specific sequences located near promoters and recruits
a variety of coregulatory complexes that perform the additional functions
required to modify transcriptional output. Recent advances in transcripttonal
regulation, which permit the unbiased identification of the regulatory regions
of genes, are providing new insight into how genes are regulated. Surpris¬
ingly, gene regulation requires the orchestrated efforts of multiple modular
enhancers often located many
kilobases
upstream, downstream, or within
the transcription units themselves. These studies are transforming our under¬
standing of how
1
,25(ОН)г0з
regulates gene transcription.
Assessment and Interpretation of Circulating 25-Hydroxyvitamin
D
and 1,25-Dihydroxyvitamin
D
in the Clinical Environment
29
Bruce W. Hollis
The unique c/s-triene structure of vitamin
D
and related metabolites makes
it susceptible to oxidation, ultraviolet (UV) light-induced conformational
changes, heat-induced conformational changes, and attacks by free rad¬
icals. Vitamin D2 is much less bioactive than vitamin D3 in humans. Meta¬
bolic activation and inactivation of vitamin
D
are well characterized and
result in a plethora of metabolites, of which only
25-hydroxyvitamin
D
(25(OH)D) and
1
,25-dihydroxyvitamin
D (1,25(OH)2D)
provide any clinically
viii Contents
relevant
information.
25(OH)D2 and
25(ОН)0з
are commonly known as cal-
cifediol and the
1
,25(OH)2D metabolites as calcitriol. In this review the cur¬
rent state of the science on the clinical assessment of circulating 25(OH)D
and
1,25(014)20
is described.
Low Vitamin
D
Status: Definition, Prevalence, Consequences, and Correction
45
Neil Binkley, Rekha Ramamurthy, and Diane Krueger
Vitamin
D
is obtained from cutaneous production when
ľ-dehydrocholes-
terol is converted to vitamin D3 (cholecalciferol) by ultraviolet
В
radiation or
by oral intake of vitamin D2 (ergocalciferol) and D3. An individual s vitamin
D
status is best evaluated by measuring the circulating 25-hydroxyvitamin
D (25(OH)D)
concentration. Although controversy surrounds the definition
of low vitamin
D
status, there is increasing agreement that the optimal cir¬
culating 25(OH)D level should be approximately
30
to
32
ng/mL or above.
Using this definition, it has been estimated that approximately three-quar¬
ters of all adults in the United States have low levels. Low vitamin
D
status
classically has skeletal consequences such as osteomalacia/rickets. More
recently, associations between low vitamin
D
status and increased risk for
various nonskeletal morbidities have been recognized; whether all of these
associations are causally related to low vitamin
D
status remains to be de¬
termined. To achieve optimal vitamin
D
status, daily intakes of at least
1000
IU or more of vitamin
D
are required. The risk of
toxicity
with high
amounts of vitamin
D
intake is low. Substantial between-individual variabil¬
ity exists in response to the same administered vitamin
D dose.
When
to monitor 25(OH)D levels has received little attention. Supplementation
with vitamin D3 may be preferable to vitamin D2.
Maternal Vitamin
D
Status: Implications for the Development of Infantile
Nutritional Rickets
61
Kebashni Thandrayen and John M. Pettifor
The mother is the major source of circulating 25-OHD concentrations in the
young infant. Thus maternal vitamin
D
status is an important factor in de¬
termining the vitamin
D
status of the infant and his/her risk of developing
vitamin
D
deficiency and infantile nutritional rickets. There is evidence
that the supplementation recommendations, particularly for pregnant
and lactating women, may be inadequate to ensure vitamin
D
sufficiency
in these groups. Thus there needs to be a wide spread and concerted
effort to ensure daily supplementation of breastfed and other infants at
high risk with vitamin
D
400
IU
from birth and pregnant women in high
risk communities with at least
600
IU. Future studies are required to deter¬
mine the optimal doses of vitamin
D
supplementation needed during preg¬
nancy and lactation; and for normalizing vitamin
D
stores in infancy to
reduce the prevalence of infantile nutritional rickets. Furthermore, opera¬
tional research studies need to be conducted to understand the best
methods of implementing supplementation programs and the factors
that are likely to promote their success.
Osteomalacia
as a Result of Vitamin
D
Deficiency
81
Arti
Bhan, Ajay D. Rao, and D. Sudhaker Rao
Osteomalacia
is an end-stage bone disease of chronic and severe vitamin
D
or phosphate depletion of any cause. Its importance has increased because
Contents
of the rising incidence of vitamin
D
deficiency. Yet, not all cases of
osteoma¬
lacia
are cured by vitamin
D
replacement, and furthermore, not all individuals
with vitamin
D
deficiency develop
osteomalacia.
Although in the past
oste¬
omalacia
was commonly caused by
malabsorption,
nutritional deficiency
now is more common. In addition, recent literature suggests that nutritional
vitamin
D
deficiency
osteomalacia
follows various bariatric surgeries for
morbid obesity. Bone pain, tenderness, muscle weakness, and difficulty
walking are all common clinical manifestations of
osteomalacia.
Diagnostic
work-up involves biochemical assessment of vitamin
D
status and may also
include a transiliac bone biopsy. Treatment is based on aggressive vitamin
D
repletion in most cases with follow-up biopsies if patients are started on anti-
resorptive or anabolic agents.
Genetic Disorders and Defects in Vitamin
D
Action
93
Peter J. Malloy and David Feldman
Two rare genetic diseases can cause rickets in children. The critical enzyme
to synthesize calcitriol from 25-hydroxyvitamin D, the circulating hormone
precursor, is 25-hydroxyvitamin D-1 a-hydroxylase
(1
α
-hydroxylase).
When
this enzyme is defective and calcitriol can no longer be synthesized, the dis¬
ease
1
α
-hydroxylase
deficiency develops. The disease is also known as
vitamin D-dependent rickets type
1
or pseudovitamin
D
deficiency rickets.
When the VDR is defective, the disease hereditary vitamin D-resistant rick¬
ets, also known as vitamin D-dependent rickets type
2,
develops. Both
diseases are rare autosomal recessive disorders characterized by hypocal-
cemia, secondary hyperparathyroidism, and early onset severe rickets. In
this article, these
2
genetic childhood diseases, which present similarly
with hypocalcemia and rickets in infancy, are discussed and compared.
Vitamin
D
and Fracture Prevention
107
Heike
A. Bischoff-Ferrari
This article discusses the amount of vitamin
D
supplementation needed
and the desirable 25-hydroxyvitamin
D
level to be achieved for optimal
fracture prevention.
Vitamin
D
in Kidney Disease: Pathophysiology and the Utility of Treatment
115
Rizwan A. Qazi and Kevin J. Martin
Vitamin
D
physiology has gained more importance and publicity than any
of its counterparts in the water- and fat-soluble vitamin groups combined.
This is partly because vitamin
D
deficiency is still widely prevalent in the
developed world and the beneficial effects are thought to extend beyond
the regulation of calcium and phosphorus homeostasis alone. Vitamin
D
deficiency becomes even more important in the various stages of chronic
kidney disease (CKD); CKD itself is also on the increase. How vitamin
D
physiology is altered in CKD and how the various treatment modalities
can alter the morbidity and mortality associated with CKD is the topic of
discussion for this article.
Vitamin
D
and the Immune System: New Perspectives on an Old Theme
125
Martin Hewison
Interaction with the immune system is one of the most well-established
nonclassic effects of vitamin D. For many years this was considered to
Contents
be a manifestation of granulomatous diseases such sarcoidosis, in which
synthesis of active
1
,25-dihydroxyvitamin D3
(1
,25(ОН)2О3)
is known to
be dysregulated. However, recent reports have supported a role for
1
,25(OH)2D3 in mediating normal function of the innate and adaptive im¬
mune systems. Crucially, these effects seem to be mediated via localized
autocrine or
paracrine synthesis of
1
,25(OH)2D3 from precursor 25-hydrox-
yvitamin D3, the main circulating metabolite of vitamin D. The ability of vita¬
min
D
to influence normal human immunity is highly dependent on the
vitamin
D
status of individuals, and may lead to aberrant response to infec¬
tion or autoimmunity in those who are lacking vitamin D. The potential
health significance of this has been underlined by increasing awareness
of impaired vitamin
D
status in populations across the globe. This article de¬
scribes some of the recent developments with respect to vitamin
D
and the
immune system, and possible clinical implications.
Vitamin D: Extraskeletal Health
141
Michael F. Holick
Vitamin
D
deficiency is the most common nutritional deficiency and likely
the most common medical condition in the world. The major cause of vita¬
min
D
deficiency has been the lack of appreciation that the body requires
5-
to 10-fold higher intakes than is currently recommended by health
agencies. There is now overwhelming and compelling scientific and
epide¬
miologie
data suggesting that the human body requires a blood level
25(OH)D above
30
ng/mL for maximum health. To increase the blood level
to the minimum
30
ng/mL requires the
ingestion
of at least
1000
IU of vita¬
min
D
per day for adults. In general, there is no downside to increasing
either a child s or adult s vitamin
D
intake.
The Role of Vitamin
D
in Cancer Prevention and Treatment
161
Aruna V. Krishnan, Donald L. Trump, Candace S. Johnson, and David Feidman
Calcitriol
(1
,25-dihydroxyvitamÍn D3),
the hormonally active form of vitamin
D, exerts growth inhibitory and prodifferentiating effects on many malig¬
nant cells and retards tumor growth in animal models. Calcitriol is being
evaluated as an
anticancer
agent in several human cancers. The mecha¬
nisms underlying the
anticancer
effects of calcitriol include inhibition of
cell proliferation, stimulation of apoptosis, suppression of inflammation,
and inhibition of tumor angiogenesis, invasion, and metastasis. This review
discusses some of the molecular pathways mediating these
anticancer
actions of calcitriol and the preclinical data in cell culture and animal
models. The clinical trials evaluating the use of calcitriol and its analogues
in the treatment of patients with cancer are described. The reasons for the
lack of impressive beneficial effects in clinical trials compared with the sub¬
stantial efficacy seen in preclinical models are discussed.
Vitamin
Đ
and Diabetes
179
Tatiana
Takiishi,
Conny Gysemans,
Roger Bouillon, and
Chantai Mathieu
Type
1
(T1D) and type
2
(T2D) diabetes are considered muMfactorial dis¬
eases in which both genetic predisposition and environmental factors par¬
ticipate in their development. Marty cellular, preclinical, and observational
Contents
studies support a role for vitamin
D
in the pathogenesis of both types of
diabetes including:
(1)
T1
D
and T2D patients have a higher incidence of hy-
povitaminosis D;
(2)
pancreatic tissue (more specifically the insulinproducing
b-cells) as well as numerous cell types of the immune system express the
vitamin
D
receptor (VDR) and vitamin D-binding protein (DBP); and
(3)
some allelic variations in genes involved in vitamin
D
metabolism and VDR
are associated with glucose (intolerance, insulin secretion, and sensitivity,
as well as inflammation. Moreover,
pharmacologie
doses of
1
,25-dihydrox-
yvitamin
D
(1
,25(OH)2D), the active form of vitamin D, prevent insulitis and
T1
D
in
nonobese
diabetic (NOD) mice and other models of T1D, possibly
by immune modulation as well as by direct effects on b-cell function. In
T2D, vitamin
D
supplementation can increase insulin sensitivity and de¬
crease inflammation. This article reviews the role of vitamin
D
in the patho¬
genesis of T1
D
and T2D, focusing on the therapeutic potential for vitamin
D
in the prevention/intervention of T1
D
and T2D as well as its complications.
Vitamin
D
Analogs
207
Glenville Jones
Vitamin
D
has gone through a renaissance with the association of vitamin
D
deficiency with a wide array of common diseases including breast, co-
lorectal and prostate cancers, cardio-vascular disease, autoimmune con¬
ditions and infections. Vitamin
D
analogs constitute a valuable group of
compounds which can be used to regulate gene expression in functions
as varied as calcium and phosphate homeostasis, as well as cell growth
regulation and cell differentiation of a wide spectrum of cell types. This re¬
view will discuss the full range of vitamin
D
compounds currently available,
some of their possible uses, and potential mechanisms of action.
Index
233
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| indexdate | 2024-07-10T00:19:38Z |
| institution | BVB |
| isbn | 9781455739318 |
| language | English |
| oai_aleph_id | oai:aleph.bib-bvb.de:BVB01-025091528 |
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| owner_facet | DE-355 DE-BY-UBR |
| physical | XIV, 242 S. Ill., graph. Darst. |
| publishDate | 2012 |
| publishDateSearch | 2012 |
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| publisher | Saunders |
| record_format | marc |
| series | Rheumatic disease clinics of North America |
| series2 | Rheumatic disease clinics of North America |
| spelling | Vitamin D guest ed.: Sol Epstein Philadelphia [u.a.] Saunders 2012 XIV, 242 S. Ill., graph. Darst. txt rdacontent n rdamedia nc rdacarrier Rheumatic disease clinics of North America 38,1 Vitamin-D-Mangel (DE-588)4252274-2 gnd rswk-swf Gesundheit (DE-588)4020754-7 gnd rswk-swf Vitamin-D-Gruppe (DE-588)4188446-2 gnd rswk-swf (DE-588)4143413-4 Aufsatzsammlung gnd-content Vitamin-D-Gruppe (DE-588)4188446-2 s Gesundheit (DE-588)4020754-7 s DE-604 Vitamin-D-Mangel (DE-588)4252274-2 s Epstein, Sol Sonstige (DE-588)141895845 oth Rheumatic disease clinics of North America 38,1 (DE-604)BV000625464 38,1 Digitalisierung UB Regensburg application/pdf http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=025091528&sequence=000002&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA Inhaltsverzeichnis |
| spellingShingle | Vitamin D Rheumatic disease clinics of North America Vitamin-D-Mangel (DE-588)4252274-2 gnd Gesundheit (DE-588)4020754-7 gnd Vitamin-D-Gruppe (DE-588)4188446-2 gnd |
| subject_GND | (DE-588)4252274-2 (DE-588)4020754-7 (DE-588)4188446-2 (DE-588)4143413-4 |
| title | Vitamin D |
| title_auth | Vitamin D |
| title_exact_search | Vitamin D |
| title_full | Vitamin D guest ed.: Sol Epstein |
| title_fullStr | Vitamin D guest ed.: Sol Epstein |
| title_full_unstemmed | Vitamin D guest ed.: Sol Epstein |
| title_short | Vitamin D |
| title_sort | vitamin d |
| topic | Vitamin-D-Mangel (DE-588)4252274-2 gnd Gesundheit (DE-588)4020754-7 gnd Vitamin-D-Gruppe (DE-588)4188446-2 gnd |
| topic_facet | Vitamin-D-Mangel Gesundheit Vitamin-D-Gruppe Aufsatzsammlung |
| url | http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=025091528&sequence=000002&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA |
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