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Did you know that ticks have antifreeze proteins?  A recent study conducted by a Yale professor of medicine focused on ticks and their unique cold resistant properties. These antifreeze proteins are called IAFGP (Ixodes scapularis anti-freeze glycoprotein) and are activated in ticks in the winter and prevent their cells and tissues from freezing.  In fact, researchers have discovered that these proteins help to decrease the damage during frostbite, thus reducing or limiting the inflammatory cascade associated with cell death.  Mice that were utilized for this study demonstrated a clear resistance to exposure to extreme cold when specially bred with genes to produce IAFGP.  There is certainly an enormous amount of potential for such proteins in terms of numerous therapeutic applications.  Read More



 

What
is CNP?

CNP stands for C-type natriuretic peptide and it is
derived from a preprohormone of 126 amino acids and a prohormone of 53 amino
acids. CNP was originally found in the
central nervous system in much greater concentrations than ANP or BNP. CNP
is produced by cardiac tissue, but is expressed primarily in the brain,
pituitary gland, vascular endothelium, kidney and female reproductive tract. It
has been discovered that it is produced in the vascular endothelial cells and after
secretion of CNP from these endothelial cells, it is regulated by cytokines and
growth factors.

Unlike ANP and BNP, CNP has a very insignificant role
in natriuretic and diuretic processes. The
physiological role of CNP is not only studied in cardiac disease, but also in
bone developmental biology, bone research, renal diseases, embryonic
developmental research, and vascular diseases. In past studies, it has been
found to play an important paracrine regulatory role in the
vasculature and involvement in neural control.

 

Biochemical Structure of CNP:

CNP produces 22 and 53 amino acid fragments.
Unlike ANP and BNP, CNP terminates in the second cysteine residue, lacking a
further C-terminal extension.

 

What is NTproCNP?

NT-proCNP is the amino-terminal peptide derived from the cleavage of the prohormone proCNP. It is an equimolar product of CNP biosynthesis and is easily measured in plasma. NTproCNP is not subject to clearance pathways and it is found in the circulation at 20- to 50-fold higher concentrations than the biologically active forms of CNP. 

 

Why Measure NTproCNP?

NTproCNP is considered to be a reliable and stable marker for measuring
CNP biosysthesis. Studies have revealed
that there is a high serum CNP concentration in critically ill subjects or individuals
who have undergone trauma. NT-proCNP has
been correlated to biomarkers of organ dysfunction and has been associated with
inflammatory and metabolic pathways.
Therefore, it has been recently been proposed as a novel biomarker for
predicting sepsis in traumatized patients.

 

 Indications for CNP:

  • Vascular Disease
  • Diabetes
  • Skeletal Development
  • Sepsis
  • Renal Disease

 

References:

  1. Clerico A et al. “Thirty years of the heart as an endocrine organ: physiological role and clinical utility of cardiac natriuretic hormones.” Am J Physiol Heart Circ Physiol 2011; 301: H12-H20.
  2. Hoffman et al. “Prognostic Value of Plasma N-Terminal Pro-Brain Natriuretic Peptide in Patients With Severe Sepsis.” Circulation; 2005:112:527-534.
  3. Koch, A. et al. “Prognostic value of circulating amino-terminal pro-C-type natriuretic peptide in critically ill patients.” Critical Care 2011, 15:R45 doi:10.1186/cc10007.
  4. Moro, Cedric et al. “Natriuretic Peptides: New Players in Energy Homeostasis.” Diabetes 2009; 12: 2726-2728
  5. Nazario, B et al. “Atrial and Brain Natriuretic Peptides Stimulate the Production and Secretion of C-type Natriuretic Peptide from Bovine Aortic Endothelial Cells.” Journal of Clinical Investigation 1995 Mar; 95(3): 1151–1157. 
  6. Olney, Robert et al. “Amino-terminal propeptide of C-type natriuretic peptide (NTproCNP) predicts height velocity in healthy children.” Clin Endocrinol (Oxf). 2012 Sep; 77(3): 416–422.
  7. Schreibe, Donald et al. “Natriuretic Peptides in Congestive Heart Failure.” Medscape 2012: Jan 10.
  8. Suzuki, T et al. “The Role of the Natriuretic Peptides in the Cardiovascular System.” Cardiovascular Research 2001; 51: 489–494.

 

 

Related Resources Citing EagleBio Kits:

          1. Stanek, B. et al. “Prognostic evaluation of neurohumoral plasma levels before and during beta-blocker therapy in advanced left ventricular dysfunction” Journal of American Cardiology 2001; 38: 436-442.

Related Kits:

NT-proCNP ELISA Assay Kit

proANP ELISA Assay Kit

BNP Fragment (Nt-proBNP 8-29) ELISA Assay Kit

Cardiovascular Assay Kits

 

Related News:

EagleBio Spotlight: Natriuretic Peptides

EagleBio Spotlight: ANP

EagleBio Spotlight: BNP

Interesting Study Highlighting Eagle Biosciences’ BNP Fragment ELISA Assay Kit

EagleBio Spotlight: ANP

 

What
is ANP?

The first
natriuretic peptide was identified in 1983 and named atrial natriuretic peptide
(ANP). ANP is a 28-amino acid polypeptide resulting from the C-terminal end of
the prohormone proANP. It is largely produced in the cardiac atria, and ANP is
quickly secreted in response to atrial stretching. ANP has the following
physiological effects:

  • Increases glomerular
    filtration rate by dilating afferent arterioles
  • Inhibits the collecting ducts from reabsorbing sodium,
    both directly and indirectly (by inhibiting aldosterone secretion)
  • Inhibits release of renin

The renin-angiotensin system and ANP
function antagonistically in the maintenance of fluid/electrolyte balance and
blood pressure.

Normal hearts
secrete extremely small amounts of ANP, but elevated levels are found in
patients with left ventricular (LV) hypertrophy and mitral valve disease.

 

Biochemical structure of ANP:

ANP is synthesized as a 126 amino acidprecursor protein which is cleaved to produce a
96 aminoacid amino-terminal fragment and a 28 amino acid
carboxyl-terminal fragment. The carboxyl-terminal 28 amino acid fragment is the biologically active peptide and
has shorter half-life than the amino-terminal fragment.

 

 

Conserved residues are shaded and the line
within the ring represents the disulfide bond. 

 

What
is proANP?

ProANP is the prohormone of ANP (ANP is stored as a
126–amino acid prohormone (proANP1–126)). After this prohormone is released it is then cleaved into
 equimolar amounts of the biologically active C-terminal peptide (ANP (99–126)) and the residual N-terminal peptide (NT-proANP (1–98)) in response to atrial wall stretch.

α-ANP has a half-life of 3-4 minutes thus is quickly cleared from circulation. ProANP (1-98) on the other hand, has a significantly longer half-life of 60-120 minutes leading to much higher concentrations in blood as compared to α-ANP. 

 

Why Measure proANP (1-98)?

Atrial natriuretic peptide (ANP) has an important physiological roles in fluid homeostasis and cardiac pathology. The longer half life of proANP (1-98) offers advantages for measuring  the ANP in the blood over α-ANP due to its lack of sensitivity to the pulsatile secretion of ANP. In fact,proANP (1-98) may provide better insight to the ANP status and its chronic secretion in the blood. Studies have shown that proANP serves as a
valuable and stable marker for several areas of research ranging from sepsis to
predicting and aiding in risk stratification for heart failure.

 

Diseases/conditions associated with increased ANP levels:

  • Diabetes and Obesity
  • Renal Disease/Renal dysfunction
  • Hypertension
  • Pneumonia
  • Asthma attacks
  • Recent heart attack
  • Heart failure/Cardiac impairment
  • Cardiomyopathy
  • Sepsis
  • Sleep apnea

 

References:

  1. Haviv, M. et al. “Atrial Natriuretic Peptidein Children with Pneumonia.” Pediatric Pulmonology 40:306–309(2005).
  2. Hoffman et al. “Prognostic Value of Plasma N-Terminal Pro-Brain Natriuretic Peptide in Patients With Severe Sepsis.” Circulation; 2005:112:527-534. 
  3. Lauridsen, Bo K et al. “ProANP Plasma Measurement Predicts All-Cause Mortality in Acutely Hospitalized Patients: A Cohort Study.” BMJ Open 2013;3:e003288 doi:10.1136/bmjopen-2013-003288.
  4. Moro, Cedric et al. “Natriuretic Peptides: New Players in Energy Homeostasis.” Diabetes 2009; 12: 2726-2728. 
  5. Robichaud, A. et al. “Plasma Atrial Natriuretic Peptide During Spontaneous Bronchoconstriction in Asthmatics. Peptides 1995;16(4):653-6.

  6. Suzuki, T et al. “The Role of the Natriuretic Peptides in the Cardiovascular System.” Cardiovascular Research 2001; 51: 489–494. 

 

 

 

Related Resources Citing EagleBio Kits:

  1. Stanek, B. et al. “Prognostic evaluation of neurohumoral plasma levels before and during beta-blocker therapy in advanced left ventricular dysfunction” Journal of American Cardiology 2001; 38: 436-442.

 

Related Kits:

proANP ELISA Assay Kit

Cardiovascular Assay Kits

Related News:

EagleBio Spotlight: Natriuretic Peptides

EagleBio Spotlight: BNP

EagleBio Spotlight: CNP

Interesting Study Highlighting Eagle Biosciences’ BNP Fragment ELISA Assay Kit

 


New Study Reveals Hong Kong Baby Girl Born 'Pregnant' with Twin Fetuses


A recent study just published in February of 2015 in the Hong-Kong Medical Journal discusses a medical case of a baby girl, born at Queen Elizabeth Hospital in Hong Kong in 2010. Doctors and other medical staff originally believed that the masses seen in prenatal ultrasounds were two tumors.  It wasn’t until the baby was born that they discovered that the masses were two fetuses that gestated up to 10 weeks.  Read More





image above from www.people.com 

EagleBio Spotlight: BNP


 

What
is BNP?

BNP stands for Brain natriuretic peptide or otherwise
known as B-type natriuretic peptide (BNP) and is produced from a preprohormone
precursor. BNP was named after it was originally identified in extracts of
porcine brain, hence brain natriuretic peptide.
Even though in humans, this peptide is produced mainly in the cardiac
ventricles its name remains the same. Following cardiac hemodynamic stress,
both atrial natriutetic peptide (ANP) and BNP are secreted from the heart (primarily produced by atrial and
ventricular cardiomyocytes). BNP is mainly expressed by ventricular myocardium
in response to volume overload and increased filling pressure. BNP
may be only activated after a prolonged period of volume overload and thus
acting like a backup hormone in response to heart stress.

The release of BNP into the blood stream causes
dilation of the blood vessels, and thereby dilation of the arteries. This begins the process of the body’s natural
response to reduce blood pressure in the body, followed by blockage of adrenalin,
and finally the release of sodium and water into the urine (natriuresis). Healthy individuals typically exhibit the
highest BNP concentrations in the atria but BNP is shifted to the ventricles in
heart failure (HF). A high concentration of BNP in the bloodstream is
indicative of heart failure. In fact, BNP
is predictive of cardiac dysfunction, in particular left ventricular
dysfunction, and is a useful marker of future outcomes in patients with acute
coronary syndromes and congestive heart failure. 

 

Biochemical structure of BNP:

BNP is produced as a 108 amino acid precursor protein
which is cleaved into a biologically active 32 amino acid carboxyl-terminal
fragment and a 76 amino acid amino- terminal fragment.


Conserved residues are shaded and the line
within the ring represents the disulfide bond.

 

The N-terminal peptide comprising amino acids 1-76 is further degraded proteolytically and thus BNP fragments in the circulation are very heterogeneous.  There are a few different circulating forms of BNP such as BNP-32 (77-108), a high molecular weight BNP and and the NT-proBNP (1-76). 

The BNP fragment (Nt-proBNP 8-29) is the preferred analyte for representation of BNP status for a few reasons.  BNP Fragment  is a stable molecule, has a long half-life and it circulates in high concentrations. 

Why Measure BNP?

BNP has a key role in cardiovascular homeostasis with biological actions including natriuresis, diuresis, vasorelaxation, and inhibition of renin and aldosterone secretion. Because of its broad range of functions in the body, measuring this analyte can be used for studying and/or monitoring the diseases/conditions below.

Diseases/conditions associated with elevated BNP levels:

  • Diabetes and
    Obesity
  • Renal Disease/Renal
    dysfunction
  • Hypertension
  • Pneumonia
  • Asthma
    attacks
  • Recent
    heart attack
  • Heart
    failure/Cardiac impairment
  • Cardiomyopathy
  • Sepsis
  • Sleep
    apnea

 

References

  1. Clerico A et al. “Thirty years of the heart as an endocrine organ: physiological role and clinical utility of cardiac natriuretic hormones.” Am J Physiol Heart Circ Physiol 2011; 301: H12-H20.
  2. Davis, William et al. “A Special Test to Diagnose Heart Failure.” Life Extension Magazine; 2007: Jun.
  3. Doust, Jenny et al. “The Role of BNP Testing in Heart Failure.” American Family Phyisician; 2006 Dec 1;74(11):1893-190.
  4. Mair, Johannes. “What are the differences between NT-proBNP and BNP, and do they matter?” Cardiac Biomarkers; 2011: Dec 1;74(11):1893-1900.
  5. Moro, Cedric et al. “Natriuretic Peptides: New Players in Energy Homeostasis.” Diabetes 2009; 12: 2726-2728.
  6. Suzuki, T et al. “The Role of the Natriuretic Peptides in the Cardiovascular System.” Cardiovascular Research 2001; 51: 489–494

 

Related Resources Citing EagleBio Kits:

  1. Stanek, B. et al. “Prognostic evaluation of neurohumoral plasma levels before and during beta-blocker therapy in advanced left ventricular dysfunction” Journal of American Cardiology 2001; 38: 436-442.

Related Kits:

BNP Fragment (Nt-proBNP 8-29) ELISA Assay Kit

proANP ELISA Assay Kit

NT-proCNP ELISA Assay Kit

 

Related News:

EagleBio Spotlight: Natriuretic Peptides

EagleBio Spotlight: ANP

EagleBio Spotlight: CNP

Interesting Study Highlighting Eagle Biosciences’ BNP Fragment ELISA Assay Kit

EagleBio’s Shikari Anti-Drug Antibody Kit Publications

 

 

EagleBio is pleased to share a list below of publications referencing use of our Shikari Kits from Matriks Biotek. Our Shikari Kits are esoteric assays and are not only the gold standard of anti-drug antibody kits world worldwide but are also incredibly user friendly.

 

Click the links below for further details.

 

Publications:

Adisen E, et al, Anti-infliximab antibody status and its relation to clinical response in psoriatic patients: A pilot study, Journal of Dermatology (2010)

Aydın C, Ataoğlu H., Demonstration of β-1,2 Mannan Structures Expressed on the Cell Wall of Candida albicans Yeast Form But Not on the Hyphal Form by Using Monoclonal Antibodies(2015).

Bodini G, et
al, Clinical relevance of Adalimumab serum concentration and Anti-Adalimumab
antibodies in patients with Chrohn’s disease during long-term follow up, Italy
(2012)

Bortlik M, et al, Impact of Anti-Tumor Necrosis Factor Alpha Antibodies Administered to Pregnant Women With Inflammatory Bowel Disease on Long-term Outcome of Exposed Children

Bortlik
M, et al, Infliximab trough levels may predict sustained response to infliximab
in patients with Crohn’s disease, Journal of Crohn’s and Colitis (2012) Bortlik
M, et al, Infliximab trough levels may predict sustained response to infliximab
in patients with Crohn’s disease, Journal of Crohn’s and Colitis (2012)

Bortlik M et al. Pregnancy and newborn outcome of mothers with inflammatory bowel diseases exposed to anti-TNF-α therapy during pregnancy: three-center study, by using Matriks Biotek®, SHIKARI® Q-INFLIXI and SHIKARI® Q-ADA (infliximab and adalimumab)) ELISA Kits IBD Clinical and Research Centre, ISCARE, Charles University , Prague , Czech Republic

Chio C, et al, Etanercept Attenuates Traumatic
Brain Injury in Rats by Reducing Brain TNF-α Contents and by Stimulating Newly
Formed Neurogenesis, Mediators of Inflammation, (2013)

Erdemli Ö., et al, In vitro evaluation of effects of sustained anti-TNF release from MPEG-PCL-MPEG and PCL microspheres on human rheumatoid arthritis synoviocytes. 

Gabriela Romero, et al, Poly(Lactide-co-Glycolide) Nanoparticles, Layer by Layer Engineered for the Sustainable Delivery of AntiTNF-α.

Grosen A., et al, Infliximab concentrations in the milk of nursing mothers with inflammatory bowel disease (2013). 

Gutierrez A, et al, Genetic susceptibility to increased
bacterial translocation influences the response to biological therapy in
patients with Crohn’s disease, Gut (2013) 

Jung Y, et al, Temperature-modulated noncovalent interaction controllable complex for the long-term delivery of etanercept to treat rheumatoid arthritis, (2013).

Kato S, et al, Elevated Serum IgE Prior to Acute Severe Infusion Reaction During Infliximab Maintenance Therapy in a Crohn’s Disease Patient, Crohn’s & Colitis Foundation of America (2011) 

Kato S, et al, Elevated Serum IgE Prior to Acute Severe Infusion Reaction During Infliximab Maintenance Therapy in a Crohn’s Disease Patient, Crohn’s & Colitis Foundation of America (2011)

Krajcovicova A. et al., Delayed hypersensitivity reaction after initial dose of infliximab: a case report (2014) 

Malickova K, et al, Phosphatidylserine-dependent
anti-prothrombin antibodies (aPS/PT) in infliximab-treated patients with
inflammatory bowel diseases, Autoimmun Highlights (2012) 

Molnar T, et al, Importance of trough levels and antibody titers on the efficacy and safety of Infliximab therapy in inflammatory bowel disease, Hungary (2012) 

Pallagi-Kunstár Éva et al., Utility of serum TNF-a, infliximab trough level, and antibody titers in inflammatory bowel disease (2014) Pallagi-Kunstár Éva et al., Utility of serum TNF-a, infliximab trough level, and antibody titers in inflammatory bowel disease (2014)

Takahashi H, et al, Plasma trough levels of adalimumab and infliximab in terms of clinical efficacy during the treatment of psoriasis, Journal of Dermatology (2012) 

Seok Lee Y, et al, Efficacy of Early Infliximab Treatment for Pediatric Crohn’s Disease: A Three-year Follow-up, Pediatric Gastroenterology, Hepatology & Nutrition (2012) 

 

Related News:

Matriks Introduces Eagle Biosciences, Inc. As Distributor in North America

New Publication Presented at UEG For Therapeutic Drug Monitoring Using EagleBio’s  SHIKARI® ELISA Kits from Matriks

 

Related Kits:

Shikari ELISA Assay Kits

EagleBio Spotlight: Endostatin




What is Endostatin?

Angiogenesis is the formation of new capillaries from preexisting blood vessels. Endostatin is a 20-kDa C-terminal fragment of collagen XVIII that plays a key role as an angiogenesis inhibitor and consists of 183-184 amino acid residues (its molecular weight is 20 kD). As a potent inhibitor of angiogenesis, endostatin has been found in recent studies to activate a series of signaling pathways thereby inducing endothelial cell apoptosis. It binds to numerous membrane proteins including integrins and heparin sulfate and this binding is further evidence of this biomarker’s involvement with multiple signaling pathways in regards to angiogenesis. In addition, other functions of endostatin in relation to cell death processes include roles in reducing cell migration, adhesion, and proliferation.

Endostatin is generated by proteoltyic cleavage by proteases or matrix metalloproteinases (MMPs) (MMPs have a variety of actions influencing fibrinolysis and angiogenesis). It is localized in the vascular basement membrane zones in various organs. Following the proteolysis, once endostatin is formed it can either stay attached to basement membranes (immobilized) or be released into circulation (soluble). Research has demonstrated that both forms of endostatin have unique biological activities. These activities at the molecular level are still being studied but thus far, it has been discovered that endostatin in combination with angiogenic factors, have an integral role in endothelial response to tissue damage such as renal injury.


Reasons to Measure Endostatin

Endostatin is a vital component for angiogenesis which is necessary for numerous pathological functions, therefore it has been indicated in a vast variety of diseases and other medical conditions. Measuring endostatin can provide remarkable value for detecting and monitoring diseases/conditions, predicting disease risk, and offering a new target for multiple therapies in related areas of research. 


Endostatin has been associated with many diseases such as:

  • Chronic Kidney Disease (CKD)
  • Renal Microvascular Disease
  • Atherosclerosis 
  • Idiopathic Pulmonary Fibrosis (IPF)
  • Cancer

References:

  1. Bellini MH et al. “Immobilized Kidney 28-kDa Endostatin-Related (KES28kDa) Fragment Promotes Endothelial Cell Survival.” Bellini MH et al., Am J Nephrol, 2010; 31(3):255-61.
  2. Chen J et al. Elevated Plasma Levels of Endostatin are Associated with Chronic Kidney Disease”. Am J Nephrol, 2012; 35(4): 335-40.
  3. Faye, Clement et al. “The First Draft of the Endostatin Interaction Network.”The Journal of Biological Chemistry 2009; 284, 22041-22047. 
  4. Iqbal CW et al. “Early-onset Coronary Artery Disease After Pediatric Kidney Transplantation: Implicating the Angiogenesis Inhibitor, Endostatin.”. Am Surg, 2011; 77(6): 731-5.
  5. Nyberg, Pia et al. “Endogenous Inhibitors of Angiogenesis.” Cancer Res 2005; 65: (10).
  6. Rehn, Marko et al. “Interaction of Endostatin with Integrins Implicated in Angiogenesis.” PNAS, 2001; 98: 1024–1029, 2001. 
  7. Richter et al. “Soluble Endostatin is a Novel Inhibitor of Epithelial Repair in Idiopathic Pulmonary Fibrosis.” Thorax 2009;64:156–161.
  8. Sodha NR et al. “Endostatin and angiostatin are increased in diabetic patients with coronary artery disease and associated with impaired coronary collateral formation.” Am J Physiol Heart Circ Physiol, 2009; 296: H428 – H434. 

Related Kits:

Endostatin ELISA

 

February 2015-  Eagle Biosciences, Inc. is pleased to introduce a new Multispecies ELISA Assay kit. This assay was developed at IBT (Immunological and Biochemical
Testsystems GmbH) in Germany. IBT’s core business surrounds the production of
high quality products in the field of Endocrinology and other related areas of
research.

This kit is designed for the simple and very
sensitive determination of Insulin-like Growth Factor 1 (IGF-1). IGF-1 is also
known as somatomedin C, and is a polypeptide of 70 amino acids and is a growth factor
for a wide range of cell types. IGF-1 is associated with cancer, neuropathy,
stroke, growth/development, aging, malnutrition/malabsorption, hypothyroidism, obesity, liver
disease, kidney disease, diabetes mellitus complications, and chronic
inflammatory disease.

“This
ELISA kit has excellent specificity for multiple species such as human, porcine, bovine and guinea pig with results in under 4 hours.”
said Dan Keefe, President of Eagle. He continued, “This product certainly
offers a lot in terms of versatility and is an exceptional addition to our
Endocrine Assay Kit line.”

These
products are currently for research use only. Check out the links below, visit
the Eagle website, www.EagleBio.com, or call 866-411-8023 for full details.

 

Multispecies IGF-1 ELISA

Endocrine Assay Kits

Vitamin D is
a steroid hormone made up of a group of fat-soluble secosteroids responsible
for enhancing intestinal absorption of calcium, iron, phosphate, magnesium, and
zinc and involved in the regulation of homeostasis. Vitamin D exists in two
forms, specifically ergocalciferol (vitamin D2), and cholecalciferol (vitamin
D3).

Vitamin
D3 is formed in the skin after exposure to sunlight or ultraviolet light, and vitamin
D2 is acquired by irradiation of plants or plant materials or foods. Both D2
and D3 forms are not yet biologically active
and are bound by a protein called VDBP (vitamin D binding protein)
in the bloodstream. Subsequently, the bound form is metabolized in the liver
where a conversion occurs into storage forms (with limited biological activity)
of the vitamin: 25-OH vitamin D2 (calcidiol) and 25-OH vitamin D3 (calcitriol).
This metabolite has been found to be the predominant circulating from of
Vitamin D and had been recognized as an accurate indicator of an individual’s
vitamin D status.

Figure 1:
D2 and D3 Structures (Norman, A. et. al)

Reasons to Measure Vitamin D

Vitamin
D is not only important for bone health but can also play a role in the
development of several non-bone related diseases. There has much debate over the past 6 decades
with regards to of which form of vitamin D to measure and which best reflects
vitamin D status. Since both D2 and D3
are used for therapy, it is necessary to measure both circulating forms. The
only way to assess a person’s vitamin D status (vitamin D deficient, sufficient,
or intoxicated) is to measure their circulating level of 25-OH Vitamin D.

Vitamin
D deficiency has been associated with many diseases such as:

  • Rickets
  • Osteomalacia
  • Osteoporosis
  • Hyperparathyroidism
  • Multiple
    Sclerosis
  • Cancers
  • Cardiovascular
    diseases
  • Depression

 

References:

1. Lips, P. et al. “Vitamin D deficiency and secondary hyperparathyroidism in the elderly: consequences for bone loss and fractures and therapeutic implications” Endocrine Rev. 22 2001; 477–501.

2. Lips P. Vitamin D physiology. Prog Biophys Mol Biol 2006; 92: 4-8.

3. Mavroeidi, A et al. “Seasonal 25-hydroxyvitamin D changes in British postmenopausal women at 57 degrees N and 51 degrees N: a longitudinal study. J Steroid.” Biochem Mol Biol 2010; 121:459-461.

4. Macdonald, HM et al. “Sunlight and dietary contributions to the seasonal vitamin D status of cohorts of healthy postmenopausal women living at northerly latitudes: a major cause for concern?” Osteoporos Int 2010.

5Norman, et. al. “From vitamin D to hormone D: fundamentals of the vitamin D endocrine system essential for good health1,2,3,4.” Am J Clin Nutr 2008; 88: 2 491S-499S.

6. Tsur, A. et al. “Effect of different dress style on vitamin D level in healthy young Orthodox and ultra-Orthodox students in Israel”. Osteoporos Int 2010; 26: 6.

7. Holick MF, Chen TC. “Vitamin D deficiency: a worldwide problem with health consequences”. Am J Clin Nutr 2008; 87: 1080-1086.

8. BW J Hollis Editiorial: “The Determination of circulating 25-Hydroxyvitamin D: No Easy Task” Clin Endocrinol Metab 2004; 89: (7):3149–3151.

9. Snellman, G. et al. “Determining Vitamin D Status: A Comparison between Commercially Available Assays.” PLoS One 2010; 13:5(7):e11555.

 

Related Kits:

Vitamin Assay Kits

Bone Metabolism Assay Kits

 

Related News:

Vitamin D Publications

10 Reasons to Keep Up with Your Vitamin D Levels