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Vitamin D Deficiency

Sunshine Delivers Free Vitamin D To Everyone.
Sunshine Delivers Free Vitamin D To Everyone.

What Is Vitamin D?

[dropcap]V[/dropcap]itamin D is the principle regulator of calcium homeostasis (balance) in the body.  This “vitamin” is really a prohormone, meaning it acts like a hormone but is not. Vitamin D does, however, contain cholesterol in its molecular structure like steroid hormones.

The physiological importance of vitamin D encompasses much more than the regulation of bone metabolism although this is a mighty function.

Q: How does vitamin D regulate bone metabolism?

A: In regulation of bone metabolism, vitamin D works in three ways: 1) enables active absorption of calcium from the small intestine, 2) enhances reabsortion of calcium by the kidneys that would otherwise be excreted in urine, and 3) plays an active role in skeletal development and bone mineralization. Mineralization gives strength to living bone tissue.

Vitamin D interacts with receptors within cells to effect transcriptional changes in many cell types including those in gut, bone, breast, prostate, brain, skeletal muscle, and the immune system.1

In regards to the essential role of vitamin D in muscle tissue, it has been recently shown that vitamin D regulates both muscle function and structure of primary myofibers.2

Vitamin D is converted in the body to a molecule that is biologically active. The active form is 1,25-dihydroxyvitamin D, usually referred to as vitamin D3. About 80% comes from sun exposure and the remaining from food.

Vitamin D3 is synthesized in the skin from 7-dehydrocholesterol via photochemical reactions requiring UV light (sunlight). That is, light that contains energy from the sun is incorporated into molecules of  7-dehydrocholesterol in the underlying dermis of skin to make this vitamin. This is why inadequate exposure to sunlight contributes to vitamin D deficiency.

Blood concentration of 25(OH)D is the best indicator of vitamin D status. It reflects vitamin D produced in the skin and that obtained from food and supplements and has a fairly long circulating half-life of 15 days.3

What Is Vitamin D Deficiency In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. McCarty DE, Chesson AL Jr, Jain SK, Marino AA. The link between vitamin D metabolism and sleep medicine. Sleep Med Rev. 2014 Aug;18(4):311-9. doi: 10.1016/j.smrv.2013.07.001. [↩]
  2. Girgis CM, Mokbel N, Cha KM, Houweling PJ, Abboud M, Fraser DR, Mason RS, Clifton-Bligh RJ, Gunton JE. The vitamin D receptor (VDR) is expressed in skeletal muscle of male mice and modulates 25-hydroxyvitamin D (25OHD) uptake in myofibers. Endocrinology. 2014 Sep;155(9):3227-37 [↩]
  3. http://ods.od.nih.gov/factsheets/VitaminD-HealthProfessional/ [↩]

Autoimmune Disorders In Celiac Disease

Lipase Enzyme. Courtesy johnsonmatthey.
Lipase Enzyme. Courtesy Johnson Matthey Catalysts.

What Is Macrolipasemia?

[dropcap]M acrolipasemia is a rare enzyme disorder characterized by altered molecules of lipase, a pancreatic enzyme needed to digest fats, that are abnormally bound with serum antibody proteins. These antibodies are commonly immunoglobulin G (IgG) and/or less likely immunoglobulin A (IgA).

Q: What happens when lipase is bound to immunoglobulins (IgA and/or IgG)?

A: The resulting molecule is too large to be filtered by the kidneys and excreted in the urine, consequently these abnormal molecules build up in the plasma causing sustained elevation of lipase levels called macrolipasemia.

Macrolipasemia occurs with or without macroamylasemia, which is the binding of immunoglobulin A and/or G to amylase, a pancreatic enzyme needed to digest starches.1

What Is Macrolipasemia In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. La Villa G, Pantaleo P, Tarquini R, Cirami L, Perfetto F, Mancuso F, Laffi G. Multiple immune disorders in unrecognized celiac disease: a case report. World J Gastroenterol. 2003;9(6):1377-1380, Available at: http://www.wjgnet.com/1007-9327/9/1377.asp. Accessed Jan 3, 2005. [↩]

Diabetes Mellitus, Type I

Image depicts tissue transglutaminase (tTg).
Image Depicts Tissue Transglutaminase (tTG).

What Are Anti-tissue Transglutaminase Antibodies?

[dropcap]A nti-tissue transglutaminase antibodies (anti-tTG) are connective tissue autoantibodies and can be detected in blood samples from affected persons who are reacting to gluten in the diet.

Autoantibodies are abnormal because they attack the body’s own tissue, which in the case of these antibodies is tissue transglutaminase 2 (TG2).

Q: What is tissue transglutaminase 2 (TG2)?

A: Tissue transglutaminase 2 (TG2) is an enzyme that appears in many cell locations and is particularly abundant in endothelial cells that line the small intestine. It has been implicated in a variety of cellular processes, such as differentiation, cell death, inflammation, cell migration and wound healing.

The cell appears to adapt the dynamics of this enzyme to meet specific sub-cellular needs or to respond to stress or other stimuli. Substantial evidence indicates that the location of TG2 within cells is critical for the regulation of its various biochemical activities, which subsequently trigger diverse downstream events,1

Although initially studied as an enzyme within cells, TG2 is now known to be secreted also into the extracellular space (between cells) or onto the cell surface.1

Abnormal activation of TG2 or deregulation of its function(s) is involved in a variety of human diseases, such as celiac disease, diabetes, neurodegenerative diseases, multiple sclerosis and rheumatoid arthritis. A role in inflammatory disorders and septic shock has also been shown. Moreover, multiple studies have revealed elevated TG2 expression in many types of cancer cells.1

What Are Anti-tissue Transglutaminase Antibodies In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Piacentini M, D’Eletto M, Farrace MG, Rodolfo C, Del Nonno F, Ippolito G, Falasca L. Characterization of distinct sub-cellular location of transglutaminase type II: changes in intracellular distribution in physiological and pathological states. Cell Tissue Res. 2014 Dec;358(3):793-805. doi: 10.1007/s00441-014-1990-x. [↩] [↩] [↩]