Vitamin D plays a crucial role in bone health by allowing your body to absorb calcium. If our bones don’t get enough of this mineral, they will grow weak. This Vitamin acts in the kidneys and the gut to soak up calcium that would normally get excreted.
We all know how calcium is important for the development of healthy bones, but most people are unaware of the role played by Vitamin D. The body is not effective at absorbing the calcium we get in our diet. Vitamin D is vital for our bones as it allows the body to make full use of the calcium we ingest. In the absence of Vitamin D, most of the calcium obtained from the diet doesn’t get absorbed, which means that we don’t get enough of this mineral to support normal bone development.
People with severe Vitamin D deficiency can only absorb small levels of calcium, causing a decline in the concentration of this mineral. Nevertheless, because calcium plays a key role in nerve and muscle function, the body cannot allow its blood concentration to fall. In order to counter this, cells called osteoclasts remove bone matrix, releasing bound calcium. When Vitamin D levels are low, the body uses calcium stored in bones to support vital bodily functions, but it doesn’t put enough calcium back to support mineralisation. This is why individuals with severe vitamin D deficiency suffer from fragile and painful bones, a disease known as rickets in children and osteomalacia in adults.
Figure 1. a) When the levels of Vitamin D are adequate, calcium is effectively absorbed into the bloodstream from the gut and kidneys. Calcium bone deposition and resoption happen at an equal rate, as a result, bones remains strong. b) Meanwhile, when an individual has severe Vitamin D deficiency, the body removes far more calcium from bones than it puts back. As a consequence, bones become weak and soft, a condition known as osteomalacia.
Vitamin D functions like a hormone in the body, binding to specific receptors, located in different parts of the body. The vitamin is like a key and the receptor is a lock that gets opened when binding occurs between the two, having a series of effects on the target cell. When Vitamin D binds to its receptor in the kidney, calcium that would normally be excreted in the urine is reabsorbed into the bloodstream and can then be used. This happens because Vitamin D causes the synthesis of calbindin in the distal tubule, a protein that binds calcium strongly and allows its reuptake into the cell. However, the actions of Vitamin D are weak in the kidney and not much calcium gets absorbed.
Vitamin D binding to receptors in the gut results in a cascade of events that facilitates intestinal calcium absorption. Some of its effects include the synthesis of calbindin and Calcium ATPases in intestinal cells called enterocytes. Calbindin binds to calcium and allows its uptake into enterocytes. Calcium ATPases are protein pumps that use energy in the form of ATP in order to transport calcium out of enterocytes and into the bloodstream. These effects ensure that the concentration of calcium inside the cell is kept low, facilitating its uptake and consequently its absorption into the circulation. Vitamin D increases the plasma concentration of calcium, which can then be utilised to support bone mineralisation.
Figure 2. Vitamin D acts in the gut to increase the numbers of calbindin and Ca2+ ATPases in enterocytes, which allows more calcium to be absorbed into the bloodstream. a) Calbindin binds very strongly to calcium in the cytoplasm, ensuring that a low concentration of calcium is kept inside the cell. This facilitates the uptake of calcium from the intestinal lumen into the cell by diffusion. b) Meanwhile, Ca2+ ATPases transport calcium out of enterocytes and into the circulation. Ca2+ ATPases function by using the energy released from the hydrolysis of a molecule called ATP, which produces ADP and inorganic phosphate (Pi) as by-products.
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