Vitamin D family

Nowadays, many people lack vitamins in their bodies, but they don’t care much about it. However, vitamins need to be supplemented to ensure the health of the body. When the body lacks certain elements, it will cause some unnecessary problems. So you can take a look at the sources of vitamin D group and make timely supplements when the body lacks vitamin D group.

Sources of Vitamin D

The main source of vitamin D in the human body is 7-dehydrocholesterol in the skin, which is converted into cholecalciferol, i.e. endogenous vitamin D3, by ultraviolet rays in sunlight.

Another source is obtained from the food we eat (exogenous). For example, animal liver, eggs, and milk all contain vitamin D. The ergosterol contained in plant foods such as vegetable oil and mushrooms must be exposed to ultraviolet rays to become calciferol, or vitamin D2, which can be absorbed by the human body. Both endogenous vitamin D3 and exogenous vitamins D2 and D3 have no biological activity and need to be further metabolized in the body to obtain a strong anti-rickets effect.

Vitamin D is first converted into 25-hydroxycholecalciferol [25-(OH)D3] in the endoplasmic reticulum and mitochondria of hepatocytes by the 25-hydroxylase system, which has a weak anti-rickets effect.

Then, in the mitochondria of the proximal tubule epithelial cells of the kidney, it is further hydroxylated into 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] by the 1-hydroxylase system. Its biological activity is greatly enhanced and it can act on distant target organs (mainly the intestines, kidneys and bones) through the blood circulation. The 25-hydroxycholecalciferol produced by the liver and the 1,25-dihydroxycholecalciferol produced by the kidneys can both regulate themselves through feedback mechanisms.

The metabolism of vitamin D2 is the same as that of vitamin D3. In addition to being regulated by its own blood concentration, vitamin D3 is also directly regulated by blood phosphorus concentration, parathyroid hormone and calcitonin, and indirectly regulated by blood calcium concentration. Hypocalcemia increases the secretion of parathyroid hormone, 1,25-(OH). D, the synthesis increases and the blood calcium rises; hypercalcemia promotes the secretion of calcitonin and inhibits the synthesis of 1,25-(OH)2D3; hypophosphatemia directly promotes the increase of 1,25-(OH)2D3 synthesis, while hyperphosphatemia inhibits it.