Magnesium plays an essential role in many fundamental cellular reactions, so its deficiency can lead to serious biochemical and clinical changes..

Experimental and clinical observations have shown important relationships of this essential ion with other electrolytes, second messengers, hormones and growth factors, their membrane receptors, signaling pathways, ion channels, secretion and action of parathyroid hormone, vitamin D metabolism and bone function..

Magnesium is involved in the synthesis of fatty acids, activation of amino acids, protein synthesis, phosphorylation of glucose and its derivatives along the glycolytic pathway, oxidative decarboxylation of citrate. Well-known protein kinases are enzymes that catalyze the transfer of phosphate to a protein substrate (more than 100 enzymes). Magnesium is required for the formation of cyclic adenosine monophosphate (cAMP).

Magnesium metabolism.

More than half of the total amount of magnesium is found in the bones, almost all of the rest is in the soft tissues.. It is a cation with a high concentration in cells. In quantitative terms, it is second only to potassium. Most intracellular magnesium exists in bound form.. Magnesium, like calcium, forms complexes with cell membrane phospholipids and nucleotides..

The percentage of magnesium absorption is regulated by its concentration in food and the presence of inhibitory or absorption-promoting dietary components.. Magnesium is absorbed in both the jejunum and the ileum. Increasing calcium intake has little effect on magnesium absorption.. In cases where magnesium absorption was increased, there was no increase in blood levels due to increased urinary excretion.. Increased oral magnesium intake leads to decreased phosphate absorption. In various malabsorption syndromes, as a rule, the absorption of magnesium in the intestine decreases..

Clinically significant magnesium malabsorption can occur with:.

• violation of the passage due to disease of the small intestine;

• reduction of the absorptive surface of the intestine due to resection, bypass anastomosis or radiation damage;

•fast transport through the intestine;

• decreased solubility of dietary or secreted magnesium binding to non-absorbable fatty acids in steatorrhea, resulting in loss of magnesium (and calcium) complexes in the stool.

The kidney plays a key role in magnesium homeostasis. Approximately 75% of serum magnesium is filtered in the glomeruli. Violation of filtration reduces the amount of magnesium entering the tubules. A severe decrease in glomerular function causes an increase in serum magnesium. The ascending limb of the loop of Henle is the main site of magnesium reabsorption and regulates excretion.. A healthy kidney at an average intake of magnesium reabsorbs approximately 95% of the amount filtered by it..

When magnesium intake is severely restricted in people with normal kidney function, magnesium excretion becomes small, less than 0.25 mmol/day.. Increasing magnesium intake to normal increases urinary excretion without altering serum magnesium levels, provided that renal function is normal and the amount administered does not exceed maximum glomerular filtration.

Magnesium deficiency and hypermagnesemia.

Magnesium deficiency symptoms: paresthesia, latent or overt tetany. Conditions in which hypomagnesemia can develop are indicated in Table.

Table 7. Clinical conditions that contribute to the depletion of magnesium reserves State Form of pathology Malabsorption syndromes Inflammatory bowel diseases Celiac disease; sprue Intestinal fistula, bypass, or resection Bile deficiency condition—eg, caecal dysfunction with steatorrhea Immune disease with villous atrophy Radiation enteritis Lymphangiectasia; другие дефекты абсорбции жира Первичная идиопатическая гипомашиемия Желудочно-кишечные инфекции  Почечная дисфункция с чрезмерными потерями  Тубулярные заболевания Метаболические расстройства Гормональные эффекты Нефротоксичные лекарства  Эндокринные расстройства  Гиперальдостеронизм Гиперпаратиреоидизм с гиперкальпиемией Постпаратиреоидэктомия (синдром «голодных костей») Гипертиреоидизм  Генетические расстройства  Первичная идиопатическая гипомашиемия Синдром сольтеряющей почки Синдром Барттера Младенцы.

The normal kidney is capable of excreting large amounts of magnesium, absorbed or excreted so quickly that serum magnesium levels usually do not reach dangerous levels.. An increase in it can occur when taking magnesium-containing antacids or laxatives in patients with chronic renal failure (CRF).

Because 20% or more of the Mg2+ from various salts can be absorbed, deterioration in renal filtration may lead to a significant increase in serum magnesium.. In acute renal failure with oliguria, especially in combination with metabolic acidosis, hypermagnesemia is possible.. Calcium infusion may counteract magnesium toxicity.

Assessment of magnesium status.

Serum magnesium levels in healthy individuals are a good indicator of nutritional magnesium. Protein-bound magnesium is subject to changes in albumin and acid-base balance.

Therefore, the level of ionized magnesium is more clinically significant than the level of total magnesium.. Urinary magnesium levels are useful in determining the cause of hypomagnesemia (taking into account magnesium intake). Low urinary magnesium indicates malabsorption, and increased urinary excretion may be due to tubular dysfunction.

Magnesium Requirements and Dietary Sources.

Need for magnesium.

The norm for adults is taken equal to 4 g / kg. This averages for men and women 350 and 280 mg / day, respectively..

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