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7. Magnesium in the Treatment and Prevention of Diseases
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Magnesium deficiency has been linked to atherosclerosis, alterations in blood lipids and blood sugar, type 2 diabetes, myocardial infarction, hypertension, kidney stones, premenstrual syndrome and psychiatric disorders . A number of common clinical symptoms and diseases in association with magnesium deficiency are described in the following.

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7.1. Magnesium, Type 2 Diabetes and Metabolic Syndrome
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イメージ 1
Diabetes
People with diabetes generally have high levels of fatty acids called triglycerides. These fatty acids may increase the risk of gallstones. Gallbladder function is impaired in the presence of diabetic neuropathy, and regulation of hyperglycaemia with insulin seems to raise the lithogenic index. A lack of melatonin could significantly contribute to gallbladder stones, as melatonin inhibits cholesterol secretion from the gallbladder, enhances the conversion of cholesterol to bile, and is an antioxidant, which is able to reduce oxidative stress to the gallbladder.

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Clinical Presentations of Gallstone Disease
For practical purpose gallbladder disease can be equated with gallstones as these are present in the large majority of patients. Most patients with gallstones have no symptoms. These gallstones are called ¡Èsilent stones¡É and may not require treatment.

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Patients with symptomatic stones most often present with recurrent episodes of right-upper-quadrant or epigastric pain, probably related to the impaction of a stone in the cystic duct. They may experience intense pain in the upper-right side of the abdomen, often accompanied by nausea and vomiting, that steadily increases for approximately 30 min to several hours. A patient may also experience referred pain between the shoulder blades or below the right shoulder region (Boas¡Ç sign). Often, attacks occur after a particularly fatty meal and almost always happen at night.

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Some patients with gallstones present with acute cholecystitis, and often secondary infection by intestinal microorganisms, predominantly Escherichia coli and Bacteroides species. Inflammation of the gallbladder wall causes severe abdominal pain, especially in the right upper quadrant, with nausea, vomiting, fever, and leucocytosis. This condition may remit temporarily without surgery, but it sometimes progresses to gangrene and perforation. Less commonly, gallstones can become lodged in the common bile duct (choledocholithiasis), sometimes with obstruction of the common bile duct and symptoms of cholestasis. Obstruction leading to jaundice though commonly caused by a stone migrating into the common bile duct, can be due to compression of the common hepatic duct by a stone in the neck of the gall bladder or cystic duct (Mirrizi syndrome). Infection in the bile ducts (cholangitis) can occur even with a seemingly minor degree of obstruction to bile flow. Stones in the common bile duct usually cause pain in the epigastrium or right upper quadrant, but may be painless. The passage of common-bile-duct stones can provoke acute pancreatitis, probably by transiently obstructing the main pancreatic duct where it passes near the common bile duct at the ampulla of Vater. Gallstones may fistulate directly into the duodenum from the gallbladder during a period of silent inflammation. This stone can impact in the duodenum leading to duodenal obstruction (Bouveret's syndrome) Alternatively, gallstones can impact at the narrowest portion of healthy small, bowel causing an obstruction termed gallstone ileus.

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The Diagnosis of Gallstone Disease
This disorder is usually diagnosed by history of recurrent episodes of right-upper-quadrant or epigastric pain, suggesting biliary colic and Boas¡Ç sign. There may be fever, tender right upper quadrant with or without Murphy's sign, tenderness when the hand taps the right costal arch (Ortner's sign).

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The three primary methods used to diagnose gallbladder disease are ultrasonography, nuclear scanning (cholescintigraphy), and oral cholecystography. Today, ultrasonography is the method most often used to detect cholelithiasis and cholecystitis. Occasionally gallstones are diagnosed during plain X-rays. Ultrasonography has a specificity and sensitivity of 90-95%, and can detect stones as small as 2 mm in diameter. It can demonstrate the presence of common-bile-duct stones, show bile-duct dilatation and detect thickening of the gallbladder wall.¡ÊÃæÎ¬¡Ë

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Treatment
Treatment of gallstones depends partly on whether they are causing symptoms or not. Recurrent episodes of upper abdominal pain related to gallstones are the most common indication for the treatment of gallstones.Delaying elective cholecystectomy until repeated episodes of pain occur results in a minimal decrease in life expectancy.

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Prophylactic cholecystectomy for gallstones has been recommended in specific groups, such as children, because symptoms develop in almost all patients.¡ÊÃæÎ¬¡Ë

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Prophylactic cholecystectomy was recommended for diabetic patients with gallstones because of an increased risk of acute cholecystitis and increased mortality with emergency cholecystectomy. Recent studies show that diabetic patients have increased operative risk with elective as well as emergency gallbladder surgery related to risk of cardiovascular disease and other coexisting conditions rather than to diabetes mellitus itself. Most authorities do not recommend cholecystectomy in diabetic patients without symptoms of gallstones.

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Open cholecystectomy was formerly the gold standard of treatment for gallstones, until the advent of laparoscopic cholecystectomy. Open cholecystectomy in an otherwise healthy, good-risk candidate requires hospital stay for some days, and has mortality of less than 1%. The greatest drawbacks to open cholecystectomy are the resulting pain and weeks of disability. Laparoscopic cholecystectomy has become widely used since it was first performed in 1988 with a complication rate probably at least as good as that of the open procedure. However a patient who has undergone abdominal surgery a number of times may not be a suitable candidate for Laparoscopic cholecystectomy because of extensive adhesions around the gallbladder. A patient who is medically too unstable to undergo open cholecystectomy is also not a good candidate for Laparoscopic cholecystectomy either. The evaluation and treatment of suspected stones in the common bile duct can be carried out by endoscopic retrograde cholangiopancreatography before laparoscopic cholecystectomy. If common-bile-duct stones are unexpectedly found by cholangiography during laparoscopic cholecystectomy,an open exploration of the common bile duct may be needed.

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The laparoscopic procedure requires more operating time than the open procedure, but usually only one night in the hospital postoperatively; postoperative pain is greatly reduced, and the patients can usually return to work early, i.e., in one to 2 weeks, as compared with 4-6 weeks after open cholecystectomy.

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Attempts to use oral bile salts to dissolve gallstones began more than 30 years ago because of those who refuse or are poor risks for surgery. Chenodeoxycholic acid (chenodiol) and ursodeoxycholic acid (ursodiol) are known to dissolve gallstones, but chenodiol causes diarrhoea and abnormal aminotransferase levels, while ursodiol does not. Therapy with bile salts is suitable for only a minority of patients with symptomatic cholesterol gallstones. It is not suitable for patients with acute cholecystitis or stones in the common bile duct, who need urgent action. Candidates for treatment with bile salts should have a patent cystic duct and noncalcified cholesterol gallstones. Gallstones frequently recur after oral bile salts are stopped.

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Contact dissolution therapy of cholesterol gallstones rapidly is possible by instilling solvents like the organic solvent methyl tert-butyl ether into the gallbladder through a percutaneous catheter placed through the liver.Alternatively, a nasobiliary catheter can be endoscopically guided into the gallbladder can be used for instilling the organic solvent. This is a technically difficult and hazardous procedure, and should be performed only by experienced doctors in hospitals where research on this treatment is being done. Serious side effects include severe burning pain.

Finally a mixture of plant terpenes may also be useful for dissolving radiolucent gallstones, particularly when used in combination with a bile acid.

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US National Library of Medicine ÊÆ¹ñ¹ñΩ°å³Ø¿Þ½ñ´Û
National Institutes of Health¡¡¹ñΩ±ÒÀ¸¸¦µæ½ê
Niger J Surg. 2013 Jul-Dec¡¡Gabriel E Njeze
イメージ 1

Abstract
Gallstone disease is a worldwide medical problem, but the incidence rates show substantial geographical variation, with the lowest rates reported in African populations.

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 Publications in English language on gallstones which were obtained from reprint requests and PubMed database formed the basis for this paper. Data extracted from these sources included authors, country, year of publication, age and sex of patients, pathogenesis, risk factors for development of gallstones, racial distribution, presenting symptoms, complications and treatment. 

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Gallstones occur worldwide, however it is commonest among North American Indians and Hispanics but low in Asian and African populations. High biliary protein and lipid concentrations are risk factors for the formation of gallstones, while gallbladder sludge is thought to be the usual precursor of gallstones. Biliary calcium concentration plays a part in bilirubin precipitation and gallstone calcification. ¡ÊÃæÎ¬¡Ë

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Introduction
Gallstones are hardened deposits of the digestive fluid bile, that can form within the gallbladder. They vary in size and shape from as small as a grain of sand to as large as a golf ball. Gallstones occur when there is an imbalance in the chemical constituents of bile that result in precipitation of one or more of the components.

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Gallstone disease is often thought to be a major affliction in modern society.However, gallstones must have been known to humans for many years, since they have been found in the gallbladders of Egyptian mummies dating back to 1000 BC. This disease is however, a worldwide medical problem, even though there are geographical variations in gallstone prevalence Gallstones are becoming increasingly common; they are seen in all age groups, but the incidence increases with age; and about a quarter of women over 60 years will develop them. In most cases they do not cause symptoms, and only 10% and 20% will eventually become symptomatic within 5 years and 20 years of diagnosis. Thus the average risk of developing symptomatic disease is low, and approaches 2.0-2.6%/year.¡ÊÃæÎ¬¡Ë

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Method
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Pathogenesis
Gallstones are composed mainly of cholesterol, bilirubin, and calcium salts, with smaller amounts of protein and other materials. There are three types of gallstones[20] (i) Pure cholesterol stones, which contain at least 90% cholesterol, (ii) pigment stones either brown or black, which contain at least 90% bilirubin and (iii) mixed composition stones, which contain varying proportions of cholesterol, bilirubin and other substances such as calcium carbonate, calcium phosphate and calcium palmitate. Brown pigment stones are mainly composed of calcium bilirubinate whereas black pigment stones contain bilirubin, calcium and/or tribasic phosphate. In Western societies and in Pakistan more than 70% of gallstones are composed primarily of cholesterol, either pure or mixed with pigment, mucoglycoprotein, and calcium carbonate. Pure cholesterol crystals are quite soft, and protein contributes importantly to the strength of cholesterol stones.

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In the simplest sense, cholesterol gallstones form when the cholesterol concentration in bile exceeds the ability of bile to hold it in solution, so that crystals form and grow as stones. Cholesterol is virtually insoluble in aqueous solution, but in bile it is made soluble by association with bile salts and phospholipids in the form of mixed micelles and vesicles.

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Three types of abnormalities have been considered to be responsible for cholesterol gallstone formation. Cholesterol supersaturation, the essential requirement for cholesterol gallstone formation, might occur via excessive cholesterol biosynthesis, which is the main lithogenic mechanism in obese persons. In the non-obese, defective conversion of cholesterol to bile acids, due to a low or relatively low activity of cholesterol 7¦Á hydroxylase, the rate limiting enzyme for bile acid biosynthesis and cholesterol elimination could result in excessive cholesterol secretion. Finally, interruption of the enterohepatic circulation of bile acids could increase bile saturation. Temporary interruption of the enterohepatic bile acid circulation during overnight fasting leads to a higher cholesterol/phospholipid ratio in the vesicles secreted by the liver. Estrogen treatment also reduces the synthesis of bile acid in women.

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Pigment stones occur when red blood cells are being destroyed, leading to excessive bilirubin in the bile. Black pigment stones are more common in patients with cirrhosis or chronic hemolytic conditions such as the thalassemias, hereditary spherocytosis, and sickle cell disease, in which bilirubin excretion is increased. Primary bile-duct stones, defined as stones that originate in the bile ducts, are usually brown pigment stones associated with infection. Bacteria in the biliary system release ¦Â-glucuronidases, which hydrolyze glucuronic acid from conjugated bilirubin. The resulting unconjugated bilirubin precipitates as its calcium salts. Primary brown pigment stones of the bile ducts often occur in Asians, associated with decreased biliary secretory Immunogloblin A (IgA.) About 15% of gallstones are calcified enough to be seen on a plain abdominal radiograph, and of these, two thirds are pigment stones.

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High biliary protein and lipid concentrations are risk factors for the formation of gallstones. Gallbladder sludge, i.e., thickened gallbladder mucoprotein with tiny entrapped cholesterol crystals is thought to be the usual precursor of gallstones. Sludge can sometimes cause biliary pain, cholecystitis, or acute pancreatitis, but sludge may also resolve without treatment. The sources of sludge are pregnancy, prolonged total parenteral nutrition,starvation, or rapid weight loss. The antibiotic ceftriaxone can also precipitate in the gallbladder as sludgeand rarely, as gallstones.

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The biliary calcium concentration plays a part in bilirubin precipitation and gallstone calcification. Many patients with gallstones have increased biliary calcium, with supersaturation of calcium carbonate.

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Intestinal hypomotility has been recently recognised as a primary factor in cholesterol lithogenesis. Fiber may protect against gallstone formation by speeding intestinal transit and reducing the generation of secondary bile acids such as deoxycholate which has been associated with increased cholesterol saturation of the bile.

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Epidemiology of Gallstones
Epidemiological studies have suggested a marked variation in overall prevalence between different populations. Gallstone is one of the diseases prevalent in developed nations, but it is less prevalent in the developing populations that still consume traditional diets. Its prevalence is especially high in the Scandinavian countries and Chile and among Native Americans. Gallstones are more common in North America, Europe, and Australia, and are less prevalent in Africa, India, China, Japan, Kashmir, and Egypt.

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Factors influencing gallstone disease
Age
All epidemiological studies showed that increasing age was associated with an increased prevalence of gallstones. Gallstones are 4-10 times more frequent in older than younger subjects. Biliary cholesterol saturation increases with age, due to a decline in the activity of cholesterol 7¦Á hydroxylase, the rate limiting enzyme for bile acid synthesis. Deoxycholic acid proportion in bile increases with age through enhanced 7¦Á dehydroxylation of the primary bile acids by the intestinal bacteria.

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Gender, parity, and oral contraceptives
In all populations of the world, regardless of overall gallstone prevalence, women during their fertile years are almost twice as likely as men to experience cholelithiasis. This preponderance persists to a lesser extent into the postmenopausal period, but the sex difference narrows with increasing age.Increased levels of the hormone estrogen, as a result of pregnancy or hormone therapy, or the use of combined (estrogen-containing) forms of hormonal contraception, may increase cholesterol levels in bile and also decrease gallbladder movement, resulting in gallstone formation.

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Genetics
Both necropsy and population studies have clearly shown the existence of racial differences that cannot completely be explained by environmental factors. Cholesterol gallstone prevalence varies widely, from extremely low (<5%) in Asian and African populations, to intermediate (10-30%) in European and Northern American populations, and to extremely high (30-70%) in populations of Native American ancestry (Pima Indians in Arizona, Mapuche Indians in Chile).¡ÊÃæÎ¬¡Ë

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Obesity and body fat distribution
Obesity is an important risk factor for gallstone disease, more so for women than for men. It raises the risk of cholesterol gallstones by increasing biliary secretion of cholesterol, as a result of an increase in 3-hydroxy-3-mthylglutaryl coenzyme A (HMGCoA) reductase activity. Epidemiological studies have found that the lithogenic risk of obesity is strongest in young women, and that slimness protects against cholelithiasis.

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Rapid weight loss
Rapid weight loss is associated with occurrence of sludge and gallstones in 10-25% of patients in a few weeks of initiating the slimming procedures. If a person loses weight too quickly, the liver secretes extra cholesterol; in addition there is rapid mobilization of cholesterol from adipose tissue stores. In fasting associated with severely fat restricted diets, gallbladder contraction is reduced, and the accompanying gallbladder stasis favors gallstone formation. Enhancing gallbladder emptying by inclusion of a small amount of dietary fat inhibits gallstone formation in patients undergoing rapid weight loss.Fasting in the short term increases the cholesterol saturation of gallbladder bile and in the longer term, causes gallbladder stasis which can lead to sludge, and eventually gallstone formation. Younger women with gallstones were shown to be more prone to skip breakfast than controls. A shorter overnight fasting is protective against gallstones in both sexes.

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Diet
Nutritional exposure to western diet, i.e., increase intake of fat, refined carbohydrates and decrease in fibre content is a potent risk factor for development of gallstones.Calcium intake seems to be inversely associated with gallstone prevalence. Dietary calcium decreases cholesterol saturation of gallbladder bile by preventing the reabsorption of secondary bile acids in the colon. Vitamin C influences 7¦Á hydroxylase activity in the bile and it was shown that ascorbic acid might reduce lithogenic risk in adults. Coffee consumption seems to be inversely correlated with gallstone prevalence, due to an increased enterohepatic circulation of bile acids. Coffee components stimulate cholecystokinin release, enhance gallbladder motility, inhibit gallbladder fluid absorption, decrease cholesterol crystallization in bile and perhaps increase intestinal motility.

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Physical activity
Regular exercise, in addition to facilitating weight control, alone or in combination with dieting, improves several metabolic abnormalities related to both obesity and cholesterol gallstones. In contrast, sedentary behaviour, is positively associated with the risk of cholecystectomy.

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Clinical Presentations of Gallstone Disease
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Magnesium in Prevention and Therapy


3. Magnesium and Nutrition
Dietary surveys of people in Europe and in the United States still reveal that intakes of magnesium are lower than the recommended amounts . Epidemiological studies in Europe and North America have shown that people consuming Western-type diets are low in magnesium content, i.e. <30%–50% of the RDA for magnesium. 

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It is suggested that the dietary intakes of magnesium in the United States have been declining over the last 100 years from about 500 mg/day to 175–225 mg/day. This is likely a result of the increasing use of fertilizers and processed foods . In 1997, the Food and Nutrition Board (FNB) of the Institute of Medicine had increased the dietary references intakes (RDA) for magnesium, based on the results of controlled balance studies. 

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The new RDA ranges from 80 mg/day for children 1–3 year of age to 130 mg/day for children 4–8 year of age. For older males, the RDA for magnesium ranges from as low as 240 mg/day (range, 9–13 year of age) and increases to 420 mg/day for males 31–70 year of age and older. For females, the RDA for magnesium ranges from 240 mg/day (9–13 year of age) to 360 mg/day for females 14–18 year of age. The RDA for females 31–70 year of age and older is 320 mg/day .

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Water accounts for ~10% of daily magnesium intake , chlorophyll (and thus green vegetables such as spinach) is the major source of magnesium. Nuts, seeds and unprocessed cereals are also rich in magnesium. Legumes, fruit, fish and meat have an intermediate magnesium concentration. Some types of food processing, such as refining grains in ways that remove the nutrient-rich germ and bran, lower magnesium content substantially. Low magnesium concentrations are found in dairy products, except milk .

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The United States NHANES 2005–2006 survey reported that nearly one half of all American adults have an inadequate intake from food and water of magnesium and do not consume the estimated average requirements (EAR) (set at 255–350 mg depending on gender and age group) . A chronic magnesium deficiency (serum magnesium <0.75 mmol/L) is associated with an increased risk of numerous preclinical and clinical outcomes, including atherosclerosis, hypertension, cardiac arrhythmias, stroke, alterations in lipid metabolism, insulin resistance, metabolic syndrome, type 2 diabetes mellitus, osteoporosis as well as depression and other neuropsychiatric disorders. Furthermore, magnesium deficiency may be at least one of the pathophysiological links that may help to explain the interactions between inflammation and oxidative stress with the aging process and many age-related diseases .

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4. Magnesium Absorption and Excretion
Magnesium homeostasis is maintained by the intestine, the bone and the kidneys. Magnesium is mainly absorbed in the small intestine, which was shown by 28Mg isotope measurements, although some is also taken up via the large intestine . Of the total dietary magnesium consumed, only about 24%–76% is absorbed in the gut the rest is eliminated in the faeces . 

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The majority of magnesium is absorbed in the small intestine by a passive paracellular mechanism, which is driven by an electrochemical gradient and solvent drag (see Figure 1). Paracellular magnesium absorption is responsible for 80%–90% of intestinal magnesium uptake. 

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 A minor, yet important, regulatory fraction of magnesium is transported via the transcellular transporter transient receptor potential channel melastatin member TRPM 6 and TRPM 7—members of the long transient receptor potential channel family—which also play an important role in intestinal calcium absorption .

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It is worth noting that intestinal absorption is not directly proportional to magnesium intake but is dependent mainly on magnesium status. The lower the magnesium level, the more of the mineral is absorbed in the gut, thus relative magnesium absorption is high when intake is low and vice versa. The kidneys are crucial in magnesium homeostasis as serum magnesium concentration is primarily controlled by its excretion in urine. 

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Under physiological conditions, ~2400 mg of magnesium in plasma is filtered by the glomeruli. Of the filtered load, ~2300 mg is immediately reabsorbed and only 3%–5% is excreted in the urine, i.e., ~100 mg . Only little magnesium is reabsorbed in the proximal tubule.Most of the filtered magnesium is reabsorbed in the loop of Henle, mostly in the thick ascending limb (up to 70% of total magnesium reabsorption). The reabsorption and excretion of magnesium is influenced by several not yet classified mechanisms. 

イメージ 3

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Most of the filtered magnesium is reabsorbed in the loop of Henle, mostly in the thick ascending limb (up to 70% of total magnesium reabsorption). The reabsorption and excretion of magnesium is influenced by several not yet classified mechanisms. 

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In this context, we could show that an overload of blood cells with magnesium in renal insufficiency can be avoided by a special cell membrane buffering system for magnesium. In severe forms of renal insufficiency, this buffering system for magnesium is destroyed and an overload with magnesium in human cells is observed . Furthermore, the exchange time for magnesium between intra- and extracellular pools is relatively long . Hypomagnesaemia is frequently linked with hypokalemia owing to disturbances in renal secretion of potassium in the connecting tubule and collecting duct .

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Magnesium absorption and excretion is influenced by different hormones. It has been shown that 1,25-dihydroxyvitamin D [1,25(OH)2D] can stimulate intestinal magnesium absorption.On the other hand, magnesium is a cofactor that is required for the binding of vitamin D to its transport protein, vitamin D binding protein (VDBP). Moreover, conversion of vitamin D by hepatic 25-hydroxlation and renal 1¦Á-hydroxylation into the active, hormonal form 1,25(OH)2D is magnesium-dependent. Magnesium deficiency, which leads to reduced 1,25(OH)2D and impaired parathyroid hormone response, has been implicated in ¡Èmagnesium-dependent vitamin-D-resistant rickets¡É. Magnesium supplementation substantially reversed the resistance to vitamin D treatment . 

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Next to 1,25(OH)2D, several other factors, such as oestrogen or parathyroid hormone (PTH), are involved in the magnesium excretion. Oestrogen is known to stimulate TRPM6 expression . Thus, oestrogen substitution therapy can normalize hypermagnesuria, which occurs frequently in postmenopausal women. Interestingly, TRPM6 expression appears to be regulated by serum magnesium levels and oestrogens, but not by 1,25(OH)2D or PTH action .

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Of special importance is PTH. Absorption of both magnesium and calcium appears to be inter-related, with concomitant deficiencies of both ions well described.For example, the stimulation of PTH secretion in response to hypocalcemia acts to restore the serum calcium concentration to normal. Hypomagnesemia impairs hypocalcemic-induced PTH release, which is corrected within in minutes after infusion of magnesium. The rapidity of correction of PTH concentrations suggests that the mechanism of action of magnesium is enhanced release of PTH. Magnesium is also required for the sensitivity of the target tissues to PTH.

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Magnesium in Prevention and Therapy
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2015 Sep 23
Uwe Gröber,1,* Joachim Schmidt,1 and Klaus Kisters1,2
2015 9·î23Æü

Magnesium is the fourth most abundant mineral in the body. It has been recognized as a cofactor for more than 300 enzymatic reactions, where it is crucial for adenosine triphosphate (ATP) metabolism. Magnesium is required for DNA and RNA synthesis, reproduction, and protein synthesis. 

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Moreover, magnesium is essential for the regulation of muscular contraction, blood pressure, insulin metabolism, cardiac excitability, vasomotor tone, nerve transmission and neuromuscular conduction. Imbalances in magnesium status—primarily hypomagnesemia as it is seen more common than hypermagnesemia—might result in unwanted neuromuscular, cardiac or nervous disorders. Based on magnesium¡Çs many functions within the human body, it plays an important role in prevention and treatment of many diseases.

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 Low levels of magnesium have been associated with a number of chronic diseases, such as Alzheimer¡Çs disease, insulin resistance and type-2 diabetes mellitus, hypertension, cardiovascular disease (e.g., stroke), migraine headaches, and attention deficit hyperactivity disorder (ADHD).

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1. Introduction
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Magnesium is an essential electrolyte for living organisms and is the fourth most abundant mineral in the human body. ¡ÊÃæÎ¬¡Ë

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Based on magnesium¡Çs many functions within the human body, it plays an important role in prevention and treatment of many diseases. Low levels of magnesium have been associated with a number of chronic and inflammatory diseases, such as Alzheimer¡Çs disease, asthma, attention deficit hyperactivity disorder (ADHD), insulin resistance, type-2 diabetes mellitus, hypertension, cardiovascular disease (e.g., stroke), migraine headaches, and osteoporosis 

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2. Functions of Magnesium
Magnesium is primarily found within the cell where it acts as a counter ion for the energy-rich ATP and nuclear acids. 
Magnesium is a cofactor in more than 300 enzyme systems that regulate diverse biochemical reactions in the body, including protein synthesis, muscle and nerve transmission, neuromuscular conduction, signal transduction, blood glucose control, and blood pressure regulation. ¡ÊÃæÎ¬¡Ë

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Magnesium is also necessary for structural function of proteins, nucleic acids or mitochondria. It is required for DNA and RNA synthesis, and for both aerobic and anaerobic energy production—oxidative phosphorylation and glycolysis—either indirectly as a part of magnesium-ATP complex, or directly as an enzyme activator.

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Magnesium also plays a key role in the active transport of calcium and potassium ions across cell membranes, a process that is important for nerve impulse conduction, muscle contraction, vasomotor tone and normal heart rhythm. ¡ÊÃæÎ¬¡Ë

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Moreover, it contributes to the structural development of bone and is required for the adenosine triphosphate-dependent synthesis of the most important intracellular antioxidant glutathione. The most important reservoir for magnesium is the bone (about 60% of total body magnesium), the remaining 40% is located extra- and intracellularly.

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 Magnesium excretion is mainly regulated by the kidney. About 100 mmol/L magnesium is filtered daily . The total magnesium content of the human body is reported to be ~20 mmol/kg of fat-free tissue. In other words, total magnesium in the average 70 kg adult with 20% (w/w) fat is ~1000 to 1120 mmol or ~24 g .

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Magnesium is beside sodium, potassium and calcium an important electrolyte for human metabolism. About 99% of total body magnesium is located in bone, muscles and non-muscular soft tissue . Approximately 50%–60% of magnesium resides as surface substituents of the hydroxyapatite mineral component of bone. Most of the remaining magnesium is contained in skeletal muscle and soft tissue. The magnesium content of bone decreases with age, and magnesium that is stored in this way is not completely bioavailable during magnesium deprivation.

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Intracellular magnesium concentrations range from 5–20 mmol/L; 1%–5% is ionized, the remainder is bound to proteins, negatively charged molecules and adenosine triphosphate (ATP)]. Extracellular magnesium accounts for about 1%–3% of total body magnesium which is primarily found in serum and red blood cells. Normal serum magnesium concentration is about 0.76–1.15 mmol/L . It is categorized into three fractions. It is either ionized (55%–70%), bound to protein (20%–30%) or complexed with anions (5%–15%) such as phosphate, bicarbonate and citrate or sulphate. Red blood cells/serum magnesium ratio is about 2.8 .

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