Created page with "過剰なリボフラビンが小腸で吸収されると、血液から速やかに除去され、尿中に排泄される。尿の色は水分補給状態のバイオマーカーとして用いられ、正常な状態では尿比重および尿浸透圧と相関する。しかし、リボフラビンを必要量を大幅に超えて補給すると、尿が通常よりも黄色く見えるようになる。通常の..."
Created page with "==欠乏== {{Anchor| Deficiency}} ===有病率=== リボフラビン欠乏症は、小麦粉やコーンミールの栄養強化プログラムを実施している米国や他の国々ではまれである。年2回実施されている米国人口調査で収集されたデータでは、20歳以上の場合、女性の22％、男性の19％がリボフラビンを含むサプリメント（通常はビタミン・ミネラル複合サプリメント）を摂取して..."
過剰なリボフラビンが小腸で吸収されると、血液から速やかに除去され、尿中に排泄される。尿の色は水分補給状態のバイオマーカーとして用いられ、正常な状態では[[urine specific gravity/ja|尿比重]]および[[urine osmolality/ja|尿浸透圧]]と相関する。しかし、リボフラビンを必要量を大幅に超えて補給すると、尿が通常よりも黄色く見えるようになる。通常の食事による摂取では、尿中の約3分の2がリボフラビンであり、残りは細胞内での酸化やその他の代謝産物として部分的にヒドロキシメチルリボフラビンに代謝されたものである。消費量が吸収能力を上回ると、リボフラビンは大腸に入り、そこで細菌によって様々な代謝物に異化され、[[feces/ja|糞便]]から検出される。吸収されなかったリボフラビンは、大腸の[[microbiome/ja|マイクロバイオーム]]に影響を与える可能性があるという推測がある。
過剰なリボフラビンが小腸で吸収されると、血液から速やかに除去され、尿中に排泄される。尿の色は水分補給状態のバイオマーカーとして用いられ、正常な状態では[[urine specific gravity/ja|尿比重]]および[[urine osmolality/ja|尿浸透圧]]と相関する。しかし、リボフラビンを必要量を大幅に超えて補給すると、尿が通常よりも黄色く見えるようになる。通常の食事による摂取では、尿中の約3分の2がリボフラビンであり、残りは細胞内での酸化やその他の代謝産物として部分的にヒドロキシメチルリボフラビンに代謝されたものである。消費量が吸収能力を上回ると、リボフラビンは大腸に入り、そこで細菌によって様々な代謝物に異化され、[[feces/ja|糞便]]から検出される。吸収されなかったリボフラビンは、大腸の[[microbiome/ja|マイクロバイオーム]]に影響を与える可能性があるという推測がある。
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==欠乏==
==Deficiency==
{{Anchor| Deficiency}}
===Prevalence===
===有病率===
Riboflavin deficiency is uncommon in the United States and in other countries with wheat flour or corn meal fortification programs. From data collected in biannual surveys of the U.S. population, for ages 20 and over, 22% of females and 19% of men reported consuming a supplement that contained riboflavin, typically a vitamin-mineral multi-supplement. For the non-supplement users, the dietary intake of adult women averaged 1.74 mg/day and men 2.44 mg/day. These amounts exceed the RDAs for riboflavin of 1.1 and 1.3 mg/day respectively. For all age groups, on average, consumption from food exceeded the RDAs. A 2001-02 U.S. survey reported that less than 3% of the population consumed less than the [[Estimated Average Requirement]] of riboflavin.
Riboflavin deficiency (also called ariboflavinosis) results in stomatitis, symptoms of which include chapped and fissured lips, inflammation of the corners of the mouth (angular stomatitis), sore throat, painful red tongue, and hair loss. The eyes can become itchy, watery, bloodshot, and sensitive to light. Riboflavin deficiency is associated with anemia. Prolonged riboflavin insufficiency may cause degeneration of the liver and nervous system. Riboflavin deficiency may increase the risk of preeclampsia in pregnant women. Deficiency of riboflavin during pregnancy can result in fetalbirth defects, including heart and limb deformities.
Risk factors
People at risk of having low riboflavin levels include alcoholics, vegetarian athletes, and practitioners of veganism. Pregnant or lactating women and their infants may also be at risk, if the mother avoids meat and dairy products. Anorexia and lactose intolerance increase the risk of riboflavin deficiency. People with physically demanding lives, such as athletes and laborers, may require higher riboflavin intake. The conversion of riboflavin into FAD and FMN is impaired in people with hypothyroidism, adrenal insufficiency, and riboflavin transporter deficiency.
Causes
Riboflavin deficiency is usually found together with other nutrient deficiencies, particularly of other water-soluble vitamins. A deficiency of riboflavin can be primary (i.e. caused by poor vitamin sources in the regular diet) or secondary, which may be a result of conditions that affect absorption in the intestine. Secondary deficiencies are typically caused by the body not being able to use the vitamin, or by an increased rate of excretion of the vitamin. Diet patterns that increase risk of deficiency include veganism and low-dairy vegetarianism. Diseases such as cancer, heart disease and diabetes may cause or exacerbate riboflavin deficiency.
There are rare genetic defects that compromise riboflavin absorption, transport, metabolism or use by flavoproteins. One of these is riboflavin transporter deficiency, previously known as Brown–Vialetto–Van Laere syndrome. Variants of the genes SLC52A2 and SLC52A3 which code for transporter proteins RDVT2 and RDVT3, respectively, are defective. Infants and young children present with muscle weakness, cranial nerve deficits including hearing loss, sensory symptoms including sensory ataxia, feeding difficulties, and respiratory distress caused by a sensorimotoraxonalneuropathy and cranial nerve pathology. When untreated, infants with riboflavin transporter deficiency have labored breathing and are at risk of dying in the first decade of life. Treatment with oral supplementation of high amounts of riboflavin is lifesaving.
The assessment of riboflavin status is essential for confirming cases with non-specific symptoms whenever deficiency is suspected. Total riboflavin excretion in healthy adults with normal riboflavin intake is about 120 micrograms per day, while excretion of less than 40 micrograms per day indicates deficiency. Riboflavin excretion rates decrease as a person ages, but increase during periods of chronic stress and the use of some prescription drugs.
Indicators used in humans are erythrocyteglutathione reductase (EGR), erythrocyte flavin concentration and urinary excretion. The erythrocyte glutathione reductase activity coefficient (EGRAC) provides a measure of tissue saturation and long-term riboflavin status. Results are expressed as an activity coefficient ratio, determined by enzyme activity with and without the addition of FAD to the culture medium. An EGRAC of 1.0 to 1.2 indicates that adequate amounts of riboflavin are present; 1.2 to 1.4 is considered low, greater than 1.4 indicates deficient. For the less sensitive "erythrocyte flavin method", values greater than 400 nmol/L are considered adequate and values below 270 nmol/L are considered deficient. Urinary excretion is expressed as nmol of riboflavin per gram of creatinine. Low is defined as in the range of 50 to 72 nmol/g. Deficient is below 50 nmol/g. Urinary excretion load tests have been used to determine dietary requirements. For adult men, as oral doses were increased from 0.5 mg to 1.1 mg, there was a modest linear increase in urinary riboflavin, reaching 100 micrograms for a subsequent 24-hour urine collection.Beyond a load dose of 1.1 mg, urinary excretion increased rapidly, so that with a dose of 2.5 mg, urinary output was 800 micrograms for a 24-hour urine collection.
History
The name "riboflavin" comes from "ribose" (the sugar whose reduced form, ribitol, forms part of its structure) and "flavin", the ring-moiety that imparts the yellow color to the oxidized molecule (from Latin flavus, "yellow"). The reduced form, which occurs in metabolism along with the oxidized form, appears as orange-yellow needles or crystals. The earliest reported identification, predating any concept of vitamins as essential nutrients, was by Alexander Wynter Blyth. In 1879, Blyth isolated a water-soluble component of cows' milk whey, which he named "lactochrome", that fluoresced yellow-green when exposed to light.
In the early 1900s, several research laboratories were investigating constituents of foods, essential to maintain growth in rats. These constituents were initially divided into fat-soluble "vitamine" A and water-soluble "vitamine" B. (The "e" was dropped in 1920.) Vitamin B was further thought to have two components, a heat-labile substance called B1 and a heat-stable substance called B2. Vitamin B2 was tentatively identified to be the factor necessary for preventing pellagra, but that was later confirmed to be due to niacin (vitamin B3) deficiency. The confusion was due to the fact that riboflavin (B2) deficiency causes stomatitis symptoms similar to those seen in pellagra, but without the widespread peripheral skin lesions. For this reason, early in the history of identifying riboflavin deficiency in humans the condition was sometimes called "pellagra sine pellagra" (pellagra without pellagra).
In 1935, Paul Gyorgy, in collaboration with chemist Richard Kuhn and physician T. Wagner-Jauregg, reported that rats kept on a B2-free diet were unable to gain weight. Isolation of B2 from yeast revealed the presence of a bright yellow-green fluorescent product that restored normal growth when fed to rats. The growth restored was directly proportional to the intensity of the fluorescence. This observation enabled the researchers to develop a rapid chemical bioassay in 1933, and then isolate the factor from egg white, calling it ovoflavin. The same group then isolated the a similar preparation from whey and called it lactoflavin. In 1934, Kuhn's group identified the chemical structure of these flavins as identical, settled on "riboflavin" as a name, and were also able to synthesize the vitamin.
Circa 1937, riboflavin was also referred to as "Vitamin G". In 1938, Richard Kuhn was awarded the Nobel Prize in Chemistry for his work on vitamins, which had included B2 and B6. In 1939, it was confirmed that riboflavin is essential for human health through a clinical trial conducted by William H. Sebrell and Roy E. Butler. Women fed a diet low in riboflavin developed stomatitis and other signs of deficiency, which were reversed when treated with synthetic riboflavin. The symptoms returned when the supplements were stopped.
