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"Child`s Health" 1 (69) 2016

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Clinical Significance of Excess Lactose in the Diet (part 1)

Authors: Abaturov A.Ye., Nikulinа A.A. - SE «Dnipropetrovsk Medical Academy of Health Ministry of Ukraine», Dnipropetrovsk; Demydenko Yu.V. - PI «Pavlograd City Hospital № 4» of Dnipropetrovsk Regional Council, Ukraine

Categories: Pediatrics/Neonatology

Sections: Clinical researches

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Summary

В статье на основании литературных источников представлены статистические данные среднегодовых уровней потребления лактозы в странах мирового сообщества, рассмотрено клиническое значение избыточного содержания лактозы в диете в зависимости от полиморфизма гена лактазы. Лактоза — основной источник энергии для детей первых месяцев жизни, который обеспечивает около 40–45 % суточной энергетической потребности организма ребенка. Нарушение всасывания лактозы (мальабсорбция), при дефиците фермента лактазы, сопровождается симптомами лактозной интолерантности. Интерес к изучению иммуномодулирующего влияния β-галактозида лактозы связан с подав­лением ею галектина 9 (Gal-9), регулирующего Т-клеточные иммунные реакции с участием Т-хелперных клеток 1-го и 17-го типов (Тh1, Тh17) и Т-регуляторных лимфоцитов (Treg), которые вовлечены во многие иммуноопосредованные заболевания человека. Галектин 9 — представитель класса галектинов типа «тандем-повтора». Наиболее высокий уровень экспрессии LGALS9 наблюдается в тканях толстого кишечника, легких, костном мозге, лимфоузлах, тимусе, печени, почках, эндокринных железах, плаценте, коже, гладких мышцах, жировой ткани.

У статті на підставі літературних джерел наведені статистичні дані середньорічних рівнів споживання лактози в країнах світового співтовариства, розглянуто клінічне значення надмірного вмісту лактози в дієті залежно від поліморфізму гена лактази. Лактоза — основне джерело енергії для дітей перших місяців життя, що забезпечує близько 40–45 % добової енергетичної потреби організму дитини. Порушення всмоктування лактози (мальабсорбція), при дефіциті ферменту лактази, супроводжується симптомами лактозної інтолерантності. Інтерес до вивчення імуномодулюючого впливу β-галактозиду лактози пов’язаний з інгібіцією нею галектину 9 (Gal-9), що регулює Т-клітинні імунні реакції за участю Т-хелперних клітин 1-го і 17-го типів (Тh1, Тh17) і Т-регуляторних лімфоцитів (Treg), що залучені до численних імуноопосередкованих захворювань людини. Галектин 9 — представник класу галектинів типу «тандем-повтору». Найбільш високий рівень експресії LGALS9 спостерігається в тканинах товстого кишечника, легенів, кісткового мозку, лімфовузлів, тимуса, печінки, нирок, ендокринних залоз, плаценти, шкіри, гладких м’язів, жирової тканини.

In the article on the basis of the literature there has been considered the statistics of average consumption of lactose in the countries of the world community, reviewed the clinical significance of the excess lactose in the diet depending on the polymorphism of the lactase gene. Lactose is the main source of energy for the children of the first months of life, which provides about 40–45 % of the daily energy needs of a body of a child. Lactose malabsorption, deficiency of the enzyme lactase is accompanied by symptoms of lactose intolerance. Interest in the study of the influence of an immunomodulatory β-galactoside lactose was caused by the suppression of its galectin 9 ­(Gal-9), the regulatory T-cell immune response involving T-helper cells 1 and 17 (Th1, Th17) and regulatory T-lymphocytes (Treg), which are involved in many immune-mediated human disea­ses. Galectin 9 is the representative of the class of galectins such as «tandem repeat». The highest level of LGALS9 expression is observed in the tissues of colon, lung, bone marrow, lymph nodes, thymus, liver, kidney, endocrine glands, placenta, skin, smooth muscle, adipose tissue.


Keywords

лактоза, полиморфизмы LCT, галектин 9, воспаление, экзогенная лактаза.

лактоза, поліморфізми LCT, галектин 9, запалення, екзогенна лактаза.

lactose, LCT polymorphisms, galectin 9, inflammation, exogenous lactase.

In the article on the basis of the literature presents the statistics of average consumption levels of lactose in the countries of the world community, reviewed the clinical significance of the excess lactose in the diet depending on the polymorphism of the lactase gene. Lactose - the main source of energy for the children of the first months of life, which provides about 40-45% of the daily energy needs of the body of the child.

Lactose malabsorption (malabsorption) accompanied by symptoms of lactose intolerance, which is characterized by the appearance of abdominal pain and indigestion within 30 minutes after consumption of lactose products and does not occur with the use of placebo. Exclusion of milk and dairy products improves the health of the child, but is problematic in infancy, when containing up to 7% lactose, breast milk is the main source of supply, ensuring the child's body with all necessary nutrients, including calcium bioequivalent. Lactose - β-galactoside, a molecule that hydrolyzes into two freely absorbed in the small intestine monosaccharide -D-glucose and D-galactose by the action of a single enzyme in mammals - lactase. Activation of the synthesis of lactase in the intestine of the fetus takes place from 8 weeks of gestation, reaching a maximum level in the secretion of breast-month period 2-4. The level of gene transcription is controlled by LCT located next to cis -regulatory element MCM6 (minichromosome maintenance complex component 6). There are two main options polymorphism enhancer MCM6, are fully associated with lactose tolerance biochemically verified. One of them is a substitution of cytosine (C) thymidine (T) at position -13910 approximately 14 kb from the locus of LCT, which saves the production of lactase in their lifetime. The second polymorphism mapped to 8 kb closer to the telomeric portion of chromosome - in the position of -22018; characterized by a guanine (G) to adenine (A). Homozygous carriers of variant T/T 13910 or A/A 22018 have lactose tolerance throughout life and the ability to consume dairy products without the risk of the development of clinical symptoms of lactose intolerance. The genotype C/T-13910 is associated with a moderate production of lactase persistence and propensity to develop secondary lactase deficiency (LD).

Homozygous carriers of variant C/C or G/G are not able to digest lactose (level synthesis of mRNA LCT reduced from 2 to 10%) and characterized by a primary lactase LD adult type. Unsplit lactose in the small intestine, is supplied in excess to the colon, where under the action of β-galactosidases of lactic acid bacteria is transformed into straight-chained fatty acids (acetate, propionate, butyrate). Formed at hypolactasia toxic metabolites (ethanol, acetone, butane-2,3-diol, acids, and aldehydes, methylglyoxal namely, acetaldehyde, protein toxins) alter cellular metabolism. Interest in the study of the influence of an immunomodulatory β-galactoside lactose associated with the suppression of its galectin-9 (Gal-9), the regulatory T cell immune response involving T- helper cells 1 and 17 kinds (Th1, Th17) and regulatory T-lymphocytes (Treg), which are involved in many immune-mediated human diseases.

Galectin 9 - the representative of the class of galectins such as "tandem repeat". The highest level of expression observed in the tissues LGALS9 colon, lung, bone marrow, lymph nodes, thymus, liver, kidney, endocrine glands, placenta, skin, smooth muscle, adipose tissue. Activating factor inducible gene expression LGALS9, are cytokines associated with Th1- response, particularly interferon-γ (IFN-γ). Under the influence of IFN-γ mRNA levels Gal-9 is increased by 22 times. Active producers of Gal-9 are: CD14+ -cell (monocytes); CD33+ -promieloсytes, CD56+ -cells (natural killer cells), CD19+ cells (B-lymphocytes), CD34+ -cells, BDCA4+ -cells CD4+ -cells and CD8+ -cells, CD4+ CD25+ Foxp3+ -cells, eosinophils, and CD71+ - early erythroides, fibroblasts, APUD cell, Kupffer cells, enterocytes.


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