MULTİPL SKLEROZ’DA K VİTAMİNİNİN ROLÜ VAR MIDIR?

Year 2020, Volume: 21 Issue: 4, 362 - 369, 14.10.2020

Merve Özdemir , Aylin Ayaz

https://doi.org/10.18229/kocatepetip.605508

Cited By: 1

Abstract

Multipl skleroz, etiyolojisi bilinmeyen inflamatuar ve nörodejeneratif bir hastalıktır. Hasta bireylerde, zamanla ilerleyen nörolojik bozulma ile takip edilen, geri dönüşümlü dönemler ile karakterize olan merkezi sinir sisteminin kronik bir demiyelinizan hastalığıdır. Tipik olarak 20-45 yaş arası yetişkinlerde görülmekle birlikte, kadınlarda erkeklerden iki kat daha fazla görülmektedir. Belirtilen semptomlar arasında uyuşukluk, halsizlik, görme bozukluğu, denge kaybı, baş dönmesi, yorgunluk ve depresyon bulunmaktadır. Vitaminlerin, vücutta farklı işlevlere sahip önemli mikro besinler olarak multipl skleroz patogenezinde önemli rolleri vardır. İn vitro, in vivo ve insan çalışmaları, bazı vitaminlerin multipl skleroz oluşumunda veya ilerlemesinde koruyucu rolünü desteklemektedir. Kan pıhtılaşmasındaki klasik rolünün dışında, K vitamini merkezi sinir sisteminin fizyolojisinde görev alan yağda çözünen bir besin ögesidir. K vitamini özellikle nöronal proliferasyon, farklılaşma, yaşlanma, transformasyon ve hücre-hücre etkileşiminde rol oynayan miyelin kılıfı ve nöron membranlarının temel bir bileşeni olan sfingolipidlerin sentezini düzenlemektedir. K vitamini ayrıca nöron fizyolojisi ve sağ kalımı etkileyen K vitamini bağımlı proteinlerin biyolojik olarak aktivasyonunu da kontrol etmektedir. K vitamini beyinde yüksek oranlarda bulunmakta ve sülfatid metabolizmasının düzenlenmesinde rol oynamaktadır. Deney hayvanları üzerinde yapılan çalışmalar, beyinde yüksek konsantrasyonlarda bulunan sfingolipidlerin biyosentezinde K vitamini rolünü desteklemektedir. Farelerde ve sıçanlarda, K vitamini eksikliğinin beyinde sülfatid seviyelerini düşürdüğü ve davranışsal değişikliklere neden olduğu belirtilmiştir. Bu derlemede yağda çözünen vitaminlerden olan ve beyinde sfingolipidlerin sentezine katılan K vitaminin multipl skleroz patogenezi, progresyonu ve tedavisindeki rolünün değerlendirilmesi amaçlanmıştır.

Keywords

Multipl Skleroz, K vitamini, sfingolipid, miyelinizasyon

DOES VITAMIN K PLAY A ROLE IN MULTIPLE SCLEROSIS?

Abstract

Multiple sclerosis is an inflammatory and neurodegenerative disease of unknown etiology. In most patients, it is characterized by reversible periods followed by a progressive neurological deterioration. It is typically seen in adults between the ages of 20 and 45. It is twice as common in women than in men. Symptoms include drowsiness, weakness, visual impairment, loss of balance, dizziness, fatigue and depression. Vitamins have important roles in the pathogenesis of multiple sclerosis as important micronutrients with different functions in the body. In vitro, in vivo, and human studies support the protective role of certain vitamins in the formation or progression of multiple sclerosis. Apart from its classic role in blood clotting, vitamin K is a fat-soluble nutrient involved in the physiology of the central nervous system. Vitamin K specifically regulates the synthesis of sphingolipids, major components of myelin sheath and neuron membranes, which play a role in neuronal proliferation, differentiation, aging, transformation and cell-cell interaction. Vitamin K also controls the biological activation of vitamin K-dependent proteins that affect neuronal physiology and survival. Vitamin K is found in high levels in the brain and plays a role in the regulation of sulfatide metabolism. Studies on experimental animals support the role of vitamin K in the biosynthesis of high concentrations of sphingolipids in the brain. In mice and rats, vitamin K deficiency has been reported to reduce sulfatide levels in the brain and cause behavioral changes. In this review, we aimed to evaluate the role of vitamin K, one of the fat soluble vitamins and involved in the synthesis of sphingolipids in the brain, in the pathogenesis, progression and treatment of multiple sclerosis.

Keywords

Multiple Sclerosis, Vitamin K, Sphingolipid, Myelination

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