Vitamin Bl deficiency

Harper, C., 2006. Thiamine (vitamin Bl) deficiency and associated brain damage is still common throughout the world and prevention is simple and safe European Journal of Neurology. 13 1078-1082. 

Wernickes encephalopathy (WE) due to thiamine (vitamin Bl) deficiency can lead to significant brain damage. 

Thiamin has a sulfur atom incorporated in the ring structure of its molecule. The compound constitutes vitamin Bl, important for many bodily functions. In children it is required for growth. Vitamin Bl deficiency may result in beriberi. 

The pyruvate dehydrogenase complex consists of three eniymes that catalyse the irreversible production of acetyl CoA from pyruvate and CoA. In aerobic conditions the NADH formed by the reaction can be oxidized in the electron transport chain. Thiamine pyrophosphate is a derivative of thiamin (vitamin Bl). Deficiency of vitamin Bl leads to a build up of pyruvate. The extra pyruvate is converted to lactate, creating an acidosis. 

The receptor for RANKL is RANK, also known as ODAR (Anderson et al. 1997 Hsu et al. 1999). RANK is expressed in osteoclast precursors, mature osteoclasts, condrocytes, fibroblasts, and immune system cells (Anderson et al. 1997 Hsu et al. 1999). The binding of RANKL with RANK on preosteoclasts initiates the OCS and the activation of osteoclasts (Anderson et al. 1997 Hsu et al. 1999 Nakagawa et al. 1998). RANK-deficient mice display a phenotype characterized by osteopetrosis and several defects in the immune system similar to that observed in RANKL-deficient mice (Dougall et al. 1999). Consistent with this hypothesis, RANK-deficient mice are resistant to bone resorption induced by TNF-a, IL-l/J, or vitamin D3 (Li et al. 2000). In agreement with this, mice deficient in molecules implied in the transduction pathway from RANK like TRAF-6 or NF-/c Bl/NK-/c B2 also show an osteopetrotic phenotype,... 

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