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Bubber, Parvesh
- Effect of Thiamine Nutritional Deficiency on the Energy Metabolism and Neurotransmission in Mice Brain
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Affiliations
1 Department of Bio Science and Bio Technology, Banasthali University, Banasthali, Distt-Tonk, Rajasthan, IN
2 Biochemistry Discipline, School of Sciences, IGNOU, Maidan Garhi, New Delhi - 110 068, IN
1 Department of Bio Science and Bio Technology, Banasthali University, Banasthali, Distt-Tonk, Rajasthan, IN
2 Biochemistry Discipline, School of Sciences, IGNOU, Maidan Garhi, New Delhi - 110 068, IN
Source
The Indian Journal of Nutrition and Dietetics, Vol 54, No 4 (2017), Pagination: 414-426Abstract
Thiamine or vitamin B1 has an antioxidant property. It plays a vital role in energy metabolism as it is directly or indirectly involved in the metabolism of lipids, glucose, amino acids and neuro transmitters. Present study emphasizes the role of thiamine deficiency (TD) on the mitochondrial enzymes involved in energy metabolism and neurotransmission. The study was carried out on Mus musculus in three groups, namely control and thiamine-deficient group for 8 (TD 8, group II) and 10 (TD 10, group III) days. Activity of TCA cycle enzymes such as succinate dehydrogenase (SDH), malate dehydrogenase (MDH) and fumarase were measured along with the activity of enzyme acetylcholine esterase (Ach E) involved in the release of neurotransmitter. These biochemical changes were further correlated with histopathological changes in TD. A significant decrease in the enzymatic activity of SDH was found in group II (p<.05) and group III (p<.001) in comparison to the control group. Similarly a significant reduction in the enzymatic activity of MDH (p<0.0001) in the TCA cycle was also found in group III (TD 10). Fumarase levels were also found to be low in both the treated groups in comparison to the control. ACh E activity was also found to be decreased in group II (p<.05) and group III (p<.001) in comparison to the control group. Histopathological analysis via transmission electron microscopy (TEM) showed neurodegenerative features in the brain of thiamine deficient mice. Diminished activity of mitochondrial enzymes and ACh E suggests impairment in energy metabolism and disturbances in the release of neurotransmitter during TD. Pathological changes were also in conformity with the fact that TD impedes metabolism and its prolong impairments would further diminish brain functions. The present results suggest nutritional corrections with thiamine might lead to the improvement from neurological disorders or neurodegenerative conditions.Keywords
Thiamine Deficiency, Energy Metabolism, Neurotransmitter, Neurological Disorders.
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