Effects of thiamine and benfotiamine on intracellular glucose metabolism and relevance in the prevention of diabetic complications.
ABSTRACT Thiamine (vitamin B1) is an essential cofactor in most organisms and is required at several stages of anabolic and catabolic intermediary metabolism, such as intracellular glucose metabolism, and is also a modulator of neuronal and neuro-muscular transmission. Lack of thiamine or defects in its intracellular transport can cause a number of severe disorders. Thiamine acts as a coenzyme for transketolase (TK) and for the pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase complexes, enzymes which play a fundamental role for intracellular glucose metabolism. In particular, TK is able to shift excess fructose-6-phosphate and glycerhaldeyde-3-phosphate from glycolysis into the pentose-phosphate shunt, thus eliminating these potentially damaging metabolites from the cytosol. Diabetes might be considered a thiamine-deficient state, if not in absolute terms at least relative to the increased requirements deriving from accelerated and amplified glucose metabolism in non-insulin dependent tissues that, like the vessel wall, are prone to complications. A thiamine/TK activity deficiency has been described in diabetic patients, the correction of which by thiamine and/or its lipophilic derivative, benfotiamine, has been demonstrated in vitro to counteract the damaging effects of hyperglycaemia on vascular cells. Little is known, however, on the positive effects of thiamine/benfotiamine administration in diabetic patients, apart from the possible amelioration of neuropathic symptoms. Clinical trials on diabetic patients would be necessary to test this vitamin as a potential and inexpensive approach to the prevention and/or treatment of diabetic vascular complications.
SourceAvailable from: scielo.clRevista medica de Chile 12/2012; 140(12):1593-1605. DOI:10.4067/S0034-98872012001200012 · 0.37 Impact Factor
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ABSTRACT: The purpose of this study was to find the effect of endurance training and thiamine supplementation on anti-fatigue during the exercise. Each nine students from K Women's University went through three cross-over treatments: placebo treatment, training treatment and thiamine treatment. Training treatment was performed with bicycle ergometer exercise for four weeks (five days per week). Each exercise was performed for an hour with intensity set at 70% (50rpm) of maximal oxygen uptake. Thiamine treatment group was given 10mg of thiamine tetrahydrofurfuryl disulfide per one kilogram for four weeks. The bicycle ergometer exercise was performed at 70% of maximal oxygen uptake in exercise intensity which 60 minutes of exercise was performed at 50rpm . Lactate concentration was significantly decreased during 15 to 30 minutes of exercise for those with training treatment and 15 to 60 minutes of exercise for those with thiamine treatment compared to placebo treatment group. Ammonia concentration was significantly decreased during 15 to 60 minutes of exercise and 15 to 30 minutes of recovery for those with training and thiamine treatment compared to placebo treatment. Resting blood thiamine concentrations of placebo treatment were significantly lower than training treatment. 60 minutes after the exercise, plasma thiamine concentration was significantly increased in all treatment group. To sum up the previous, thiamine intake during exercise positively benefits carbohydrate metabolism in a way that will decrease lactate concentration, ammonia concentration, and anti- fatigue by reducing the RPE. Therefore, we can consider thiamine intake to be utilized as similar benefits as endurance training.
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ABSTRACT: Objective Refeeding syndrome can occur in several contexts of relative malnutrition in which an overaggressive nutritional support is started. The consequences are life-threatening with multiorgan impairment, and severe electrolyte imbalances. During refeeding, glucose-involved insulin secretion causes abrupt reverse of lipolysis and a switch from catabolism to anabolism. This creates a sudden cellular demand of electrolytes (phosphate, potassium and magnesium) necessary for ATP synthesis, glucose transport and other synthesis reactions, resulting in decreased serum levels. Laboratory findings and multiorgan impairment similar to refeeding syndrome are also observed in acute thiamine deficiency. Methods We describe two patients with leukemia who developed acute thiamine deficiency with an electrolyte pattern suggestive of refeeding syndrome, severe lactic acidosis and evidence of proximal renal tubular dysfunction. Results A single thiamine administration led to rapid resolution of the tubular dysfunction and normalization of acidosis and electrolytes imbalance. This demonstrated that thiamine deficiency was responsible for the electrolyte imbalance, caused by tubular electrolytes losses. Conclusions Our report indicates that, despite sharing many laboratory similarities, refeeding syndrome and acute thiamine deficiency should be viewed as separate entities in which the electrolyte abnormalities reported in cases of refeeding syndrome with thiamine deficiency and refractory lactic acidosis may be due to a renal tubular losses instead of a shifting from extracellular to intracellular compartment. In oncologic and malnourished patients, categories at particular risk of developing refeeding syndrome, in presence of these biochemical abnormalities, acute thiamine deficiency should be suspected and treated, because it promptly responds to thiamine administration.Nutrition 07/2014; 30(7-8). DOI:10.1016/j.nut.2014.02.019 · 3.05 Impact Factor