Thiamine Vitamin B1 Metabolism Functions Deficiency

Thiamine is a water-soluble vitamin, Vitamin B1, and serves as a cofactor for enzymes with Mitochondrial localization. Since it is not endogenously synthesized, the available dietary sources of thiamine are beef, poultry, nuts, cereals, and nuts. It plays a critical function in oxidative and nonoxidative carbohydrate metabolism in the energy transformation process. Other functions of thiamine are the antioxidation effect on neurotrophins, which oppresses oxidative stress-induced activation that plays a critical role in activating the immune system, signaling and maintenance in cells, and cell uptake mechanisms.1 Intestinal enzyme phosphate Hydrolyzes thiamine into a free form absorbed in the small intestines. The Phosphorylated is stored in the heart, kidneys, brain, and liver. Thiamine has a half-life of 1 to 12 hours and can be stored in the body between 14 to 18 days. Consequently, regular dietary intake is necessary to avoid the development of a deficiency.

The recommended thiamine intake differs with age and gender but a standard intake of 1.2mg/day among men and 1.1mg/day for women with increments to 1.4 mg/day for pregnancy and lactation, respectively.3. Regular intake is imperative to maintain the correct thiamine levels in the body. The intestinal uptake of thiamine is regulated by a molecular mechanism that involves thiamine transporters-1 and -2, which are products of Solute Carrier Family 19 Member 2 (SLC19A2) and genes. SLC19A2 encodes thiamine transporter 1 (THTR1) across cell membranes. The homozygous mutation of thiamine cause thiamine responsive megaloblastic anemia, sensorineural deafness, and diabetes. Therefore, thiamine deficiency results in insulin secretion in conjunction with mitochondrial dysfunction, cell cycle arrest, and the loss of immunity against oxidative stress.

In the blood system, the thiamine diphosphokinase enzyme converts thiamine into its active form, thiamine pyrophosphate (TPP), which plays different roles during metabolisms such as glucose, Krebs cycle, pentose phosphate pathway, and metabolism. During the preparation of diets, a considerable loss of thiamine is caused during cooking or heat-induced food processing. In countries where there is a large dependence on processed foods on day-to-day basis results in thiamine deficiency.2 Processed foods have a high caloric density, but lack recommended dietary guidelines for micronutrients intake. This condition is referred to as high-calorie malnutrition. More than 29% of the obese individuals who undergo bariatric surgery are thiamine deficient. Different states of thiamine play indifferent roles in intercellular synthesis. Thiamine monophosphate frees thiamine into the intercellular synthesis of thiamine triphosphate and diphosphate

TPP activates decarboxylation of pyruvate during the pyruvate dehydrogenase complex. The complex involves a group of cofactors and enzymes from acetyl CoA that condenses with oxaloacetate forming citrate, the first compound in the citric acid cycle. Since pyruvate is formed from the breakdown of glucose through the Embden–Meyerhof pathway. In the critic acid cycle, it also plays a linking role as a decarboxylating component of alpha-ketoglutarate dehydrogenase.3 Thiamine triphosphate appears in the neurophysiological function localized in the cell membrane structure. Thiamine triphosphate (TTP) acts as an activator of chloride channels with high conductance. As established, thiamine deficiency results in various disorders, such as Korsakoff’s Syndrome, Alzheimer’s Disease (AD), diabetes mellites, depression, and Polyneuropathy, that affect cell physiology or cognitive functions.

Thiamine can be administered orally, intramuscularly, or intravenously. The administration is useful in treating congestive heart failure, Alzheimer’s disease, and cataracts. The administration of thiamine orally is not recommended since it is not adequate for symptomatic patients. Intravenous administration is considered the best option since the administration of 100mg thiamine for one to two weeks or until improvement or symptoms clear, eliminating risks associated with oral intake.2 Intramuscular supplementation with thiamine is considered for patients who do not have IV access during an emergency.