Thiamine (
Vitamin B1) is considered an essential
micronutrient for humans; its deficient intake brings about the
Wernicke-Korsakoff syndrome (
encephalopathy and
psychosis) or
beriberi (a neurological and
cardiovascular disease). Once
thiamine enters the cells it is phosphorylated by
thiamine pyrophosphokinase (TPPK), and converted into the
coenzyme thiamine pyrophosphate (TPP), the active form of
thiamine. TPP is a relevant cofactor for
transketolase (TK), α-ketoglutarate
dehydrogenase (αKDH), and
pyruvate dehydrogenase (PDH), all these
enzymes are fundamental for
glucose metabolism.
Diabetes mellitus (DM), however, is considered both a deficient
thiamine and deficient energy state, as a consequence of the limited TPP synthesis. Recent evidences have shown that the administration of
thiamine or
lipid-soluble derivatives, such as
benfotiamine (developed to improve the bioavailability of
thiamine), has positive effects in the diabetic patient (after
thiamine is transformed into TPP). For this reason, administration of supplements with TPP in the diabetic patients is recommended to avoid complications, like neuropathy and nephropathy. It has been suggested that these beneficial effects are a consequence of the activation of TK (
pentose pathway) or the PDH complex in mitochondria.
Nitric oxide (NO) is synthesized by the endothelial cell and is also an important
element for the viability and functionality of this cell type. However, in the DM patient, a deficient synthesis of NO has been reported. It is relevant to mention that recent evidences have led to propose mitochondrial activity as an important regulator of
nitric oxide synthesis (ON). We consider that the exogenous administration of TPP facilitates the utilization of this molecule, regulating some metabolic processes such as phosphorylation of
thiamine by TPPK, energy consumption (
ATP), as well as mitochondrial activity, inducing eventually NO synthesis. If this is confirmed, the administration of TPP to the diabetic patient would provide additional protection to endothelial cells, reducing the risk of vascular damage, to which the diabetic patient is highly susceptible.