Precursor of the biologically active form called thiamine pyrophosphate (TPP), this essentially plays the role of coenzyme of various cellular processes.
Provided both from plant foods and from the animal kingdom, thiamine is widespread, but not particularly abundant in the diet; it is absorbed in the small intestine, a process hindered by ethyl alcohol, and transported throughout the body by the bloodstream. It is mainly concentrated in the organs.
The deficiency typically causes beriberi or similar syndromes, an eventuality that can be avoided by taking about 0.4 mg per 1000 kcal. Toxicity is unlikely, especially with food alone.
Let's go into detail.
and of an amino group.
Thiamine is chemically structured from a derivative of pyrimidine and thiazole, linked by a methylene group.
In vivo, is subjected to phosphorylation to obtain mono-di- and tri-phosphate; thiamine pyrophosphate (TPP) - obtained thanks to the thiamine-pyrophosphate synthetase enzyme - is considered the biologically active form.
; at low concentrations (<2 mg / L) this occurs via the active transport mechanism, while at higher densities it takes advantage of passive diffusion.The process can be inhibited by the excessive consumption of alcoholic beverages, due to an increase in the intestinal alcohol level.
, kidneys, liver, brain and skeletal muscles; compared to the organs, the latter are proportionally poorer in the vitamin but, given the considerably higher mass, they contain about 40% of the total.
Phosphorylation of thiamine to TPP occurs in all tissues and mainly in the liver. The process, as we have anticipated, is catalyzed by a specific enzyme called thiamine-pyrophosphate synthase, which intervenes by transferring a pyrophosphate from ATP to the hydroxyl group of the vitamin.
Any excess with respect to requirements is rapidly eliminated in the urine as such or suitably degraded.
Employee TPPs are:
- Pyruvic dehydrogenase: converts pyruvic acid into acetyl-CoA;
- α-ketoglutaric-dehydrogenase: which transforms α-ketoglutarate into succinyl CoA;
- Dehydrogenase of branched-chain α-ketoacids: transforms the latter into the corresponding acyl CoA.
Oxidative decarboxylation reactions occur only in the presence of coenzyme A (CoA), lipoic acid and NAD; decarboxylase binds TPP, transacetylase binds lipoic acid and FAD dependent dehydrogenase regenerates reduced lipoic acid.
The transketolase present in the cytoplasm transfers a glycoaldehyde group from some α-keto sugars (xylulose 5-P, sedoheptulose 7-P etc.) to carbon 1 (C1) of some aldoses; it acts in a reaction of the pentose phosphate pathway for the oxidation of glucose.
A role of thiamine other than coenzyme has been observed in nerve cells, where the active form appears to be TTP; this would be hydrolyzed following a nerve stimulus and would modify the permeability of the Cl ˉ channels.
, cardio-circulatory and nervous; the symptoms vary subjectively, also depending on the diet, but generally they are all always present.The overt thiamine deficiency determines beriberi which can manifest itself in three different forms:
- dry beriberi or neuritic;
- edematous wet beriberi;
- cerebral beriberi.
This disease, before taking on a precise physiognomy, manifests itself with inappetence, asthenia, gastrointestinal disorders, edema (at times), sensitivity disorders, uncertainty in movements, pain and muscle spasms.
Dry beriberi is characterized by polyneuritis, which begins with walking problems and evolves towards a flaccid, symmetrical paralysis, especially in the lower limbs, with complications of muscle atrophy and disappearance of tendon reflexes; cardiovascular alterations are quite frequent but of little entity.
In humid beriberi, cardiovascular and respiratory symptoms take over with tachycardia, exertional dyspnea, palpitations, followed by homogeneous cardiomegaly (radiological investigation) and specific signs of heart failure in the form of edema may occur; heart failure can lead to sudden death.
Cerebral beriberi is the most frequent form in industrialized countries associated with alcohol abuse (Wernicke-Korsakoff syndrome or Wernicke encephalopathy). It is characterized by psychic signs (space-time disorientation, apathy, confusion, numbness), neurological manifestations (ophthalmoplegia, ataxia, nystagmus) and is often associated with polyneuropathy.
Beriberi can also occur in infants (2 ÷ 6 months of life), especially if breastfed by mothers lacking in thiamine, with anorexia, vomiting, diarrhea, sleep disturbances, cyanosis, tachycardia, convulsions. It has a fulminant course, due to heart failure, if you do not intervene quickly with adequate treatment.
, higher doses can cause headaches, convulsions, weakness, cardiac arrhythmia and allergic reactions.
Two thiamine antagonist enzymes have been discovered in animal and plant tissues: thiaminase I and thiaminase II. Thiaminase I is responsible for some cases of hypovitaminosis in countries where raw fish is consumed and for Chastek's paralysis, which affects minks and foxes fed on animal viscera. Thiaminase II, produced mainly by intestinal bacteria, can in some cases also cause hypovitaminosis.
(in particular swine), offal, eggs, cereals (which are the main source for many populations) and legumes.Whole grains are richer in thiamine as it is concentrated mainly in the pericarp and in the perisperm of the caryopsis, which are instead eliminated during grinding and sifting.
In parboiled rice the content of thiamin is higher than in polished rice, because before refining it is subjected to a technological process that allows the transfer of the vitamin from the outer layers towards the endosperm.
and in detail that of carbohydrates, also taking into account the difficulty in reaching the recommended ration, the latter refers to the energy intake and more precisely to 1,000 kcal of the ration.
According to the LARN (Recommended Nutrient Intake Levels for the Italian population) the recommended ration is 0.4 mg / 1,000 kcal, with the recommendation not to drop below 0.8 mg in adults with an energy intake <2,000 kcal / day.
