scholarly journals Developmental maturation of the colonic uptake process of the microbiota-generated thiamin pyrophosphate

Author(s):  
Subrata Sabui ◽  
Jose M Romero ◽  
Hamid M Said

The water-soluble vitamin B1 is essential for normal human health and physiology. In its main biologically active form, i.e., thiamin pyrophosphate (TPP), the vitamin plays many critical roles in cell metabolism; thus, its deficiency leads to a variety of adverse effects. Humans/mammals obtain vitamin B1 from two exogenous sources: diet and gut microbiota. Considerable amount of the microbiota-generated vitamin B1 exists in the form of TPP, and colonocytes can efficiently absorb this TPP via a high-affinity and specific carrier-mediated mechanism that involves the recently cloned colonic TPP transporter (cTPPT; product of SLC44A4 gene). There is nothing currently known about colonic uptake of TPP during early stages of life, and whether the process undergoes developmental regulation. We addressed this issue using the mouse as animal model. Our results showed that colonic uptake of TPP undergoes developmental up-regulation as the animal moves from the suckling period to weanling and adulthood. This up-regulation in uptake was found to be associated with a parallel induction in level of expression of the cTPPT protein, mRNA and heterologous nuclear RNA (hnRNA), suggesting possible involvement of transcriptional mechanism(s). We also found a parallel up-regulation in level of expression of the two nuclear factors that drive activity of the SLC44A4 promoter (i. e., CREB-1 and Elf-3) with maturation. These results demonstrate, for the first time, that colonic TPP uptake process and cTPPT expression are developmentally up-regulated, and that this up-regulation is likely driven via transcriptional mechanism(s).

2017 ◽  
Vol 100 (5) ◽  
pp. 1511-1515
Author(s):  
Frédéric Martin ◽  
Liliane Meyer ◽  
Konstantinos Zelianos ◽  
Esther Campos Gimenez

Abstract The purpose of this work was to understand low recoveries of thiamine (vitamin B1) when extracted from cocoa-containing beverage powders fortified with water-soluble vitamin B1, and to develop and validate a new procedure to improve these results. Based on the literature, previous trials have focused on two main factors: pH value prior to paper filtration and the need for solid-phase extraction (SPE) clean up. We demonstrate that by following European Standard EN 14122, recovery of thiaminein cocoa-containing beverage powders is low and dependent on the test portion (86 and 72% for 0.5 and 1.5 g test portions, respectively). Our improved method resolved this problem by keeping the pH low (around 1) prior to paper filtration, leading to a 96.3% recovery and high precision (RSDr of 3.5%). The use of strong cation-exchange SPE cartridges for cleanup prior to the thiamine oxidation reaction proved to be essential. A comparison between our improved method and EN 14122 on nine cocoa-containing beverage samples available on local market from different manufacturers showed a systematic increase in thiamine content (up to 70%) when the improved methodwas applied. The highest difference was observed forthe sample that contained the highest amount of cocoa. However, for beverage powders that contained bothcocoa and milk, no difference was observed.


Author(s):  
Frédéric Sedel ◽  
Carla E. M. Hollak

Thiamine is a water-soluble vitamin acting in the mitochondria as a cofactor for energy metabolism and, in the cytoplasm, in the pentose phosphate biosynthetic pathway. Its transport through the plasma membrane requires two transporters with overlapping functions: THTR1 encoded by SLC19A2, and THTR2 encoded by SLC19A3. Thiamine is transformed into its active form, thiamine pyrophosphate (TPP) by a kinase encoded by the TPK1 gene. Then it may enter the mitochondria through a TPP transporter encoded by SLC25A19. Mutations in SLC19A2 cause thiamine-responsive megaloblastic anemia (TRMA). Mutations in SLC19A3 cause biotin/thiamine–responsive basal ganglia disease. Mutations in SLC25A19 may cause early microcephaly with death in infancy (also called Amish microcephaly) or a later-onset bilateral striatal necrosis with progressive peripheral neuropathy. Recently, mutations in the TPK1 gene have been associated with recurrent encephalopathy with mild lactic acidosis.


1930 ◽  
Vol 24 (6) ◽  
pp. 1764-1779 ◽  
Author(s):  
Harriette Chick ◽  
Alice Mary Copping

2020 ◽  
pp. 1753495X2096090
Author(s):  
Nivedita Hegde ◽  
AJ Ashwal ◽  
Shrayva Deekonda ◽  
KK Suresh

Thiamine (vitamin B1) is a sulfur-containing, water-soluble vitamin that plays an essential role in energy metabolism and the tricarboxylic acid cycle. There is an increased need for vitamin B1 (1–1.2 mg daily) during pregnancy and lactation. Hyperemesis during pregnancy can cause severe polyneuropathy (Wernicke’s encephalopathy) as a result of thiamine deficiency. Thiamine deficiency has also been associated with beriberi. A number of atypical cases with reversible right heart failure and severe pulmonary hypertension have also been reported in non-pregnant individuals, but have never been reported in pregnancy. Here we present five such cases of thiamine deficiency with neurological and cardio-pulmonary manifestations.


Author(s):  
S. U. Digraskar ◽  
S. T. Borikar ◽  
A. S. Tawheed ◽  
B. S. Nithin ◽  
S. Neelam ◽  
...  

Thiamine (vitamin B1) deficiency in birds is caused by malnutrition or thiaminase-rich foods (raw freshwater fish) or foods high in anti-thiamine factors (betel nuts).Thiamine is an essential water soluble vitamin contributing phosphate derivatives that are involved in many cellular processes as coenzymes in the catabolism of sugars and amino acids. Also thiamine triphosphate (TTP) helps in proper functioning of neuronal membranes (Cooper and Pincus, 1979) and its deficiency leads to polyneuritis which is manifested as lethargy, head tremors, impaired digestion, general weakness, star-gazing and frequent convulsions


2017 ◽  
Vol 5 (19) ◽  
pp. 11 ◽  
Author(s):  
Mohamed Shehab-Eldin

Thiamine (vitamin B1), a water-soluble vitamin, is an essential factor in cellular metabolismand fundamental cofactor in important biochemical cycles. Thiamine deficiency is a wellknowncause of neurological and cardiologic disorders, especially in patients with alcoholdependence. Recently, several researchers have studied the role of thiamine deficiency incritically ill patients and the link between thiamine supplementation and changes in lactatelevels in septic shock patients. The role of thiamine in this group of patients is still unclear;however, thiamine supplementation does not cause toxic side effects or increase morbidityor mortality. In this review, we discuss the most common conditions associated with thiaminedeficiency and the limited literature available on thiamine supplementation in critically illpatients.


2021 ◽  
Vol 50 (6) ◽  
pp. 551-561
Author(s):  
Chang-Guk Boo ◽  
Sung Min Cho ◽  
Hyang Yun Jeong ◽  
So Jeong Yoon ◽  
Seong Jun Hong ◽  
...  

2018 ◽  
Vol 8 (3) ◽  
pp. 197-200
Author(s):  
Maria Sofia Cotelli ◽  
Patrizia Civelli ◽  
Marinella Turla

Wernicke’s encephalopathy (WE) is an acute, neuropsychiatric syndrome which results from a deficiency in vitamin B1 (thiamine), which in its biologically active form, thiamine pyrophosphate, is an essential coenzyme in several biochemical pathways in the brain, often due to alcohol abuse (alcoholic WE). Non-alcoholic WE variant manifests in many different clinical settings, such as gastrointestinal tumors, hyperemesis gravidarum, chemotherapy, acquired immunodeficiency syndrome, prolonged therapeutic fasting, protracted parenteral nutrition and bariatric surgery, anorexia nervosa and can even be secondary to socioeconomic factors. The classic triad of encephalopathy, oculomotor dysfunction, and gait ataxia is only seen in approximately one-third of patients and is more common in alcoholics; only some of these symptoms are usually present. Here we describe a case of an occasional neuroradiological finding of Wernicke Encephalopathy not related to symptoms or signs.


2021 ◽  
Author(s):  
Simon Strobbe ◽  
Jana Verstraete ◽  
Christophe Stove ◽  
Dominique Van Der Straeten

Abstract Thiamin (or thiamine) is a water-soluble B-vitamin (B1), which is required, in the form of thiamin pyrophosphate (TPP), as an essential cofactor in crucial carbon metabolism reactions in all forms of life. To ensure adequate metabolic functioning, humans rely on a sufficient dietary supply of thiamin. Increasing thiamin levels in plants via metabolic engineering is a powerful strategy to alleviate vitamin B1 malnutrition and thus improve global human health. These engineering strategies rely on comprehensive knowledge of plant thiamin metabolism and its regulation. Here, multiple metabolic engineering strategies were examined in the model plant Arabidopsis thaliana. This was achieved by constitutive overexpression of the three biosynthesis genes responsible for B1 synthesis, HMP-P synthase (THIC), HET-P synthase (THI1) and HMP-P kinase/TMP pyrophosphorylase (TH1), either separate or in combination. By monitoring the levels of thiamin, its phosphorylated entities, and its biosynthetic intermediates, we gained insight into the effect of either strategy on thiamin biosynthesis. Moreover, expression analysis of thiamin biosynthesis genes showed the plant’s intriguing ability to respond to alterations in the pathway. Overall, we revealed the necessity to balance the pyrimidine and thiazole branches of thiamin biosynthesis and assessed its biosynthetic intermediates. Furthermore, the accumulation of non-phosphorylated intermediates demonstrated the inefficiency of endogenous thiamin salvage mechanisms. These results serve as guidelines in the development of novel thiamin metabolic engineering strategies.


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