This document discusses vitamin B1 (thiamine). It provides information on the structure of thiamine, dietary sources, roles in the body including as a coenzyme in important metabolic reactions, deficiency manifestations such as beriberi, and absorption/transport of thiamine in the body. The key points are that thiamine is a water-soluble vitamin required for important metabolic processes, it acts as a coenzyme (thiamine pyrophosphate) in the oxidative decarboxylation of pyruvate and alpha-ketoglutarate, and deficiency can cause diseases like beriberi if intake is inadequate.
Biotin (vitamin b7) biological functions, clinical indications and its techn...rohini sane
An illustrative presentation on Biotin (Vitamin B7), clinical indications and technological applications for Medical, Dental, Pharmacology & Biotechnology students to facilitate easy- learning.
a ppt about vitamins especially about vitamin b9 or folate or folic acid
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An illustrative presentation on Biotin (Vitamin B7), clinical indications and technological applications for Medical, Dental, Pharmacology & Biotechnology students to facilitate easy- learning.
a ppt about vitamins especially about vitamin b9 or folate or folic acid
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Vitamin B12- definition, functions, absorption, storage, transportation, deficiency, pernicious anemia, relationship between vitamin B12 and folate deficiency, sign & symptoms, deficiency in case of maternal & child health care, RDA, sources, prevention and treatment.
Rickets - Bony manifestation of altered Vit. D, Calcium, and phosphorus metabolism
- Rickets – child;
- Osteomalacia – adult form
there is an inability to mineralize chondroid and osteoid
- lack of available calcium or phosphorus (or both) for mineralization of newly formed osteoid
- osseous changes in both adults and children
--- Definition - a defect in mineralization of osteoid matrix caused by inadequate calcium and phosphate deposition prior to closure of physis.
- Clinical features arise from un-mineralized matrix at the growth plate.
- less mineralized bone per unit volume of bone
- classic changes of rickets will typically occur in children younger than 6-7 years of age
-- Pathophysiology of Rickets
- Vitamin D => increase the absorption of calcium from intestine
PTH => mobilizes calcium from bone and increases urinary excretion of phosphate
Calcitonin => inhibits bone resorption
CLINICAL FEATURES
Head:
Craniotabes — softening of cranial bones. also seen in osteogenesis imperfect, hydrocephalus and syphilis
Frontal bossing
Delayed dentition and tooth caries
Delayed closure of fontanel
Craniosynostosis.
Chest
Rachitic rosary — widening of osteochondral junction
Harrison’s groove — occurs due to pulling of softened ribs in inspiration by diaphragm. Softened ribs also predispose to atelectasis and pneumonia because of decreased air entry
Pectus carinatum (pigeon breast)
Spine
Scoliosis (uncommon)
Kyphosis (rachitic cat back)
Accentuation of lumbar lordosis
Limbs and Joints
Bone pain and tenderness
Coxa vara
Genu valgum or varum
Windswept deformity
Bowing of tibia, femur, radius and ulna
Widening of wrist, elbow, knee and ankle because of enlargement of ends of long bones
Rachitic saber shins
Sausage like enlargement of ends of phalanges and metacarpals, with regular constrictions corresponding of the joints string of pearls deformity
Double malleoli sign
General
Failure to thrive
Protuberant abdomen
Apathy, listlessness and irritability
Proximal muscle weakness
Ligament laxity
Symptoms of hypocalcemia—tetany, seizures and stridor due to laryngeal spasm
Bilateral lamellar cataract (Vitamin D deficiency in early infancy).
RADIOLOGICAL SIGNS
Generalized osteopenia
Bowing deformities of the long bones, femur and tibia
Widening of the growth plate
Cupping or flaring of the metaphysis
Radiographic findings in vitamin D resistant rickets
similar to those in infantile rickets
Bowing deformities and shortening of the long bones => more pronounced in early rickets
More common in distal ends of radius and ulna (more so in ulna)
Changes in the shaft appear a few weeks later than metaphysis.
The epiphysis is cloudy and indistinct and periosteum is thick.
The shaft shows diffuse rarefaction, thin cortices with coarse texture of spongiosa.
Umbau zones (Looser’s zones) => sharply defined radiolucent transverse zones
-- Findings of healing rickets:
Earliest finding => reappearance of the provisional zone of calcification, which gradually thickens
Report about some facts about vitamin B complex and the importance, origin, signs and symptoms of deficiency and food sources of Vitamin B1 (thiamine), Vitamin B2 (riboflavin), Vitamin B3 (niacin), Vitamin B6 (pyrodixine), and Vitamin B12 (cyanocobalamin), It also has very detailed origin on how each vitamin was discovered
The effects of a deficiency of one vitamin would not ordinarily be expected to be highly dependent on the presence or absence of another vitamin in the diet, since the symptoms of deficiency of each vitamin are usually quite distinct. Nevertheless, antagonistic or synergistic interactions between vitamins may occur to a greater or less extent. While several mechanisms can be proposed whereby vitamins can be synergistic, it is more difficult to conceive of one which could explain vitamin antagonism.
This Medicoapps Masterclass discusses about Cori cycle. Various Topics Discussed are given below
Cori cycle Various Steps
Significance of Cori’s Cycle
Exam points of Cori’s Cylce
Vitamin B12- definition, functions, absorption, storage, transportation, deficiency, pernicious anemia, relationship between vitamin B12 and folate deficiency, sign & symptoms, deficiency in case of maternal & child health care, RDA, sources, prevention and treatment.
Rickets - Bony manifestation of altered Vit. D, Calcium, and phosphorus metabolism
- Rickets – child;
- Osteomalacia – adult form
there is an inability to mineralize chondroid and osteoid
- lack of available calcium or phosphorus (or both) for mineralization of newly formed osteoid
- osseous changes in both adults and children
--- Definition - a defect in mineralization of osteoid matrix caused by inadequate calcium and phosphate deposition prior to closure of physis.
- Clinical features arise from un-mineralized matrix at the growth plate.
- less mineralized bone per unit volume of bone
- classic changes of rickets will typically occur in children younger than 6-7 years of age
-- Pathophysiology of Rickets
- Vitamin D => increase the absorption of calcium from intestine
PTH => mobilizes calcium from bone and increases urinary excretion of phosphate
Calcitonin => inhibits bone resorption
CLINICAL FEATURES
Head:
Craniotabes — softening of cranial bones. also seen in osteogenesis imperfect, hydrocephalus and syphilis
Frontal bossing
Delayed dentition and tooth caries
Delayed closure of fontanel
Craniosynostosis.
Chest
Rachitic rosary — widening of osteochondral junction
Harrison’s groove — occurs due to pulling of softened ribs in inspiration by diaphragm. Softened ribs also predispose to atelectasis and pneumonia because of decreased air entry
Pectus carinatum (pigeon breast)
Spine
Scoliosis (uncommon)
Kyphosis (rachitic cat back)
Accentuation of lumbar lordosis
Limbs and Joints
Bone pain and tenderness
Coxa vara
Genu valgum or varum
Windswept deformity
Bowing of tibia, femur, radius and ulna
Widening of wrist, elbow, knee and ankle because of enlargement of ends of long bones
Rachitic saber shins
Sausage like enlargement of ends of phalanges and metacarpals, with regular constrictions corresponding of the joints string of pearls deformity
Double malleoli sign
General
Failure to thrive
Protuberant abdomen
Apathy, listlessness and irritability
Proximal muscle weakness
Ligament laxity
Symptoms of hypocalcemia—tetany, seizures and stridor due to laryngeal spasm
Bilateral lamellar cataract (Vitamin D deficiency in early infancy).
RADIOLOGICAL SIGNS
Generalized osteopenia
Bowing deformities of the long bones, femur and tibia
Widening of the growth plate
Cupping or flaring of the metaphysis
Radiographic findings in vitamin D resistant rickets
similar to those in infantile rickets
Bowing deformities and shortening of the long bones => more pronounced in early rickets
More common in distal ends of radius and ulna (more so in ulna)
Changes in the shaft appear a few weeks later than metaphysis.
The epiphysis is cloudy and indistinct and periosteum is thick.
The shaft shows diffuse rarefaction, thin cortices with coarse texture of spongiosa.
Umbau zones (Looser’s zones) => sharply defined radiolucent transverse zones
-- Findings of healing rickets:
Earliest finding => reappearance of the provisional zone of calcification, which gradually thickens
Report about some facts about vitamin B complex and the importance, origin, signs and symptoms of deficiency and food sources of Vitamin B1 (thiamine), Vitamin B2 (riboflavin), Vitamin B3 (niacin), Vitamin B6 (pyrodixine), and Vitamin B12 (cyanocobalamin), It also has very detailed origin on how each vitamin was discovered
The effects of a deficiency of one vitamin would not ordinarily be expected to be highly dependent on the presence or absence of another vitamin in the diet, since the symptoms of deficiency of each vitamin are usually quite distinct. Nevertheless, antagonistic or synergistic interactions between vitamins may occur to a greater or less extent. While several mechanisms can be proposed whereby vitamins can be synergistic, it is more difficult to conceive of one which could explain vitamin antagonism.
This Medicoapps Masterclass discusses about Cori cycle. Various Topics Discussed are given below
Cori cycle Various Steps
Significance of Cori’s Cycle
Exam points of Cori’s Cylce
Thiamine is also called as vitamin B1, Aneurine (it can relieve neuritis), or antiberberi
factor.
• In 1900, Christian Eijkman produced beriberi in chicken by feeding polished rice (Nobel
Prize, 1929).
• Adolf Windaus (Nobel Prize, 1928) elucidated the structure of the vitamin.
Structure of Thiamine:
Biosynthesis:
Deficiency Manifestations of Thiamine
Thiamine, also known as thiamin or vitamin B₁, is a vitamin found in food and manufactured as a dietary supplement and medication. Food sources of thiamine include whole grains, legumes, and some meats and fish
Thiamine (vitamin B1) and biochemical aspects of beriberirohini sane
A comprehensive presentation on Thiamine and biochemical aspects of Beriberi for MBBS, BDS, B Pham and Biotechnology students to facilitate easy leaning.
Chemistry of vitamin B1, Biochemical functions of vitamin B1, Recommended dietary Allowance of Thiamine, Dietary sources of Thiamine ,Deficiency symptoms of Thiamine
Healing takes energy. Energy requires thiamine. Modern foods, lifestyles, medications and chemical exposures threaten thiamine status in a large percentage of the population. Modern thiamine deficiency does not look like classic thiamine deficiency, and thus, goes largely unrecognized by the medical community. Modern thiamine deficiency does not originate from starvation, but rather, from a state of being well fed and sometimes over-fed. As a result, many of the symptoms are incongruent with current textbook definitions. This presentation discusses the chemistry and symptomology of modern thiamine deficiency.
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As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
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Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
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Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
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Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
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CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
2. VITAMINS
Vitamins may be regarded as organic
compounds required in the diet in small
amounts to perform specific biological
functions for normal maintenance of
optimum growth and health of the
organism.
4/3/2020 2
5. DEFICIENCY OF VITAMINS MAY OCCUR DUE TO
a. Reduced intake
b. Impaired absorption
c. Impaired metabolism
d. Additional requirements
e. Increased losses.
4/3/2020 5
7. THIAMINE (VITAMIN B1)
Thiamine is also called as vitamin B1
Aneurine (it can relieve neuritis) or antiberberi
factor.
Christian Eijkman produced beriberi in chicken by
feeding polished rice .
Adolf Windaus elucidated the structure of the
vitamin.
4/3/2020 7
8. SOURCES
Aleurone layer of cereals (food grains) is a rich
source of thiamine.
whole wheat flour and unpolished handpound rice
have better nutritive value than completely
polished refined foods.
When the grains are polished, aleurone layer is
usually removed.
Yeast is also a very good source.
Thiamine is partially destroyed by heat.
4/3/2020 8
9. STRUCTURE OF THIAMINE
Thiamine contains a substituted pyrimidine ring
connected to a substituted thiazole ring by
means of methylene bridge.
The vitamin is then converted to its active co-
enzyme form by addition of two phosphate
groups, with the help of ATP .
It is catalyzed by thiamine pyrophospho
transferase.
4/3/2020 9
10. Vitamin B1
It is required for the essential decarboxylation
reactions catalyzed the pyruvate and 2-
oxoglutarate by omplexes.
4/3/2020 10
12. Chemistry
The structure of thiamine [3-(4-amino-2-methyl-pyrimidyl-5-
methyl)-4-methyl-5-(β-hydroxyethyl)thiazole] is that of a
pyrimidine ring, bearing an amino group, linked by a
methylene bridge to a thiazole ring .
The thiazole has a primary alcohol side chain at C5, which can
be phosphorylated in vivo to produce thiamine phosphate
esters, the most common of which is TPP (also known as
thiamine diphosphate [cocarboxylase]).
Monophosphate and triphosphate esters also occur.
The basic vitamin is isolated or synthesized and handled as a
solid thiazolium salt (eg, thiamine chloride hydrochloride).
Thiamine is somewhat heat labile, particularly in alkaline
solutions, where base attacks occur at C2 of the thiazolium
ring.
4/3/2020 12
13. Dietary Sources
Small amounts of thiamine and its phosphates
are present in most plant and animal tissues,
but more abundant sources include unrefined
cereal grains, liver, heart, kidney, and lean cuts
of pork.
The enrichment of flour and derived food
products, particularly breakfast cereals, has
considerably increased the availability of this
vitamin.
4/3/2020 13
18. PHYSIOLOGICAL ROLE OF THIAMINE
i. Pyruvate dehydrogenase: The co-enzyme for is
thiamine pyrophosphate(TPP).
It is used in oxidative decarboxylation of alpha
keto acids, e.g. pyruvate dehydrogenase
catalyzes the breakdown of pyruvate, to acetyl
CoA, and carbon dioxide.
4/3/2020 18
19. (a) TPP is the coenzyme form of
vitamin B1 (thiamine). The reactive
carbon atom in the thiazolium ring of
TPP is shown in red. In the reaction
catalyzed by pyruvate decarboxylase,
two of the three carbons of pyruvate
are carried transiently on TPP in the
form of a hydroxyethyl, or “active
acetaldehyde,” group.
4/3/2020 19
20. (b), which is subsequently
released as acetaldehyde.
4/3/2020 20
21. The thiazolium ring of TPP
stabilizes carbanion
intermediates by providing an
electrophilic (electrondeficient)
structure into which the
carbanion electrons can be
delocalized by resonance.
Structures with this property,
often called “electron sinks,” play
a role in many biochemical
reactions—here, facilitating
carbon–carbon bond cleavage.
4/3/2020 21
28. PHYSIOLOGICAL ROLE OF THIAMINE
ii. Alpha ketoglutarate dehydrogenase: An
analogousbiochemical reaction that requires TPP is
the oxidative decarboxylation of alpha
ketoglutarate to succinyl CoA and CO2 (See citric
acid cycle).
4/3/2020 28
31. PHYSIOLOGICAL ROLE OF THIAMINE
iii. Transketolase: The second group of enzymes that
use TPP as co-enzyme are the transketolases, in the
hexose monophosphate shunt pathway of glucose .
iv. The main role of thiamine (TPP) is in carbohydrate
metabolism. So, the requirement of thiamine is
increased along with higher intake of
carbohydrates.
4/3/2020 31
38. DEFICIENCY MANIFESTATIONS OF THIAMINE
A. Beriberi
B. Wet beriberi
C. Dry beriberi
D. Inantile beriberi
E. Wenicke-Korsakoff syndrome (cerebral beriberi)
F. Polyneuritis
4/3/2020 38
40. BERIBERI
Deficiency of thiamine leads to beriberi.
It is a Singhalese word, meaning “weakness”.
The
early symptoms are anorexia, dyspepsia,
heaviness
and weakness. Subjects feel weak and get
easily
exhausted.
4/3/2020 40
41. BERIBERI continue…………..
B. Wet beriberi: Here cardiovascular manifestations
are prominent. Edema of legs, face, trunk and
serous cavities are the main features.
Palpitation, breathlessness and distended neck
veins are observed. Death occurs due to heart
failure.
4/3/2020 41
42. BERIBERI continue…………..
C. Dry beriberi: In this condition, CNS manifestations
are the major features.
Walking becomes difficult.
Peripheral neuritis with sensory disturbance leads
to complete paralysis.
D. Infantile beriberi: It occurs in infants born to
mothers suffering from thiamine deficiency.
Restlessness and sleeplessness are observed.
4/3/2020 42
43. E. Wernicke-Korsakoff syndrome:
It is also called as cerebral beriberi.
Clinical features are those of encephalopathy
(ophthalmoplegia, nystagmus, cerebellar ataxia)
plus psychosis.
It is seen only when the nutritional status is
severely affected.
4/3/2020 43
44. Wernicke-Korsakoff Syndrome Is Exacerbated by a
Defect in Transketolase continue….
alcoholism than in the general population, because
chronic, heavy alcohol consumption interferes with
the intestinal absorption of thiamine.
The syndrome can be exacerbated by a mutation in
the gene for transketolase that results in an enzyme
with a lowered affinity for TPP—an affinity one-
tenth that of the normal enzyme.
This defect makes individuals much more sensitive
to a thiamine deficiency.
The result is a slowing down of the whole pentose
phosphate pathway.
4/3/2020 44
45. WERNICKE ENCEPHALOPATHY &
KORSAKOFF SYN DROME
Wernicke encephalopathy i s characterized b y confusion, ataxia,
and nystagmus leading to ophthalmoplegia (lateral rectus muscle
weakness, conjugate gaze palsies) ;
peripheral neuropathy may also be present. It is due to thiamine
deficiency and in the patients with alcoholism.
It may also occur in patients with AIDS or hyperemesis
gravidarum, and after bariatric surgery.
In suspected cases, thiamine ( 1 00 mg) is given intravenously
immediately and then intramuscularly on a daily basis until a
satisfactory diet can be ensured.
Korsakoff syndrome occurs in more severe cases; it includes
anterograde and retrograde amnesia and sometimes
confabulation, and may not be recognized until after the initial
delirium has lifted.4/3/2020 45
46. WKS
Glucose administration increases the thiamine
requirement and can precipitate Wernicke-
Korsakoff syndrome if thiamine is not co
administered.
Parenteral nutrition without thiamine causes
severe refractory lactic acidosis from deranged
pyruvate metabolism.
4/3/2020 46
47. F. Polyneuritis:
It is common in chronic alcoholics.
Alcohol utilization needs large doses of
thiamine.
Alcohol inhibits intestinal absorption of
thiamine, leading to thiamine deficiency.
Polyneuritis may also be associated with
pregnancy and old age.
Thiamine deficiency in alcoholism may cause
impairment of conversion of pyruvate to acetyl
CoA.
Increased plasma concentration of pyruvate and
lactate, leading to lactic acidosis.4/3/2020 47
48. Biochemical Parameters
blood thiamine is reduced, but pyruvate, alpha
ketoglutarate and lactate are increased.
Erythrocyte transketolase activity is reduced.
Erythrocyte transketolase levels may be reduced in
comatose patients, alcoholics, chronic renal failure,
malnutrition as well as in elderly patients.
A lipid soluble acylated derivative (benfotiamine) is
now being recommended for diabetic patients to
decrease glycation of proteins (AGE) and to improve
diabeteic neuropathy.
4/3/2020 48
49. ANTITUMOR DRUG
The thiamine analog oxythiamine, which blocks the
action of a transketolase-like enzyme that converts
xylulose 5-phosphate to glyceraldehyde 3-
phosphate is in preclinical trials as an antitumor
drug.
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51. Absorption, Transport, Metabolism, and
Excretion
proximal smallintestine by a saturable (thiamine transporter)
process at a low concentration (≤1 μmol/L) and by simple passive
diffusion beyond that, although percentage absorption diminishes
with an increased dose.
Absorbed thiamine undergoes intracellular phosphorylation,
mainly to the pyrophosphate, but at the serosal side, 90% of
transferred thiamine is present in the free form.
Thiamine uptake is enhanced by thiamine deficiency and is
reduced by thyroid hormone, diabetes, and ethanol ingestion.
Thiamine is carried by portal blood to the liver.
The free vitamin is present in plasma, but the coenzyme, TPP, is
the primary cellular component. Approximately 30 mg is stored in
the body, with 80% as pyrophosphate, 10% as triphosphate, and
the rest as thiamine and its monophosphate.
About half of body stores are found in skeletal muscle, with much
of the remainder in the heart, liver, kidneys, andnervous tissues
(including the brain, which contains most of the triphosphate).4/3/2020 51
52. Absorption, Transport, Metabolism, and Excretion
continue………………..
The three tissue enzymes known to participate in the formation of
phosphate esters are (1) thiaminokinase (a pyrophosphokinase),
which catalyzes formation of TPP and adenosine monophosphate
(AMP) from thiamine and adenosine triphosphate (ATP).
(2) TPP-ATP phosphoryltransferase (cytosolic 5′-adenylic kinase),
which forms the triphosphate and adenosine diphosphate from
TPP and ATP.
(3) thiamine triphosphatase, which hydrolyzes TPP to the
monophosphate.
Although thiaminokinase is widely distributed in the body,
phosphoryl transferase and the membrane-associated
triphosphatase are found mainly in nervous tissue.
With the use of labeled thiamine probes, a study of thiamine
metabolism at normal loads produced an estimated half-life of
thiamine of 9.5 to 18.5 days, and showed a large number of
breakdown products in the urine.
Several of these urinary catabolites are shown in Fig.4/3/2020 52
55. Functions
Thiamine is required by the body as the pyrophosphate (TPP) in two
general types of reactions: (1) the oxidative decarboxylation of 2-oxo
acids catalyzed by dehydrogenase complexes; and
(2) the formation of α-ketols (ketoses) as catalyzed by transketolase
and as the triphosphate (TTP) within the nervous system.
TPP functions as the magnesium (Mg)-coordinated coenzyme for the
active aldehyde transfers in multienzyme dehydrogenase complexes
that affect decarboxylative conversion of α-keto (2-oxo) acids to acyl-
coenzyme A (acyl-CoA) derivatives, such as pyruvate dehydrogenase
and α-ketoglutarate dehydrogenase.
These are often localized in the mitochondria, where efficient use in
the Krebs tricarboxylic acid (citric acid) cycle follows.
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56. Functions
Three types of subunit proteins constitute such
dehydrogenase complexes: (1) a TPP-dependent
decarboxylase, which converts the 2-oxo acid to an α-
hydroxyalkyl–TPP complex;
(2) a transacylase core, which contains lipoyl residues
that are acylated by the α-hydroxyalkyl–TPP.
(3) a flavin adenine dinucleotide (FAD)-dependent
dihydrolipoyl dehydrogenase, which re-oxidizes the
reduced lipoyl residues produced after transfer of their
acyl functions to reduced CoA.
the initial pyruvate dehydrogenase–catalyzed step
provides acetyl-CoA as a biosynthetic precursor to lipids
and acetylcholine of the parasympathetic nervous
system.4/3/2020 56
57. Functions
Transketolase is a TPP-dependent enzyme found in
the cytosol of many tissues, especially liver and
blood cells, in which the principal carbohydrate
pathways exist.
In the pentose phosphate pathway, which
additionally supplies reduced nicotinamide-adenine
dinucleotide phosphate (NADPH) necessary for
biosynthetic reactions.
this enzyme catalyzes the reversible transfer of a
glycoaldehyde moiety from the first two carbons of a
donor ketose phosphate to the aldehyde carbon of
an aldose phosphate.
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58. Functions
thiamine as its pyrophosphate contributes to nervous system
composition and function in such essential reactions as
energy production and biosynthesis of lipids and
acetylcholine, a further specific, non-cofactor role for
thiamine has been proposed in excitable cells.
TTP is believed to be involved in the regulation of ion
channels, specifically, chloride channels of large unitary
conductance (the “maxi-chloride channels”).
TTP may also have more basic metabolic functions, including
acting as a phosphate donor for the phosphorylation of
proteins, suggesting a potential role in cell signaling.
A subacute necrotizing encephalomyelopathy has been seen
in patients with Leigh syndrome, resulting from the presence
of an inhibitor of TPP-ATP phosphoryl transferase and a
consequent reduction in TTP concentration.4/3/2020 58
59. Requirements and Reference Nutrient
Intakes
Thiamine is necessary mainly for the metabolism of
carbohydrates, fats, and alcohol, a direct correlation has been
noted between physiologic requirements and the amount of
metabolizable food intake.
A greater requirement is present under situations in which
metabolism is increased (eg, in normal conditions of
increased muscular activity, pregnancy, and lactation, and in
abnormal cases of protracted fever, posttrauma, and
hyperthyroidism).
Clinical signs of deficiency in adults can be prevented with
intakes of thiamine of more than 0.15 to 0.2 mg/1000 kcal,
but 0.35 to 0.4 mg/1000 kcal may be closer to a
concentration necessary to maintain urinary excretion and
TPP-dependent erythrocyte transketolaseactivity within
normal reference intervals.
4/3/2020 59
60. RDA
1.2 mg/day for men 19 years and older and 1.1 mg/day
for women 19 years and older.
The requirement for pregnant women increases early in
pregnancy and then remains constant; 1.4 mg/day is
recommended.
The lactating woman secretes 0.1 to 0.2 mg of
thiamine/day in milk, so 1.4 mg/day is suggested.
Based on the thiamine content of human milk and with
an increment considered to provide a margin of safety,
0.2 mg/day is the allowance for infants up to 6 months,
and 0.3 mg/day for infants 7 to 12 months.
For children, due to growth, 0.5 mg/day is suggested
for up to 3 years of age, and between 4 and 8 years, 0.6
mg/day is suggested.4/3/2020 60
61. Intravenous Supply
Traditionally, the intravenous recommendation was
3 mg/ day for adults, usually provided as thiamine
hydrochloride, but also as thiamine mononitrate or
tetrahydrate.
this was increased to 6 mg/ day, with recognition of
the likelihood of increased demands for thiamine
caused by hypercatabolism in such patients and the
serious potential complications o deficiency.
4/3/2020 61
62. Deficiency
Inadequate intake caused by diets largely dependent
on milled, nonenriched grains such as rice and wheat.
Raw fish containing thiaminases, which hydrolytically
destroyt the vitamin in the gastrointestinal tract.
Tea may also contain anti-thiamine factors.
Chronic alcoholism often leads to thiamine deficiency
caused by reduced intake, impaired absorption,
impaired use, and reduced storage, and may lead
clinically to the Wernicke-Korsakoff syndrome.
who receive parenteral nutrition without adequate
thiamine supplementation, older adult patients taking
diuretics,and patients undergoing long-term renal
dialysis.
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63. DEFICIENCY
In infants symptoms appear suddenly and severely, often involving cardiac
failure and cyanosis.
Commonly, the distinction between wet (cardiovascular) and dry (neuritic)
manifestations of beriberi relate to duration and severity of the deficiency,
the degree of physical exertion, and caloric intake.
The wet or edematous beriberi results from severe physical exertion and
high carbohydrate intake.
the dry or polyneuritic beriberi stems from relative inactivity with caloric
restriction during a long-term deficiency.
cardiovascular system are peripheral vasodilatation leading to a high-output
state, biventricular myocardial failure, and retention of sodium (Na) and
water, leading to edema.
Nervous system involvement includes peripheral neuropathy, Wernicke
encephalopathy, and the amnesic psychosis of Korsakoff syndrome.
More rarely, but especially in seriously ill patients in hospitals, an acute
form of cardiac failure has been described (Shoshin beriberi), which may be
fatal, but can be successfully and rapidly reversed with high-dose
intravenous thiamine.4/3/2020 63
64. DEFICIENCY
Beriberi (origin: Sinhalese from a word meaning
weakness) is the disease that results from thiamine
deficiency.
Clinical signs of thiamine deficiency primarily
involve the nervous and cardiovascular systems. In
the adult, the most frequently observed symptoms
include mental confusion, anorexia, muscular
weakness, ataxia, peripheral paralysis,
ophthalmoplegia, edema (wet beriberi),.
muscle wasting (dryberiberi), tachycardia, and an
enlarged heart.
4/3/2020 64
65. DEFICIENCY
In thiamine-responsive megaloblastic anemia, the gene has
been mapped and cloned, and designated as SLC19A2 as a
member of the solute carrier gene superfamily.
Mutations of this gene, the product of which is a membrane
protein that transports thiamine with submicromolar affinity,
have been found in all thiamine-responsive megaloblastic
anemia kindreds studied.
Thiamine-responsive pyruvate dehydrogenase complex
deficiency, which presents with lactic acidosis, can be caused
by a point mutation within the TPP-binding region .
and a thiamine-responsive, branched-chain keto acid
dehydrogenase complex deficiency, which presents as a form
of maple syrup urine disease, is caused by mutations in the E1
α-subunit of the enzyme complex.
Therapeutic doses of 5 to 20 mg/day of thiamine have proved
beneficial in these cases.
4/3/2020 65
66. Toxicity
stimulators of transketolase enzyme synthesis, such
as thiamine, support the high rate of nucleic acid
ribose synthesis necessary for tumor cell survival,
chemotherapy resistance, and proliferation.
4/3/2020 66
67. Laboratory Assessment of Status
A rapid HPLC method for measuring both
thiamine and its phosphate esters .
Measurements of certain urinary metabolites,
thiamine acetic acid, have been suggested as
reflecting thiamine status but are not
routinely requested.
4/3/2020 67
68. Preanalytical Variables
Whole blood collected into containers with the
preservatives Li heparin or ethylenediaminetetraacetic acid
(EDTA) is recommended.
4/3/2020 68
69. Reference Intervals
(1) erythrocytes, whole blood, or plasma is used as a
sample; (2) cellular concentrations are expressed per
liter of packed red cells or grams of Hb.
erythrocyte transketolase activity, 0.75 to 1.30 U/g Hb
(48.4–83.9 kU/ mol Hb) is used.
Percent TPP effect (activation), 0% to 15% is normal,
16% to 25% is marginally deficient, and more than 25%
is severely deficient with clinical signs.
For direct TPP : 173 to 293 nmol/L for erythrocytes and
90 to 140 nmol/L for whole blood, 280 to 590 ng/g Hb
in erythrocytes, and 275 to 675 ng/g Hb in whole blood
with less than 150 ng/g Hb indicating clinical deficiency.
4/3/2020 69