Nutrition pdf - د. رباح

Vitamin A (retinol)

Metabolites

: are retinaldehyde and retinoic acid

Function

 retinaldehyde

is important of vision

 retinoic acid

for the cell growth and

differentiation

 retinoid

synthetic molecule

Vitamin A (retinol)

plays a role in

iron utilization

humeral immunity

T cell–mediated immunity

natural killer cell activity

phagocytosis

Vitamin A (retinol)

Metabolism

The

liver

contains 90% of the vitamin A is bound

to retinol-binding protein

transthyretin

trimolecular complex

specific cell-

surface receptors

bound to a series of

cellular retinol-binding proteins, function as
transporting agents as well as co-

ligands

for

certain nuclear receptors that act as transcription

factors.( retinoid-mediated gene transcription)
receptors for cell proliferation and differentiation

• * The trimolecular complex [retinol (vit.A) + retinol-binding protein

(RBP) + transthyretin(TTR)] prevents the glomerular filtration of the
low molecular weight RBP (and so vit.A).

* Transthyretin (TTR) is a carrier for retinol-binding protein, and also
thyroxine (T4). [This is how transthyretin gained its name,

trans

ports

thy

roxine and

retin

ol]

* RBP plays an important role in transporting retinol in circulation,
and delivering it to the cells by binding to specific cell-surface
receptors, releasing retinol to the cell after binding with the receptor,
then recirculate as the apo-form of BPR. Thus

• RBP is involved in multiple molecular interactions: it binds
• retinol and interacts with TTR and the cell-surface receptor

Vitamin A (retinol)

Dietary source

animal source

: liver and fish (excellent source)

plant source

: dark-green vegetable and fruits

by the splitting of carotenes.

Vitamin A (retinol)

Deficiency

1. chronic dietary deficit

(developing countries)

Southern Asia, Sub-Saharan Africa, some areas

of Latin America

More than

125 million

preschool-age children

with vitamin A deficiency, ~

4 million

have an

ocular manifestation of deficiency .

quarter

of a million children each year

developed blindness.

Vitamin A (retinol)

2. Malabsorption:

celiac disease, short bowel syn.

3. Zinc deficiency:

interfere with vitA mobilization

from the liver

4. Alcohol :

interfere with conversion of

retinol

to retinaldehyde in the

retina

(dehydrogenase)

5. Drugs :

interfere with the absorption of vitA

neomycin, cholestyramine (bile acid

sequestrant, so it can also bind fat-
soluble vitamins  interference with absorbtion.

Vitamin A (retinol)

Clinical features

• night blindness

(loss of dark adaptation)

and may develop to complete blindness (endemic

blindness).

• conjunctival xerosis

(dryness)

(xerophalmia)

(because of loss of mucus secreting cells)

• Bitot's spots

(white patches of keratinized

epithelium on the sclera)

• Keratomalacia

(softening of the cornea) leads

corneal ulceration and

necrosis

result in corneal scarring

• increased risk of infection

dysentery

respiratory disease.

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• * Vit.A deficiency in children is dangerous, and

increases mortality, because vit.A is essential
to maintain intact epithelia tissue as a physical
barrier to infection; it is also involved in
maintaining a number of immune cell types
from both the innate and acquired immune
systems.

• Prevention of deficiency :

1- A pregnant woman is advised to eat dark-green leafy vegetables,
and yellow fruits  retinol in baby’s liver. (she shouldn’t take
vit.A supplements (high doses), because they have serious side
effects< and are teratogenic to the baby).

2- 60 mg retinol as palmitate is given to pre-school children leads to
a decrease in mortality by gastroetnteritis, respiratory infections,
and also measles.

• Toxicity :

1- Repeated moderate of high doses  liver damage,
hyperostosis (excessive growth of bone), and
teratogenecity.

• 2- Acute overdose  nausea, headache, elevated

intracranial pressure, skin desquamation.

3- Excessive intake of carotenes causes benign condition
(hypercarotenaemia), in which skin pigmentation
occurs and gradually fates when intake is stopped

Vitamin A (retinol)

Diagnosis

1.Serum retinol level
2.Test of dark adaptation
3.Impression cytology of the conjunctiva
4.Store assessment by liver BX

Vitamin A (retinol)

Treatment

 30mg IM

or 60mg orally

 Vitamin A

supplementation can markedly

reduce risk of child mortality where
deficiency is widely prevalent.

 NB.

Used in patient with M3 leukemia (acute

promyelocytic leukaemia) and cystic acne
(cream).

Vitamin D

Synthesis and Metabolism

• steroid

hormone

involved in mineral ion

homeostasis (calcium and phosphate)

• can be synthesized In response to ultraviolet

radiation of the skin (a photochemical cleavage
from 7-dehydrocholesterol).

source

 animal sources(vitD3):

dairy products, fish

oils

egg yolks

 plant sources (vitamin D

cereals

Vitamin D

Causes of the deficiency

Vitamin D deficiency

  Impaired cutaneous production
  decrease dietary
  Malabsorption

Accelerated loss of vitamin D

Increased metabolism (barbiturates, phenytoin, rifampin)
Impaired enterohepatic circulation

* Anti-epileptic drugs (AEDs)

can also cause a deficiency in 25(OH)D,

even at sub-therapeutic serum levels of the drug, so theoretically it
can be worthwhile to supplement calcium and vitamin D even
before initiation of antiepileptic therapy.

Vitamin D

Clinical features

Asymptomatic

(Mild to moderate deficiency)

Osteomalacia

(defective bone mineralization)

 Muscle and bone pain
 Malaise
 Fragility fracture (pseudofractures or Looser’s zone)
 Proximal myopathy (waddling gait)
 Bone tenderness

Rickets

( growth retardation, bone deformities)

Looser zone

Vitamin D

Diagnosis

1. Biochemical tests

 decrease serum 25(OH)D
 low or normal s. Ca. , ph.
 increasing PTH levels
 increase alkaline phosphatase

2. Radiological tests of oteomalacia

 decrease in cortical thickness
 osteopenia of the skeleton
 pseudofractures, or Looser's zones in the ribs

and pelvis and long bones and vertebra

3. Bone biopsy

Vitamin D

Treatment

 VitD 50,000 IU

weekly for 3–12 Weeks

followed by maintenance therapy (800 IU
daily).

 Calcium supplementation include 1.5–2.0 g

 800 IU of vitamin D, with calcium

supplementation, decreases the risk of hip
fractures in elderly women.

Vitamin E ( tocopherols)

Function

• acts as

antioxidant

and radical

scavenger

which protects low-

density lipoprotein and polyunsaturated fats in membranes from
oxidation, and especially effective for protecting nerve cells, red
blood cells, and immune system function; aiding in the
prevention of and healing of neurological disorders, chronic viral
illness and anemia. Several studies have been performed in
relation to fertility health, revealing its importance for
reproductive function and health.

Absorption and Metabolism

• After absorption, vitamin E is taken up from

chylomicrons

by the

liver, and a hepatic tocopherol transport protein mediates
intracellular vitamin E transport and incorporation into very low-
density lipoprotein

(VLDL)

Vitamin E ( tocopherol)

Dietary source

widely distributed in the food supply

 High

: sunflower, soybean and corn oils

meats, nuts, and cereal grains

 small amounts

: fruits and vegetables.

Vitamin E ( tocopherol)

Causes of the deficiency:

Dietary deficiency

( does not exist).

prolonged

malabsorptive diseases

prolonged

cholestasis

abetalipoproteinemia

cannot absorb or

transport vitamin E.

familial form

of isolated vitamin E

deficiency (defect in the tocopherol
transport protein).

Vitamin E ( tocopherols)

Clinical features

axonal degeneration of the large myelinated

axons and results in

posterior column

 Peripheral neuropathy
 Sensory ataxic gait
 Ophthalmoplegia
 skeletal myopathy
 pigmented retinopathy

Vitamin E ( tocopherols)

Diagnosis

low blood levels of tocopherol

Treatment

• 800–1200

mg of tocopherol per day.

Vitamin k

Function

• vitamin K

phylloquinone, from vegetable and

animal sources

• vitamin K

, menaquinone, synthesized by

bacterial flora and found in hepatic tissue

• Vitamin K3

, menadion, synthetic

• required for the

carboxylation

of glutamic

acid, which is necessary for calcium binding to
-carboxylated proteins such as prothrombin
(factor II); factors VII, IX, and X; protein C;
protein S).

Vitamin k

Dietary Sources

 green leafy vegetables

(spinach)

 liver

 vegetable oils

: olive, soybean oils.

* It’s also synthesized by bacteria in the
colon ( intestinal flora), so intestinal
disorders and broad spectrum antibiotics
will affect the flora  decrease vit.K supply
by the flora.

Vitamin k

Causes of the deficiency

small-intestinal disease

(e.g., celiac disease)

cholestatic

liver disease (obstructive jaundice).

3. Broad-spectrum

antibiotic

treatment (especially with

anticoagulant drugs as warfarin) killing intestinal flora
decreased normal vit.K supplement by the flora G.I.T bleeding
(because of the drugs and low vit.K level which is needed for
coagulation).

drug

therapy, the antiobesity drug orlistat (Absorption of fat-

soluble vitamins and other fat-soluble nutrients is inhibited,
because orlistat acts by inhibiting the gastric and pancreatic
lipase).

• In new born, primary deficiency results from :

1- Inefficient placental vit.K transferring.

   2- Neonatal bowel has not yet acquired the
flora.
  3- Breast milk contains little amounts of vit.K.

So, vit.K supplements are given to the new born
babies routinely to prevent haemorrhigic
diseases of the new born .

Vitamin k

The diagnosis

• elevated

prothrombin time

or reduced

clotting factors

• vitamin K may also be measured directly.

Treatment

• Vitamin K deficiency is treated using a

parenteral dose of

mg.

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