Biochemical Disease Mechanisms

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Nutritional Biochemistry I

This set of lecture is strictly for personal use

and may not be copied, reproduced, used, or
distributed in any way. 1

Lecturer: Esra Dandin

 Information

Some underlying mechanisms and some possible

treatments of diseases are discussed in a
biochemical point of view in order to get the
concept of relationship between biochemistry,
pathophysiology and nutrition sciences.
 Gall-Stones
 Bile composition: Bile salts, cholesterol,
phospholipids.

 If concentration of cholesterol in bile increases

compared to phospholipid and bile salts, then
cholesterol crystallizes and bile stones are
formed.

 Causes can be over concentration of cholesterol in

gall bladder, excessive liver secretion by liver.
 If large gall stone is lodged in common bile duct
and therefore prevent bile entering to
duedenum, fat digestion and absorption get
negatively affected.

 Absorption of fat and fat-soluble vitamins

decreases.

 As a result of decrease in fat-soluble vitamin

absorption, blood clotting problems (vit.K), and
calcium malabsorption (vit. D) can occur.
 If malabsorbed fat enters large intestine due to
malabsorption, then fat appears in feces:
steatorrhea.
 Ulcers
 Stomach protects itself against to be digested by acidic
content and pepsin.
 Such as: alkaline mucus layering over the luminal
surface
 When protective mechanisms are not efficient enough,
ulcer can occur.
 Not only in stomach but also in esophagus and
duedenum.
 It occurs when mucosal barrier is broken and underlying
tissue is exposed to corrosive acid and pepsin.
 Genetics, drugs, alcohol, smoking, bile salts,
excessive acid and pepsin contribute to ulcer
formation.

 Also, Helicobacter pylori crosses the mucosal

layer ot stomach damaging underlying cells.

 Symptoms: Pain, weight loss, nausea, vomiting,

loss of appetite, abdominal bloating.

 Acid-blocking meds, antibiotics…

 GERD
 Movement of acid from stomach into the
esophagus is called heartburn.

 Severe one: GastroEsophageal Reflux Disease

(GERD)

 Occurs when gastroesophageal sphincter relaxes

not only time of swallowing but also other times
when it must not.
 Constipation
 Voluntary inhibition of normal bowel reflexes for long
periods

 Calcium, iron supplements, some drugs can cause

constipation

 Fiber stimulates peristalsis and draws water into large

intestine preventing stool get hard and dry.

 Water enhances fiber’s function

 Physical activity for regular bowel movements

 Cystic Fibrosis
 Overproduced mucus can block pancreatic duct
and inhibits enzyme entry to intestine

 Ends up with maldigestion

 Enzyme replacement
 Celiac Disease
 Allergic reaction to gluten protein

 Ends up with destruction of absorptive enterocytes,

flattening of villi (reduced surface area for
absorption)

 Limits absorption

 Elimination of gluten containing food such as wheat

and rye.
 Lactose Intolerance
 Insufficient lactase enzyme

 Symptoms: Diarrhea, pain, gas.

Diabetes Mellitus
 Interfered GLUT4 translocation
 When insulin binds to its receptor on cell
membrane, a signal is sent to GLUT4 to be
activated and go to cell membrane, function like
a tunnel for glucose to pass through.
 If there is a problem in GLUT4 translocation,
insulin cannot function on cells especially on
muscle and adipose cells. So, body responses to
it by producing more insulin. Then, beta cells get
tired and die causing hyperglycemia in long term.
 Atherosclerosis
 Tissue damage due to LDL, smoking, high blood
pressure, diabetes, stress…
 Plaque building: if LDL is not readily taken up from
bloodstream, it is oxidized and scavenger cells in
arteries capture it and cholesterol content of LDL
contributes to plaque formation. Collagen
formation and calcium accumulation contributes
to hardening and narrowing of arteries.
 High blood pressure makes damage worse.
 As a result of inflammatory response, monocytes
engulfs oxidized LDL and accumulates in
epithelium creating a fatty-streak which causes
thrombocytes to come and turn it into a fibrous
cap. Sometimes this fibrous cap can break off
and block bloodstream in arteries.
 Relationship between DM and CVD

 Elevated glucose concentration in blood causes

oxidative stress and alters osmotic phenomena
in blood. So, blood vessels get damaged.

 Risk factor for CVD comes up when damage in

vessels are coupled with saturated, elevated and
oxidized LDL.
 Pernicious Anemia
 Auto-immune destruction
of parietal cells in stomach
that produce intrinsic factor

 Due to malabsorption of
vitamin B12

 Large and immature blood

cells
Thanks!