Important point biochem mid2
Lec1:
Carbohydrates digestion:
Mouth: salivary a-amylase
Stomach: no digest salivary a-amylase can’t catch to work there.
Intestine:
Pancreatic bicarbonate > neutralization
Pancreatic a-amylase > oligosaccharide and disaccharide
^ Those enzymes from pancreas
lactese, Sucrase, maltes > free glucose
^ From intestine
Glucose and galactose transport by sodium dependent glucose cotransporter-1 <
need energy
Fructose transport by sodium-independent transporter (GLUG-5) < no need
energy
Example Q:
Infant drink milk with watery diarrhea has abdominal discomfort and gases?
Answer: lactose intolerance < lactase deficiency
Or defect in intestine
Treated by milk free lactose
Maybe the cause a drug damages the intestine wall.
Protein digestion:
Mouth: no digest.
Stomach: secret pepsin “zymogen” activated by HCL < breakdown the protein
Intestine:
Pancreatic enzymes: trypsin, chymotrypsin, elastase, carboxypeptidase
Most digest in pancreas.
All the enzyme zymogen “inactive” activated by trypsin after it activated by
entrokinase.
Elastase> endopeptide
Carboxypeptidase> exopeptide
Intestine enzyme: aminopeptidase
Example Q:
Enzyme digest protein from pancreas?
Carboxypeptidase.
Lec2:
Enzymes digest lipid:
Lingual lipase, gastric lipase, pancreatic lipase
1-Gastric lipase> breakdown short and medium chain “milk” baby depend on it.
2-Bile salt > emulsification “ increase surface area for pancreatic enzyme to work
faster”
Form from liver and stored in gall bladder, derived from cholesterol.
3-Pancreatic lipase: the important one in lipid digestion.
Work in Triacylglycerol in carbon 1,2 to give 2 monoacylglycerol and 2 F.A
Colipase >anchore for pancreatic lipase
* Orlistat inhibit pancreatic lipase > will not digest so not absorbed and loss in
stool.
Phospholipid: break down by phospholipase 2 < remove F.A from carbon 2.
The remnant lysophospholipid break down by lysophospholipase
Cholesterol ester> by cholesterol ester hydrase > to give free cholesterol
After all break down “digested”
Short and medium chain direct from intestine to portal by albumin
The long chain:
Bile salt > micelles “to absorbed”
The micelles contain: 2 monoacylglycerol, free F.A, free cholesterol < will go
inside intestine cell
Then will resynthesis to TAG, PL, CE.
Transport: by chylomicrons
Apo B48 > carrier in the circulation, HDL> give apoC, apoE
To enter the adipose tissue need apo C to active liopproteinlipase
Lipopropteinlpase> F.A and glycerol
Remnant of chylomicron: apoC go back to HDL
The apoE active uptake the remnant to the liver.
Example Q:
1- In deficiency of lipoproteinlipase what will elevate in blood?
Answer: chylomicron or trygylecrol.
2- Deficiency in aopE what will elevate in blood?
Answer: remnant of chylomicron or cholesterol.
3-patient with malabsorption and statorriha and has live cirrhosis, the defect
will be in?
Answer: no bile salt
3- Patient with pancreas disease treatment will be?
Answer: diet with short chin and medium chin, milk product.
Lec3:
b-oxidation of F.A occurs in mitochondria.
Long chain more than 12 carbons need for transport CAT1 and CAT2
Carnitine inhibited by F.A synthesis *malonyl* and increase in acetyl coA
CAT1 bind carnitine with F.A in outer mitochondria transport F.A inside
inner mitochondria
*Inner mitochondria is impermeable*
CAT2 break down CAT1 into carnitine and F.A
**Defect in canitine no transport for F.A so no energy caused by 2ry causes:
liver diseases and malnutrition and increase in demand> pregnancy
1ry causes:
1-Defect in CPT1 < affect liver
Patient has Hypoglycemia < if no carbohydrate in diet
2-Defect in CPT2< affect muscle and heart
No energy muscle weakness, cardiomyopathy
^^ Treated by diet with carbohydrate and milk product < if they say milk free
is WRONG!!
MCAD> defect in first enzyme “dehydrogenases”
^F.A not breakdown < in medium chain
Happened in children cause they rely on milk.
Treatment carbohydrate diet.
F.A oxidation > 129 ATP
Refsum diseases:
The branched F.A need a-oxidation to break it down
^ If there’s defect on it will lead to toxicity < deafness and blindness
Ketones bodies:
Synthesis in liver and breakdown in all tissue except liver
And synthesis in prolonged fasting and in DM< no insulin, increase in
lipolysis.
Lec4:
Protein degradation by:
1-ubiquitin > need energy, intracellular
2- lysosomes> no need energy, extracellular
a.a > remove a-amino group > give ammonia
And the remaining carbon skeleton > give energy
Transporter for ammonia:
What the carrier for ammonia in brain? Glutamine
What the carrier for ammonia in muscle? Alanine
Transamination reaction not gives free ammonia or free amino group
Oxidative deamination done by glutamate dehydrogenase work on glutamate
give > free ammonia and a-ketoglutarate
Example Q:
Oxidative deamination done by?
Answer: glutamate dehydrogenase
Or amino acid dehydrogenase
**Make sure is glutamate not GLUTAMINE.
Urea form in liver for disposal ammonia and excretion mainly in urine via
kidney
And stool and reabsorbed to blood via intestine
Hyperammonemia:
Acquired:
1-liver diseases
2-GIT bleeding < increase amount of reabsorbed ammonia in blood
Heredity: defect in enzymes in urea cycle
**Renal failure:
Can’t excrete urea in urine so it’ll transfer to intestine that will increase the
amount of ammonia absorbed to the blood lead to hyperammonemia
For treatment give oral neomycin antibiotic to reduce intestinal Bactria that
responsible for production of ammonia