Carbohydrates

Question 1

General Formula

Answer 1

(CH2O)n

Question 2

General structure

Answer 2

Have aldehyde groups (C=O), ketone groups
(-C=O-C)
And lots of hydroxyl groups

Question 3

Carbs function

Answer 3

Glucose main metabolic fuel
Essentially:
Carbohydrate ——> Monosaccharides ——> Pyruvate ———> Acetyl CoA

Acetyl CoA can then enter into the KREBS Cycle or into Fatty Acid Synthesis

Question 4

3 main monosaccharides

Answer 4

Glucose
Fructose (Fruit sugar)
Galactose

Question 5

Disaccharides

Answer 5

Sucrose (Glucose-Fructose)
Lactose (Galactose-Glucose)
Maltose(Glucose-Glucose)

Question 6

Polysaccharides

Answer 6

Glycogen (Storage polymer of glucose in animals)
Starch (Storage polymer of glucose in plants)

Question 7

Cellulose not digestible in humans why?

Answer 7

Don’t posses enzyme to break the Beta 1-4 glycosidic bond

Question 8

Lactose Intolerance

Answer 8

Due to low activity of ENZYME LACTASE

Question 9

Lactose Intolerance Symptoms

Answer 9

Diarrhoea
Bloating
Discomfort

Question 10

Lactose Intolerance Symptoms Explained

Answer 10

Lactose moves into large intestine. Osmotic pressure increases so water moves into large intestine (diarrhoea). Bacteria begin breaking it down releasing gases (bloating/discomfort)

Question 11

Dietary Polysaccharide metabolism

Answer 11

Starch and Glycogen hydrolysed by category of enzymes called glycosidase enzymes in mouth and duodenum
Produce glucose, maltose and Dextrins
Maltose and Dextrins and dietary Lactose and sucrose digested in duodenum and jejenum

AMYLASE IN SALIVA
LACTASE, SUCRASE, PANCREATIC AMYLASE (BREAKS a 1-4 bonds) , ISOMALTASE (BREAKS a 1-6 bonds)

The enzymes are found attached to brush border membrane of epithelial cells in small intestine

Question 12

Primary Lactase Deficiency

Answer 12

Absence of Lactase persistence allele in adults
So LACTASE ENZYME not produced

Question 13

Secondary lactase deficieny

Answer 13

Caused by injury to small intestine:
Gastroenteritis
Coeliac Disease
Ulcerative colitis
Chron’s Disease

The transmembrane enzymes damaged

Question 14

Congenital lactase deficiency

Answer 14

AUTOSOMAL RECESSIVE defect in lactase gene. Cant digest breast milk

Question 15

Glycolysis main features

Answer 15

Is anaerobic
Oxidation of glucose IS EXERGONIC
2 NADH produced per glucose
4 ATP produced Net production of 2 ATP
2 ATP used in substrate phosphorylation of glucose
Finishes with 2 pyruvate molecules

Question 16

Glycolysis Key Regulatory enzymes

Answer 16

Hexokinase(glucokinase in liver)
Converts glucose to glucose 6 phosphate

Phosphofructokinase-1 (key control enzyme of glycolysis) Fructose 6 phosphate to Fructose 2-6 bisphosphate

Pyruvate Kinase converts phosphoenolpyruvate to pyruvate

Question 17

Cells/tissues requiring glucose

Answer 17

RBCs
Neutrophils
Inner cells of kidney medulla
Lens of eye
Either have low 02 environment or lack mitochondria

Question 18

1-3 bis phosphoglycerate important from glycolysis

Answer 18

2-3 bis phosphoglycerate is derived from it and it regulates oxygen affinity of haemoglobin

Question 19

Dihydroxyacetone = important glycolysis metabolite

Answer 19

Undergo reaction to produce Glycerol Phosphate.
Important to make Triacylglycerols (Triglycerides)

Question 20

Phosphofrucktokinase Regulates Glycolysis

Answer 20

Allosterically controlled:
High ATP INHIBITS, High Citrate INHIBITS, STIMULATED By High AMP

Hormonal controlled: Insulin STIMULATES, GLUCAGON INHIBITS

Question 21

Lactate Dehydrogenase (LDH) Importance

Answer 21

Converts Pyruvate to Lactate and Lactate to Pyruvate
Replenishes the amount of oxidised NAD+ when pyruvate is converted to Lactate
Uses up NADH oxidising it
ESSENTIAL WHEN NO 02 FOR OXIDATIVE PHOSPHORYLATION SO REDUCING POWER CANT BE REGENERATED SO GLYCOLYSIS WOULD CEASE

Question 22

[Blood Lactate] Controlled By

Answer 22

Rate of production
Rate of Utilisation
Rate of disposal by kidney

Question 23

Fructose and Galactose metabolism

Answer 23

They get metabolised so that they end up as G-3-P which can be converted to pyruvate so the normal metabolic pathway can resume

Question 24

Galactosaemia

Answer 24

Unable to utilise Galactose as a result of a deficiency in 1 of 2 enzymes:
-Galactokinase
-Galactose-1P uridyltransferase or just uridyl transferase

Question 25

Galactokinase deficient galactosaemia

Answer 25

Milder form than uridyl transferase deficient Only galactose accumulates Leads to galactose entering ALDOSE REDUCTASE PATHWAY PRODUCES galactitiol

Question 26

ALDOSE REDUCTASE PATHWAY

Answer 26

Galactose converted into galactitol (reduced alcohol) This depletes the NADPH stores in the eye lens damaging the crystallin protein in the eye The denatured protein makes the lens cloudy

Question 27

Galactose-1P Uridyl Transferase Deficient Galactosaemia

Answer 27

Common worse form of Galactosaemia Both Galactose and Galactose-1-P Galactose-1-P affects liver, kidney and brain (organ damage)

Question 28

Galactosaemia Treatment

Answer 28

NO LACTOSE IN DIET

Question 29

Galactosaemia Symptoms

Answer 29

Cataracts Enlarged Liver Vomiting Diarrhoea Galactose in Urine

Question 30

Pentose Phosphate Pathway

Answer 30

Starts with Glucose-6-Phosphate Important source of NADPH for: Biosynthesis, detoxification, maintains GSH levels Makes 5 Carbon sugar ribose (Needed for making. Nucleotides, DNA/RNA)

Question 31

Glucose-6-phosphate dehydrogenase

Answer 31

Rate limiting enzyme in Pentose Phosphate Pathway

Question 32

Glucose-6-Phosphate dehydrogenase (G6PDH) deficiency (ENZYME ESSENTIAL IN PROTECTING AGAINST OXIDATIVE STRESS/ROS since NADPH needed to maintain high GSH levels)

Answer 32

In RBCs affected. NADPH levels fall, so cell vulnerable to ROS, disulphide bridges form in RBC denaturing the haemoglobin, Heinz bodies present, haemolysis

Question 33

G6pd found in RBCs

Answer 33

It protects RBCs Without it RBCS become damaged meaning less RBCs can take oxygen around the body making you anaemic and therefore tired/lacking energy

Question 34

GSH (Glutathione)

Answer 34

Protects cell against oxidative damage

Question 35

Why is NADPH important for GSH

Answer 35

Its needed to recycle GSH back into its active reduced form

Question 36

Active Glutathione Role (GSH)

Answer 36

Prevent damage from free radicals on cells

Question 37

RBCs vulnerable in G6PD deficiency

Answer 37

Pentose Phosphate Pathway only source of NADPH (NO MITOCHONDRIA SO NON KREBS CYCLE), vulnerable to oxidative damage. Haemoglobin gets cross linked by disulphide bonds, causing oxidative damage forming Heinz bodies. Cells get destroyed (haemolytic)

Question 38

Pyruvate Dehydrogenase

Answer 38

Catalyses conversion of pyruvate into acetyl CoA so the Krebs Cylcle (TCA Cycle) can happen

Question 39

Phosphofructokinase regulation

Answer 39

Stimulated by AMP (Low energy signal, when ratio of ATP:ADP is low, cell needs to make more ATP) Inhibited by ATP (High energy signal also is product inhibition)

Question 40

Absorption of monosaccharides from small intestine into blood

Answer 40

Active Transport via Sodium GLucose Transporter 1 (SGLT1) into intestinal epithelial cells Facilitated Diffusion Via GLUT2 transporter into BLOOD

Question 41

5 Glucose Transporters

Answer 41

GLUT 1 GLUT 2 GLUT 3 GLUT 4 GLUT 5

Question 42

All c