Lecture 2.1: Energy Production from Carbohydrates (1) Flashcards
What is Anabolism?
The synthesis of larger molecules from simple molecules
(Monomers to Polymer)
What is Catabolism?
The breakdown of complex molecules in living organisms to form simpler ones
(Polymer to Monomer)
What are the 4 Stages of Catabolism?
1: Extracellular, GI Tract. Lipids, Carbs broken down into smaller parts so they can be taken into cells
2: Intracellular in cytosol and mitochondria [Glycolysis]
3: Intracellular in mitochondria [Krebs Cycle]
4: Intracellular in mitochondria [Oxidative Phosphorylation]
Recommend Daily Intake of C,L&P
Carbs: 15%
Lipids: 8%
Proteins: 5%
What are Carbohydrates?
General formula: (CH2O)n
Contain aldehyde or ketone group
Hydrophilic
Monosaccharides
Glucose
Fructose
Galactose
Aldose
Aldehyde containing sugar
Ketose
Ketone containing sugar
Isomers of Glucose
D and L
But only D isomer is naturally occurring
Common Disaccharides
Lactose: Galactose + Glucose
Maltose: Glucose + Glucose
Sucrose: Glucose + Fructose
α-glucose vs β-glucose
α-glucose: -OH group is below on Carbon 1
β-glucose: -OH group is above on Carbon 1
Monosaccharide Shape
Not Planer
They assume “boat” or “chair” shapes in 3D space
Oligosaccharides
Contain 3 –12 monosaccharides
Polysaccharides
Contain 10 – 1000 monosaccharides
Glycogen
– Human Starch, stored in liver and skeletal muscle
– α-glucose
– Contains α1,4 and α1,6 glycosidic bonds
– Highly Branched Structure [allows more rapid breakdown from all ends for
energy production]
Starch
– Polymer of glucose found in plants
– Mixture of amylose (α1-4 bonds) and amylopectin and α1-4 andα1-6
glycosidic bonds
– Less branched than glycogen
– GI tract enzymes release glucose and maltose
Cellulose
– Structural polymer of glucose in plants
– β1-4 linkages
– No GI enzymes to digest β1-4 Linkages
– It forms dietary fibre that is important for GI function
Digestion of Dietary Carbohydrates: where? what enzymes?
Mouth: Salivary α-amylase
Pancreas: α-amylase
Small intestine: Pancreatic amylase
Disaccharidases attached to brush border membrane of epithelial cells (enterocytes): lactase, sucrase, maltase, isomaltase
Carbohydrate Transport
Glucose, galactose and fructose are transported to enterocytes by facilitated or active transport
GLUT2 (glucose transporter type 2)
SGLT1 (Na+/glucose/galactose cotransporter)
GLUT5 (fructose transporter type 5)
They are transported from enterocytes to blood by GLUT2 and then transported to target tissues via various transporters
GLUT Transporters and their corresponding organs
Brain: GLUT3
Heart/Fatty Tissue/Skeletal Muscle: GLUT4
Enterocytes: GLUT1
Liver/ Pancreatic β-cells/ Intestines/ Kidney: GLUT2
Jejunum/ Kidney: GLUT5
Lactose Intolerance: Science
Loss of / reduced lactase activity
→ Therefore Inability to hydrolyse lactose
Results from reduced expression of the LCT gene
Onset from late childhood to early adulthood
Lactose Intolerance: Consequences
Undigested lactose is passed to the large intestine
Increases osmotic pressure and draws in H2O causing osmotic diarrhoea
Fermented by colonic bacteria produces organic acids (acetic and lactic
acids) and H2, CO2 and CH4 gases causing abdominal cramps and flatulence
Lactose intolerance: Symptoms, Clinical Tests, Management
No immune system involvement/ Not allergic reaction
Symptoms: abdominal pain, bloating, diarrhoea, and nausea appear in 30
to 120 minutes following consumption of lactose
Clinical Tests: Positive hydrogen breath test, Positive stool acidity test
Management: Decrease or elimination of the amount of lactose in diet, Consumption of lactase-treated foods or lactase supplements
Anaerobic Glycolysis: Lactate Dehydrogenase (LDH) Reaction
Overall reaction of the 11- step anaerobic glycolysis:
Glucose + 2 Pi + 2 ADP → 2 lactate + 2 ATP + 2 H2O
Where Does Lactate Go?
The lactate produced by skeletal muscle and RBCs is released into the blood
It is then metabolised by the liver, heart and kidney
2 NADH + (2 H+) + 2 pyruvate (2 NAD+) + 2 lactate
This is facilitated by LDH in both directions
Plasma Lactate Concentrations
Blood concentration normally constant: <1 mM
Hyperlactaemia: 2-5 mM in blood, Below renal threshold, No change in blood pH (buffering capacity)
Lactic acidosis: Above 5 mM in blood, Above renal threshold, Blood pH lowered
Essential fructosuria
Caused by fructokinase deficiency
Fructose accumulates in urine
No symptoms
Fructose Intolerance
Caused by aldolase deficiency
Fructose-1-P accumulates in liver, liver damage and hypoglycaemia
Symptoms: poor feeding as baby, vomiting, nausea, abdominal pain
Treatment- elimination of sucrose and fructose from diet
Galactokinase Deficiency‐Non‐Classical Galactosaemia
Very rare
↑ Galactose in blood (Galactosaemia) and urine (Galactosuria)
Galactose and Galactitol accumulation causes cataracts
Treatment ‐ dietary restriction (lactose and galactose)
GALT Deficiency‐ Classical Galactosaemia
Galactosaemia and Galactosuria
Galactose-1-P and Galactitol accumulate causing cataracts
Brain and Liver damage
Treatment ‐ dietary restriction (lactose and galactose)