Lecture 4.1: Energy Storage- Carbohydrates and Lipids Flashcards
Types of fuel reserves in body (4)
Triacylglycerol
Liver Glycogen
Muscle Glycogen
Muscle Protein
Which tissues have an absolute need for glucose as fuel?
Erythrocytes and leukocytes
Testes
Kidney medulla
Lens and cornea of the eye
Brain
Hypoglycaemia (4 glucose levels)
2.8mmol/L : Confusion
1.7mmol/L : Weakness, Nausea
1.1mmol/L : Muscle Cramps
0.6mmol/L : Brain Damage, Death
Glucose Utilisation Over Time
2 hrs after meal: Glucose from food
2-8 hrs after: Glycogenolysis (Glycogen)
8-10 hrs after: Gluconeogenesis (Lactate, Glycerol, Amino acids)
How is Glycogen Stored?
As granules in muscle and liver cells
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]
Glycogenesis (Glycogen Synthesis)
Diagram on iPad
Regulation of Glycogen Metabolism: Glucagon, Adrenaline
Mechanism is phosphorylation
Glycogen synthase decreased
Glycogen phosphorylase increased
Regulation of Glycogen Metabolism: Insulin
Mechanism is de-phosphorylation
Glycogen synthase increased
Glycogen phosphorylase decreased
Glycogen Storage Diseases (GSD I-XI)
Arise from deficiency or dysfunction of enzymes involved in glycogen metabolism
Severity depends on enzyme/tissue affected
11 distinct types
Why is excess glycogen storage harmful?
Can lead to tissue damage
Why is insufficient glycogen degradation harmful?
Can lead to hypoglycaemia (low glucose levels)
Poor exercise tolerance
Types of GSDs (4 out of 11)
McArdle Disease (GSD V)
Von Gierke Disease (GSD I)
Cori Disease (GSD III)
Pompe’s Disease (GSD II)
McArdle Disease (GSD V)
Muscle glycogen phosphorylase deficiency
Exercise-induced muscle pain and cramps
Fatigue/ Tiredness
Von Gierke Disease (GSD I)
Cori Disease (GSD III)
Pompe’s Disease (GSD II)
Gluconeogenesis (de novo glucose synthesis)
Synthesis of glucose from non-hexose precursors
Beyond 8-10 hours of fasting, liver glycogen stores start to deplete and an alternative source of glucose is required
Occurs in liver and to lesser extent in kidney cortex, major precursors include: Lactate, Glycerol, Pyruvate, Glucogenic amino acids (mainly alanine)
Key Enzymes In Gluconeogenesis
Phosphoenolpyruvate carboxykinase (PEPCK)
Fructose 1,6-bisphosphatase
Glucose-6-phosphatase
Regulation of Gluconeogenesis
Glucagon, Cortisol: Increases PEPCK and Fructose 1,6 bisphosphatase, Stimulates Gluconeogenesis
Insulin: Decreases PEPCK and Fructose 1,6 bisphosphatase, Inhibits Gluconeogenesis
Lipid (Triacylglycerol) Storage
Highly efficient energy store
Energy content per gram twice that of carbohydrate or protein
Excess energy is converted to triacylglycerol (TGs) for storage
Stored as anhydrous white adipose tissue
The storage and mobilisation of TGs is under hormonal control
