8. the starved state Flashcards
when does the fasting state start?
what type of state is the body in during this time?
when does the starved state start?
2-4 hours after a meal
catabolic
3 days- metabolically different to fasted state
during starvation, what two factors determine how long you can survive for?
amount of adipose tissue and protein levels
what can protein depletion lead to?
organ malfunctioning and infections
two priorities of the body during starvation
-Maintain adequate blood glucose
Mobilise fatty acids & synthesise/release ketone bodies for other tissues
why isn’t it practical to store all energy as glycogen?
binds water as polar molecule
organ fuel use: brain
- Glucose is primary fuel (except during starvation)
- Ketones used in starvation
- FAs can’t cross BBB as bound to albumin
Organ fuel use:muscle
- Glucose, FA, & Ketone Bodies
- Glycogen store can be converted to glucose by glucose-6-phosphate for contraction
- FAs are used by resting muscle (85%) of needs
- Glucose prioritized for contraction
organ fuel use: heart
- FAs, ketone bodies, lactate
- No glycogen reserves. So prefers fatty acids and ketones
organ fuel use: adipose tissue
what is needed to create triacylglycerols?
what else is needed?
- Needs glycerol 3-phosphate to create triacylglcyerols
- ∴ need glucose for glycolytic intermediate Dihydroxyacetone phosphate (reduction = G-3-P)
organ fuel use: liver
- Provides fuel to brain, muscle & peripheral organs
- Metabolises carbohydrates (~ 2/3rds of glucose) to form glycogen
- Turns fatty acids into ketone bodies
Utlises α-ketoacids derived from amino acids
carbohydrate metabolism in liver:
what is the main role? what else is produced?
which metabolic pathway is used first?
what does in increase glucagon: insulin lead to?
where are the skeletons from gluconeogenesis derived from?
- the main role is to produce glucose by glycogenolysis & gluconeogenesis. Also , ketone bodies are produced for non-glucose dependent tissues.
- Glycogen degradation occurs first, followed by gluconeogenesis
-Increased glucagon-to-insulin ratio = PKA-mediated phosphorylation of glycogen phosphorylase kinase
Increased phosphorylation of glycogen phosphorylase
•The skeletons from gluconeogenesis are derived from glucogenic amino acids, lactate from muscle and glycerol from adipose tissue
- Gluconeogenesis is favored by fructose 1,6-bisphosphatase activation & PEPCK induction
•Some amino acids are used for biosynthetic functions
- e.g. heme synthesis, neurotransmitters formation
•Nitrogen is converted to urea (output decreases as starvation continues)
fat metabolism in liver
•Fatty acid oxidation is the major energy source in liver tissue
- Malonyl CoA drop permits CPT-1 to activate & β-oxidation occurs
- NADH produced inhibits the TCA cycle
- Acetyl CoA produced activates Pyruvate carboxylase &inhibits pyruvate dehydrogenase
- Gluconeogenesis is increased
•Increased Ketone body synthesis occurs (acetoacetate & 3-hydroxybutyrate)
- Not used by liver as lacking thioporase
- Favoured when acetyl CoA exceeds TCA cycle capacity
adipose tissue: carbohydrate metabolism
Glucose transport is depressed as GLUT-4 is insulin sensitive
- Reduced glycolysis etc.
- Reduced TAG synthesis
adipose: fat metabolism
- Adipose triacylglycerols are mobilized by lipolysis
- releases FAs & glycerol
- PKA-mediated phosphorylation and activation of HSL
- enhanced by elevated catecholamines
- FA usage increases with length of fast
•Increased Release of Fatty acids
- Hydrolysis of TAGs releases FAs
- Bound to albumin they act as fuel for a variety of tissues
- Glycerol can also be used as a gluconeogenic precursor in the liver
•Decreased uptake of Fatty acids
- Adipose LPL activity is low
resting skeletal muscle
•During fasting, resting muscle moves further from glucose to FAs & ketone bodies
- For contraction: as glycogen depleted, FAs mobilized from TAG (Adipose tissue) become the dominant energy source.
