Feed/Fast Cycle Flashcards
Mention the 2 body priorities during fasting state
- The need to maintain adequate plasma levels of glucose to sustain energy for brain, RBCs & other glucose-requiring tissues
- The need to mobilize FA from adipose tissue & to synthesize ketone bodies in liver for all other tissues
Describe CHO metabolism in liver during well-fed state
- Inc phosphorylation of glucose by glucokinase
- Inc glycolysis by activating rate-limiting enzymes & inc PDH activity (as PDH kinase is inhibited by pyruvate). Acetyl CoA is used for FA synthesis or in TCA
- Inc glycogen synthesis: G6P is an allosteric effector of glycogen synthetase
- HMP inc activity due to in G6P & NADPH consumption
- Dec gluconeogenesis
Describe fat metabolism in liver during well-fed state
- Inc FA synthesis due availability of acetyl coA & NADPH, also acetyl CoA carboxylase is activated by dephosphorylation & citrate.
- Inc TAG synthesis due to availability if FA from de novo synthesis or CM, glycerol 3-phosphate is obtained from glycolytic metabolism of glucose. TAG is packaged in VLDL & distributed to body.
Describe AA metabolism in liver during well-fed state
Inc AA degradation as there is more than the liver can used for synthesis of proteins/N-containing compounds. Thus they are not stores & are either released into blood for other tissues OR deaminated with C-skeleton used to synthesise pyruvate, acetyl CoA or TCA cycle intermediates.
Describe CHO metabolism in Adipose tissue during well-fed state
- Inc glucose uptake which is inuslin dependent
- Inc glycolysis supplies Glycerol 6-P & Acetyl CoA for TAG synthesis
- Inc activity of HMP pathway (NADPH for FA synthesis)
Describe lipid metabolism in Adipose tissue during well-fed state
- inc synthesis of FA & TAG
- Dec TAG degradation, dec activity of HSL
Describe CHO & fat metabolism in SKM during well-fed state
- Inc glucose uptake
- Inc glycogen synthesis esp if stores are depleted by exercise
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FAs are released from CM & VLDL by LPL, but are 2ry energy source during well-fed state as glucose is the main energy source.
Describe protein metabolism in SKM during well-fed state
- Inc protein synthesis & inc AA uptake
- Inc uptake of branched chain AAs, valine, isoleucie, leucine as SKM is main site for their degradation as it contains required transaminases. They are used in protein synthesis or for energy.
Describe brain metabolism well-fed state
- It uses glucose exclusively as fuel, oxidized about 140 g/day completely dependent on availability of BG
- Brain has not TAG stores & FAs can’t cross BBB
Describe CHO metabolism in liver during fasting
- Inc glycogenolysis, nearly exhausted after 10-18 hrs of fasting
- Inc gluconeogenesis
Liver removes amino acids from circulation for gluconeogenesis
Describe lipid metabolism in liver during fasting
- Inc FA oxidation: as acetyl coA carboxylase is inactivated by phosphorylation, thus malonyl CoA drops relieving inhibition on CAT1
- Inc ketogenesis, conc of acetyl CoA from FA oxidation exceeds the capacity of TCA, it starts in first days (3 days) of fasting & rise in level of ketone bodies causes inhibition of muscle proteolysis.
Describe metabolism in adipose tissue during fasting
- Glucose uptake & utilization are depressed by low insulin
- Activation of HSL leadng to lipolysis, FFAs are bounf to albumin & utilized by various tissues as source of energy
- Glycerol is used in gluconeogenesis
Describe metabolism in SKM during fasting
- Glucose uptake & utilization are dec due to dec I/G ratio
- During 1st two weeks of fasting, muscle uses FAs & ketone bodies but during the third week it uses FAs almost exclusively
- During first few days of fasting there is rapid proteolysis to provide AAs to liver for gluconeogenesis. Alanine & glutamine are quatitatively most imp, but this process dec as brain starts using ketone bodies as source of energy.
Describe metabolism in brain during fasting
In the first days if fasting, the brain continues to use glucose. In prolonged fasting, plasma KBs significantly rise & replace glucose as 1ry source of energy.
Describe the role of kidney in long-term fasting
As fasting continues into early starvation,
1. Kidney expresses gluconeogenic enzymes including glucose 6-phosphatase
2. Kidney provides compensation for acidosis that accomapies in KBs. Glutamine released from muscle is acted upon by renal glutaminase & glutamate dehydrogenase producing a-ketoglutarate for TCA & ammonia which combines with H+ ions to form ammonium which is excreted in urine.
