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gihep 15: post-absorption processing of lipids (TG breakdown (lipolysis)…
gihep 15: post-absorption processing of lipids
FAs
in fed state get converted to TGs
major energy source, principal storage form
too large + hydrophobic to travel in blood
transported as chylomicrons (bind to lipoproteins)
released from lipoproteins by lipoprotein lipase
not in liver or brain
unregulated by insulin
relocated to muscle when fasting
in fasting state...
converted to ACoA by beta oxidation
converted to ketone bodies in liver by ketogenesis
carried to tissues by albumin
TG synthesis
increased by insulin
increase no. of glucose transporters
produces more glycerol 3P (byproduct of glycolysis)
increases lipoprotein lipase activity
induces glyclrolphosphate-acyl transferase (catalyses 1st step)
TG breakdown (lipolysis)
stepwise removal of 3 FAs
1st cleavage = rate limiting step
catalysed by hormone sensitive adipose tissue lipase
activated by decreased insulin
activated when phosphorylated by PKA
lipolytic hormones
NA + adrenaline
act via beta-adrenergic Rs (cAMP, PKA)
most important
glucocorticoids, GH, thyroid hormone
symp NS ensures TGs are hydrolysed in response to cold, stress + exercise
beta-oxidation
in all cells except neutrons + RBCs
in mitochondria
short FAs enter by passive diffusion
long FAs converted to CoA-thioesters by thiokinase, then transported by carnitine
inhibited by malonyl-CoA
each cycle removes 2 Cs + produces NADH, H+, FADH2
high ATP yield
4 enzymes
acyl-coA dehydrogenase (long, medium or short chain)
enoyl-CoA dehydratase
3-L-hydroxyacyl-CoA dehydrogenase
beta-ketothiolase
Ketone bodies
acetoacetate + beta-hydroxybutyrate
formed in liver mitochondria from ACoA (ketogenesis)
metabolised in TCA cycle
acetone
small amounts formed by spontaneous decarboxylation of acetoacetone
released on the breath
major energy source, esp in heart, adrenal gland, renal cortex
circulating levels low, rise in fasting + diabetes mellitus
Brown adipose tissue
for thermogenesis instead of ATP release
good blood supply, lots of mitochondria + cytochromes
decreased ATP syntheses activity
oxidation of glucose + FAs
medium chain acyl CoA dehydrogenase deficiency (MCADD)
fat stores can't be oxidised
fasting intolerance, hypoglycaemia, impaired ketogenesis
manage via diet
don't fast
glucose supplements