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16 Cards in this Set

  • Front
  • Back

Structure of TAG (triacylglycerols)

3 FA's esterified to glycerol


1: saturated


2: unsaturated


3: either

TAG storage

Form oily droplets, anhydrous


= major E reserve for body

Sources of glycerol phospate

- initial acceptor of FA's in TAG synthesis




- liver & adipose tissue: from glucose


-> DHAP, glycerol phosphate dehydrogenase => glycerol phosphate




- liver: glycerol, glycerol kinase => glycerol phosphate

TAG synthesis

FA + CoA, ATP -> FA-CoA + AMP, PPi




- 3 additions to glycerol-Pi => TGA


w/ acetyl transferase (& phosphatase before the last step)

Fates of TAG in liver, intestines, adipose tissue

adipose tissue: depot fat (storage)




liver: little storage; most produces VLDL (w/ cholesteryl esters, cholesterol, phospholipid, protein [apolipoprotein B-100])




intestines: transported w/ chylomycrons

Classes of phospholipids

glycerophospholipids [phosphoglicerides]: glycerol as a backbone; phosphatidic A-derived




sphingophospholipids: sphingosine backbone

Glycerophospholipids formation

Phasphatidic A + alcohol (attached to the P)




Either one needs to be activated by CDP-


Synthesized in the sER -> Golgi -> membranes/excreted

Cardiolipin

= PA + glycerol + PA (in mito)


(2 phosphatidylglycerols connected by the common alcohol, glycerol)




- antigenic


- inner mito & bacterial membranes

Sphingophospholipids synthesis

sphingosine + FA (@ amino group) -> ceramide -> OH group @ C1 esterified -> sphingomyelin




- in cell PM, high affinity to cholesterol


- constituent of myelin




Ceramide can also be linked w/ glucose/galactose @ C3 -> glycolipids

Degradation of phosphoglycerides

Phospholipases -| phosphodiester bonds


@ C1/2 -> lysophosphoglyceride


-> lysophospholipases -> ...




- forming (substrates of) messengers


- remodeling

Degradation of sphingomyelin

Sphingomyelinase (type of PLC) -| phosphorylcholine -> ceramide -> ceramidase -> sphingosine + FA




- messengers


- if malfunctional: Niemann-Pick disease (A/B)

Structure of cholesterol

~ a kind of sterols




4 fused hydrocarbon rings


A, B, C - 6-membered rings


D - 5-membered ring




+ 8C branched HC @ C17 of D, OH @ C3 of A, etc.

Cholesteryl Esters (CE)

Form of most plasma cholesterol (FA @ C3 of A)


-> even more hydrophobic

Cholesterol synthesis

Synthesized in all tissues, cyto


All C's from acetate; reducing equivalents: NADPH




2 Acetyl-CoA -> aceloacetyl-CoA


+ Acetyl-CoA, HMG-CoA synthase -> HMG-CoA


+ HMG-CoA reductase, 2 NADPH -> mevalonic A, CoA (rate-limiting step)


->> 2 ATP -> 5-pyrophosphomevalonate


->> ATP -> CO2 + IPP -> DPP; + IPP -> GPP; + IPP -> FPP;


2 FPP -> squalene ->> NADPH -> lanosterol ->> cholesterol

Regulation of cholesterol synthesis

Major control pt: HMG-CoA reductase ~rate-limiting enzyme




- Sterol-dependent regulation of gene expression (SREBP2 -> SRE => ↑)


- ↑ cholesterol -> ↓ stability


- Sterol-independent de-/phosphorylation (Pi-|)


- Hormonal regulation


- Inhibition by drugs

Degradation of cholesterol

Conversion -> bile A's/salts -> excretion in feces


Modification by bacteria -> coprostanol, cholestanol


=> all: neutral fecal sterols




- precursor for oxysterols & steroid hormones