Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
27 Cards in this Set
- Front
- Back
|
what are the major types of lipids and their functions? |
FFA (fatty acids) -it's delivered from adipose to liver for use -major component of triglycerides and LPs -precursor is arachidonic acid (important in inflammation) triglycerides -form of energy storage in adipose tissue phospholipids -part of cell & organelle membranes & LPs -precursor to 2nd messengers in intracellular signaling & for myelin in CNS/nerves cholesterol -part of membranes -precursor to steroid and bile acids lipoproteins=TG+cholesterol+phospholipids+apolipoproteins -transporters of triglycerides & cholesterol b/w sites of lipid absorption/synthesis & storage |
|
|
what are eicosanoids derived from (i.e. prostaglandin)? |
like fatty acids, they're derived from arachidonic acids |
|
|
what metabolic processes are fatty acids primarily synthesized from? |
from carbon (Acetyl CoA), which is produced by carb or AA metabolism in the mitochondria, feeding into the TCA cycle (thus TCA cycle feeds this anabolic pathway via one of its intermediates) |
|
|
what is the key enzyme/step in FFA synthesis (lipogenesis)? |
AcCoA Carboyxlase (ACC) |
|
|
what is the key hormone regulating lipogenesis? How does this hormone regulate the process |
insulin it regulates ACC, which is the key enzyme in lipogenesis |
|
|
given that fatty acids are derived from acetyl CoA (taken from TCA cycle), how does Acetyl CoA get from the mitochondria to the cytosol? |
Acetyl Coa gets from mitochondria (in TCA cycle) to cytosol via citrate (intermediate of TCA) As citrate leaves the mitochondria into the cytosol, citrate lyase cleaves it into Acetyl CoA and Oxaloacetate |
|
|
why is dietary macronutrient composition important for lipogenesis?
|
it's important because it determines how much lipogenesis will occur
lipogenesis can only occur if there's an excess of carbs (glucose) & AA being metabolized, if there's not excess glucose, Acetyl CoA will continue toward TCA cycle to form energy
Also, lipogenesis only occurs if there's an excess AA. If there's no excess, AA can't be converted to fatty acids for energy storage
|
|
|
in what organ does lipogenesis primarily occur? |
liver rodents: in adipose tissue |
|
|
the presence of which regulatory molecule stimulates the polymerization of ACC (active form) to allow it to convert Acetyl CoA into malonyl CoA... thus turning on lipogenesis?
|
citrate |
|
|
the presence of which regulatory molecule stimulates depolymerization of ACC (inactive form) to inhibit ACC function, thus turning off lipogenesis? |
palmitoyl-CoA |
|
|
what phosphorylation state is ACC in in order to be active? |
ACC active =dephosphorylated b/c it allows ACC units to polymerize ACC inactive= phosphorylated units |
|
|
what regulatory enzyme directly activates ACC? what regulates this enzyme? |
phosphatase b/c it dephosphorylates ACC, thereby by allowing the multimeric units to polymerize regulatory factor: Pase is activated by insulin (which is stimulated during times of high energy); Pase is inactivated by glucagon/epi (which are signs of low energy status/hypoglycemia), via cAMP-dep PK |
|
|
what regulatory enzyme directly inactivates ACC? what regulates this enzyme |
AMP-K b/c it phosphorylates ACC, thus preventing the units from rebinding together regulatory factor: the presence of of low ATP (don't want to build fat during low energy status) |
|
|
T/F: FAS (fatty acid synthase) is a single enzyme
|
false; it's an enzyme complex |
|
|
how does FAS facilitate lipogenesis? |
once ACC produces malonyl CoA from Acetyl CoA & ATP; FAS complex: 1. combines malonyl CoA to ACP (acyl carrier protein) to form malonyl-ACP. 2. adds 2 C Acetyl CoA subunits to malonyl-ACP to form palmitate (major 16 C FFA) FAS does this via: energy using reducing power from NADPH provided by pentose phosphate pathway |
|
|
what effects do the following factors have on [ACC] & [FAS] (both which facilitate lipogenesis): insulin starvation dietary PUFA (polyunsaturated fatty acids) |
insulin stimulates their concentrations (it indicates there's energy to conduct lipogenesis) starvation and dietary PUFA decrease their concentrations (starvation = lack of energy to make fat; PUFA=another source of dietary fat, so why make more?) |
|
|
what enzyme binds the 3 fatty acids to glycerol to make triglyceride? |
acyltransferase enzyme |
|
|
T/F: lipids are stored as fatty acids
|
false they're stored as triglycerides
|
|
|
are 'free' fatty acids truly circulating in the blood 'free' of any attachment?
: |
No, it's bound to albumin as it's transported via blood |
|
|
where are fatty acids stored that are produce by: 1. adipose tissue (rodents) 2. liver |
FFAs produced by adipose are stored in adipose FFAs produced by liver are exported as VLDL (lipoprotein) to transport to adipose for storage |
|
|
why is it more efficient to store energy as triglycerides than glycogen? |
fat's stored in anhydrous state, but glycogen's in a hydrous state thus fat has more kcal/g (fat has > 2x calories as carbs) as a result, this energy storage lasts longer, allowing for hibernation |
|
|
what is the rate limiting step/enzyme in cholesterol synthesis? |
HMG-CoA reductase (this is the target of statin drugs like lipitor) |
|
|
what is the major apoprotein(s) in the following lipoproteins: 1. VLDL 2. LDL 3. chylomicrons 4. HDL (good cholesterol) |
1. apolipoprotein B (apo-B)
2. Apo-B100 3. Apo-B48 4. Apo-A1 |
|
|
what is the function of LPL (lipoprotein lipase)? |
it's the enzyme (located on the endothelium of capillaries in FFA storage tissue (adipose & muscles)) that cleaves TGs that are delivered by VLDL and chylomicrons in other words, it's the transporter of lipids from site of absorption (intestine) or synthesis (liver) to site of storage (fat/muscle) thus it allows lipids to pass through capillaries of muscles and adipose for storage |
|
|
what upregulates the LPL expression activity in adipose & muscle? |
insulin (remember, need energy to store fats, thus insulin is a signal of high energy status) insulin thus increases the lipolysis of chylomicrons and VLDL |
|
|
what is the rate limiting enzyme in the hydrolysis of TG into FFAs & glycerol? how is it regulated? |
HSL (hormone sensitive lipase) regulated by phosphorylation state via cAMP: inhibited by insulin (signs of higher energy; thus you want to keep fat stored, NOT released) activated by glucagon/epi/norepi (signs of starvation; want to use up your fat storage and release it) |
|
|
what is the function of HSL (hormone sensitive lipase)? |
it's the transporter of lipids from site of storage (fat/muscle) to site of absorption (intestine) or synthesis (liver) (opposite of LDL)
it facilitates fatty acid release from storage tissue into blood stream |
