01d: FA Oxidation, Gluconeogenesis Flashcards
FA undergo oxidation in tissues, esp (X), for E. They can also be ocnverted to (Y) for storage in adipose tissue.
X = muscle and liver Y = triacylglycerols
List the four basic functions of FA.
- Major fuel source
- Building blocks (phospholipids, glycolipids)
- Protein modifies (hydrophobicity)
- Hormones/intracell messenger precursors
Palmitic acid has (X) number of C’s and the (sat/unsat) version is called (Y) with (Z) number of C’s.
X = 16
Unsat;
Y = palmitoleic acid
Z = 16
Oleic acid has (X) number of C’s and the (sat/unsat) version is called (Y) with (Z) number of C’s.
X = 18
Sat;
Y = stearic acid
Z = 18
T/F: Linoleic and linolenic acids are both unsaturdated with 18 carbons.
True (differ in number of double bonds)
Lipolysis, aka (X) breakdown, is a(n) (Y)-sensitive process.
X = triglyceride/triacylglycerol Y = hormone
(X) acts on triglyceride to produce DAG, which is then acted on by (Y).
X = adipose TG lipase Y = hormone-sensitive lipase
TAG broken down to DAG then MAG. What acts on MAG to produce (X) product(s)?
MAG lipase;
X = glycerol and FA
List hormones that play important role in stimulating lipolysis.
Epi and glucagon
First step in FA oxidation is (X). This step involves ATP (production/breakdown) (to/from) (Y).
X = FA activation
Breakdown;
To
Y = AMP and PPi, which is then cleaved to 2Pi (two high-E bonds broken!!)
T/F: In FA activation, ATP is broken down into ADP and PPi.
False - into AMP and PPi, then PPi cleaved to 2 Pi
Activation of free FA is carried out by (X) enzyme. Essentially, FA and (Y) become (Z).
X = Acyl-CoA Synthetase Y = CoA Z = Acyl-CoA
Second step in FA Oxidation is (X). What needs to be done for this step to occur?
X = Transfer to mitochondria
Carnitine replaces CoA on Acyl-CoA (to allow it to pass through translocase)
FA Ox: (X) enzyme responsible for addition of carnitine to FA Acyl group. (Y) enzyme responsible for putting the CoA back once FA is in (Z) compartment.
X = CPT-I Y = CPT-II Z = mitochondrial matrix
CPT = carnitine palmitoyl transferase = carnitine acyltransferase
The translocase that’s important for shuttling FA to (X) compartment is in (Y) membrane and recognizes (Z).
X = mitochondrial matrix Y = inner mito Z = carnitine
Third step in FA Oxidation is (X). In general, it starts with (Y) and ends with (Z) products.
X = beta-oxidation Y = Acyl-CoA Z = Acetyl-CoA and Acyl-CoA (that's 2 C shorter)
How many NADH or FADH2
(required/produced) per cycle of FA beta-oxidation?
Produced;
1 of each
An important point of control in FA Oxidation is at that of (X) enzyme. Specifically, it’s inhibited by (Y), which is made by (Z).
X = CPT-I Y = malonyl-CoA Z = acetyl-CoA carboxylase (ACC)
High levels of ACC enzyme is important for (stimulation/inhibition) of (X) enzyme/process. You’d expect ACC to be quite active as a result of (low/high) E states.
Inhibition;
X = FA oxidation (via CPT-I enzyme step)
High E
In addition to controlling (X) process, ACC enzyme can be controlled. Specifically, (Y) inhibit(s) it in (low/high) E states.
X = FA oxidation (inhibits translocase step)
Y = PKA and AMPK (AMP-activated protein kinase)
Low E
High PKA has (stimulatory/inhibitory) effect on FA oxidation by its direct (stimulatory/inhibitory) effect on (X).
Stimulatory;
Inhibitory (via phosphorylation);
X = ACC enzyme
One of the most common inborn errors of metabolism is related to FA oxidation, a(n) (excess/deficiency) in (X) enzyme.
Deficiency;
X = Medium Chain Acyl-CoA Dehydrogenase (MCAD) deficiency
Patient with Medium Chain Acyl-CoA Dehydrogenase (MCAD) deficiency would be (hyper/hypo)-glycemic. List the two reasons for this.
Hypoglycemic;
- Tissues forced to consume glucose since FA not available
- Gluconeogen not possible without FA Ox
(X) is an important alternate E product/fuel for brain in severe starvation. These are produced primarily in (Y) from (Z) compound.
X = ketone bodies Y = liver mitochondria (ketogenesis) Z = acetyl-coa
Ketone body synthesis: interconversion can occur when (X) compound undergoing either decarboxylation, to yield (Y), or reduction, to yield (Z).
X = acetoacetate Y = acetone Z = D3-Hydroxybutyrate
Which, if any, ketone bodies can be efficiently reconverted via (ketogenesis/ketolysis) to (X). What’s the fate of (X)?
Ketolysis;
Acetoacetone and D3-hydroxybutyrate
X = acetyl-coa (2 molecules)
TCA Cycle
In (X) disease, there’s a very high blood level of ketone bodies. This is because (presence/absence) of (Y) results in unrestrained (Z).
X = diabetic ketoacidosis
Absence
Y = insulin
Z = lipolysis (even in presence of high glucose)
T/F: Gluconeogenesis has same energy requirements as glycolysis (2 ATP per glucose).
False - 6 ATP (or GTP) per glucose
The (first/second/third) enzyme of gluconeogenesis, (X), has a required activator: (Y).
First;
X = pyruvate carboylase
Y = acetyl-coa
Insulin (stimulates/inhibits) gluconeogenesis. This is (direct/indirect) via (stimulating/inhibiting) (X).
Inhibits;
Indirect;
Inhibiting
X = FA lipolysis (and thus acetyl-coa formation, which is required for gluconeogen)
The first two steps of gluconeogen, involving (X) enzymes, are highly coordinated by liver with corresponding (Y) enzyme.
X = pyruvate carboxylase and PEP carboxykinase Y = pyruvate kinase
The liver exercises high control/regulation over (X) and (Y) early glycolytic enzymes. It also regulates the two corresponding gluconeogenesis enzymes, which are:
X = glucokinase Y = PFK
Glucose-6-phosphatase and fructose-1,6-BPase
Fructose-2,6-BP, which (stimulates/inhibits) PFK, (stimulates/inhibits) the corresponding gluconeogenesis enzyme (X).
Stimulates;
Inhibits;
X = Fructose-1,6-BPase
Key enzyme involved in Cori cycle is (X). And in alanine cycle is (Y).
X = lactate dehydrogenase Y = alanine aminotransferase (ALT)
(Alanine/Cori) cycle is active in high muscle activity.
Cori
Unlike (X), ketone bodies don’t need to be carried on albumin to travel in bloodstream. Why?
X = FAs
They’re water-soluble
Reciprocal control: Fructose-1,6-BPase is inhibited by high levels of (X), which are the factors that stimulate (Y) glycolytic enzyme.
X = Fructose-2,6-BP and AMP Y = PFK
Control of gluconeogenesis and glycolysis is possible by adaptive responses. In other words, starvation/low carb diet will have which general effect on gluconeogen/glycolytic enzymes?
Gluconeogen enzymes upregulated
(X) glycolytic enzyme must be inhibited for gluconeogenesis to proceed. This justifies the heavy regulation put on (X), such as its required activator: (Y).
X = pyruvate kinase Y = fructose-1,6-BP
The main points of Cori/alanine cycles is that liver receives lactate/alanine, converts them to (X) via (Y), and sends the much-needed product back to (Z).
X = pyruvate, then glucose Y = gluconeogenesis Z = muscle (via blood)
EtOH ingestion inhibits gluconeogenesis due to (depletion/accumulation) of (X).
Accumulation;
X = NADH
Fuel stores in muscle include (X); these stores are for (muscle/other tissues).
X = glycogen and TAGs;
Muscle alone
Fuel stores in liver include (X); these stores are for (liver/other tissues).
X = glycogen; Other tissues (brain, muscle)
Fuel stores in adipose include (X); these stores are for (muscle/other tissues).
X = TAGs; Other tissues (liver, muscle)
T/F: An overflow of excess lipids results in fat accumulation outside adipose tissue (muscle, liver).
True
