Biochem lipids exam 2

What is the most common form of dietary lipid

Triacylglycerol (TAG)

How are fatty acids classified based on carbon chain length

"• Short-chain: 2 to 4 carbons
• Medium-chain: 6 to 12 carbons
• Long-chain: 14 to 20 carbons
• Very long-chain: $\ge 22$ carbons

"
Which chain lengths of fatty acids are found in significant quantities in milk

Chain lengths of 4 to 10 carbons (short and medium chain)

Structural lipids and triacylglycerols contain primarily fatty acids of at least how many carbons

At least 16 carbons (e.g., Palmitic acid)

Which two fatty acids are classified as essential fatty acids in the human diet

Linoleic acid (18:2) and $\alpha$-Linolenic acid (18:3)

Which 20-carbon polyunsaturated fatty acid serves as the direct precursor of prostaglandins

Arachidonic acid (20:4)

Which stomach enzymes initiate lipid digestion, and which fatty acids are their primary targets

Gastric lipase and lingual lipase

they target short- and medium-chain fatty acids.

What role does Cholecystokinin (CCK) play in intestinal lipid digestion

CCK stimulates bile release from the gallbladder, promotes pancreatic enzyme secretion, and decreases gastric motility.

What hormone stimulates the secretion of bicarbonate ($\text{HCO}_3^-$) from the pancreas into the duodenum

Secretin (neutralizes acidic gastric contents to allow optimal pancreatic enzyme activity).

What rate-limiting enzyme catalyzes the synthesis of primary bile acids from cholesterol

$7\alpha$-Hydroxylase Diagram showing cholesterol conversion to 7alpha-hydroxycholesterol catalyzed by 7alpha-hydroxylase

What are the two primary bile acids formed from cholyl-CoA

Taurocholic acid and Glycocholic acid

How are secondary bile acids (e.g., deoxycholic acid and lithocholic acid) produced in the gut

Intestinal bacteria deconjugate and $7\alpha$-dehydroxylate primary bile acids.

What percentage of bile salts released into the intestine are reabsorbed and recycled via enterohepatic circulation

95% (reabsorbed primarily in the ileum

5% excreted in feces) Diagram illustrating 95 percent reabsorption of bile salts in enterohepatic circulation

What are the primary breakdown products when pancreatic lipase hydrolyzes a dietary triacylglycerol

2-Monoacylglycerol and two free fatty acids

What is the specific function of colipase in pancreatic lipid digestion

Colipase binds to pancreatic lipase and anchors it to the lipid droplet surface, preventing bile salts from inhibiting lipase activity.

Which bond position does pancreatic Phospholipase $A_2$ specifically hydrolyze in a phospholipid

Position 2 (releasing a free fatty acid and a lysophospholipid)

What structures facilitate the intestinal absorption of dietary lipid digestion products across enterocyte membranes

Mixed micelles (composed of fatty acids, 2-monoacylglycerols, cholesterol, fat-soluble vitamins, and bile salts)

Following absorption into enterocytes, how are dietary lipids processed before export

TAGs and cholesterol esters are resynthesized and packaged into chylomicrons containing Apoprotein B-48.

What path do newly synthesized chylomicrons take to enter the systemic bloodstream

Excreted into intestinal lacteals $\rightarrow$ thoracic duct $
ightarrow$ systemic venous circulation

Which apolipoprotein on chylomicrons activates endothelial Lipoprotein Lipase (LPL) in capillary beds

ApoC-II

What action does Lipoprotein Lipase (LPL) perform on circulating chylomicrons

Hydrolyzes core triacylglycerols into free fatty acids and monoacylglycerols for tissue uptake.

Which hormones stimulate lipolysis in adipose tissue during fasting

Glucagon and Epinephrine (via phosphorylation and activation of Hormone-Sensitive Lipase)

How are free fatty acids (FFAs) transported in plasma after release from adipose tissue

Bound non-covalently to plasma albumin

Which enzyme activates cytosolic free fatty acids before they enter metabolic pathways

Fatty acyl-CoA synthetase (Thiokinase)

How many high-energy phosphate bonds are consumed during the activation of a fatty acid to Fatty Acyl-CoA

2 high-energy phosphate bonds (ATP $\rightarrow$ AMP + $\text{PP}_i$, followed by hydrolysis of $\text{PP}_i \rightarrow 2 \text{P}_i$ by inorganic pyrophosphatase)

Why is the carnitine shuttle required for mitochondrial long-chain fatty acid oxidation

The inner mitochondrial membrane is impermeable to long-chain Fatty Acyl-CoA.

Where is Carnitine Palmitoyltransferase I (CPT-I) located, and what is its reaction

Located on the outer mitochondrial membrane

converts Fatty acyl-CoA and carnitine into Fatty acylcarnitine and free CoA.

Which transport protein transfers fatty acylcarnitine across the inner mitochondrial membrane

Carnitine-acylcarnitine translocase (exchanges fatty acylcarnitine into the matrix for free carnitine moving out)

What reaction is catalyzed by Carnitine Palmitoyltransferase II (CPT-II) inside the mitochondrial matrix

Recombines the fatty acyl group with matrix CoA to reform Fatty Acyl-CoA and releases free carnitine. Diagram of the carnitine shuttle mechanism across outer and inner mitochondrial membranes

What are the four repeating enzymatic steps of the mitochondrial $\beta$-oxidation spiral

"1. Dehydrogenation (Oxidation generating $\text{FADH}_2$)
2. Hydration
3. Dehydrogenation (Oxidation generating NADH)
4. Thiolytic cleavage (releasing Acetyl-CoA)"
What reducing equivalents and carbon units are generated during one single cycle of $\beta$-oxidation

How many cycles of $\beta$-oxidation are required for the complete breakdown of Palmitoyl-CoA (C16), and how many Acetyl-CoA are produced

7 cycles of $\beta$-oxidation yielding 8 Acetyl-CoA molecules

What is the NET ATP yield from the complete mitochondrial oxidation of one molecule of Palmitate (C16)

106 ATP (108 ATP gross minus 2 ATP equivalents used during initial activation)

What metabolite synthesized during hepatic lipogenesis potently inhibits CPT-I to prevent simultaneous $\beta$-oxidation

Malonyl-CoA (produced by Acetyl-CoA carboxylase under insulin stimulation)

How do elevated cellular ratios of ATP/ADP and NADH/$\text{NAD}^+$ regulate fatty acid oxidation

High ATP and high NADH levels signal sufficient cellular energy and inhibit key enzymes of $\beta$-oxidation.

What 3-carbon intermediate is produced at the final step of odd-chain fatty acid $\beta$-oxidation

Propionyl-CoA

Which coenzyme is required by Propionyl-CoA carboxylase to convert Propionyl-CoA to D-Methylmalonyl-CoA

Biotin (Vitamin $B_7$)

Which coenzyme is required by Methylmalonyl-CoA mutase to produce Succinyl-CoA from L-Methylmalonyl-CoA

Coenzyme $B_{12}$ (Adenosylcobalamin) Pathway converting Propionyl-CoA to Succinyl-CoA via biotin and vitamin B12 dependent enzymes

What are the primary clinical features of adolescent or adult-onset CPT-II deficiency

Skeletal muscle pain and myoglobinuria triggered by prolonged exercise or fasting.

What diagnostic plasma biomarker accumulates in Medium-Chain Acyl-CoA Dehydrogenase (MCAD) deficiency

Elevated C8–C10 acyl-carnitines in plasma

Why does MCAD deficiency manifest as non-ketotic hypoglycemia during fasting

Impaired medium-chain fatty acid oxidation reduces hepatic acetyl-CoA supply, disabling both gluconeogenesis support and ketone body formation.

What is the primary organ site where ketogenesis occurs

Liver (specifically within hepatocyte mitochondria)

What is the rate-limiting enzyme in hepatic ketone body synthesis

Mitochondrial HMG-CoA synthase

Which ketone body is formed first by the cleavage of HMG-CoA by HMG-CoA lyase

Acetoacetate

Which enzyme reversibly converts Acetoacetate to D-$\beta$-hydroxybutyrate depending on mitochondrial NADH/$\text{NAD}^+$ levels

D-$\beta$-hydroxybutyrate dehydrogenase

How is acetone produced during hyperketonemia, and how is it eliminated

Produced by spontaneous, non-enzymatic decarboxylation of acetoacetate

eliminated by expiration through the lungs (fruity odor).

Which enzyme converts Acetoacetate to Acetoacetyl-CoA during ketone body utilization in extrahepatic tissues

$\beta$-Ketoacyl-CoA transferase (Thiophorase)

Why is the liver unable to oxidize ketone bodies for its own energy needs

The liver lacks the enzyme $\beta$-Ketoacyl-CoA transferase (Thiophorase). Diagram showing ketone body activation in extrahepatic tissues via thiophorase

Why does active hepatic gluconeogenesis during prolonged starvation accelerate ketogenesis

Gluconeogenesis consumes oxaloacetate (OAA). Depleted OAA prevents acetyl-CoA from entering the TCA cycle, diverting acetyl-CoA into ketone body synthesis.

During prolonged starvation, which circulating fuel source shows the most significant concentration increase in blood

$\beta$-Hydroxybutyrate Graph showing plasma concentrations of glucose, free fatty acids, acetoacetate, and beta-hydroxybutyrate during starvation

What are the three main regulatory checkpoints controlling hepatic ketogenesis

"1. Adipose lipolysis rate (FFA supply in blood)
2. CPT-I gateway activity (entry of FFA into hepatic mitochondria)
3. Partitioning of mitochondrial Acetyl-CoA between the TCA cycle and ketogenesis