Metabolism, Digestion, and ATP Energetics

Flashcards covering catabolism stages, digestion mechanisms, zymogens, carb/protein/lipid transport, clinical insights, and ATP bioenergetics based on lecture notes.

What are the three stages of catabolism described in the lecture notes?

1. Food digests into large molecules, which catabolize into small units. 2. Small units catabolize into key basic units (linking anabolism and catabolism). 3. Key basic units oxidize into ATP.

How are zymogens (proenzymes) stored, secreted, and activated in the digestive system?

Zymogens are stored in granules near the cell membrane. Upon signaling, the granules fuse with the cell membrane and expel their contents into the lumen of the intestine. They are activated when a part of the inactive precursor is cleaved by another protease.

What enzyme activates trypsinogen, and what is active trypsin's role in the pancreas zymogen cascade?

Inactive trypsinogen is converted to active trypsin by enteropeptidase/enterokinase (attached to epithelial cells). Active trypsin then activates the other pancreatic proenzymes/zymogens.

What chemical components make up saliva, and what is the specific cleavage action of salivary $\alpha$-amylase?

Saliva is made of $Na^+$, $K^+$, $Cl^-$, $HCO_3^-$, mucoproteins (components of mucus), and $\alpha$-amylase, which cleaves at $\alpha\text{-1,4}$ glycosidic linkages.

What steps initiate protein digestion in the stomach?

1. Stomach acid ($\text{pH } 1$ and $2$) denatures proteins, exposing peptide linkages. 2. Pepsin (a protease) breaks down the proteins into protein fragments. 3. Intestinal proteases further break down these fragments.

How do secretin and cholecystokinin (CCK) function during intestinal digestion?

Low pH stimulates the small intestine to release secretin, which triggers pancreatic release of sodium bicarbonate to neutralize food pH. Oligopeptide products stimulate release of CCK, prompting the pancreas to release enzymes and bile into the intestine.

What enzyme generates stomach acidity, and how is Gastroesophageal Reflux Disease (GERD) treated?

Stomach acidity is generated by $H^+-K^+ \text{ ATPase}$. GERD is treated with $H^+-K^+ \text{ ATPase}$ inhibitors such as omeprazole.

Why are gluten-derived peptides resistant to digestive breakdown in patients with celiac disease?

Gluten proteins are rich in the amino acids proline and glutamine, which are resistant to digestion by pepsin and pancreatic proteases.

What are the specific enzymatic cleavage products of sucrase, maltase, isomaltase, and trehalase?

Sucrase breaks sucrose into glucose + fructose; maltase breaks maltose into $2$ glucose; isomaltase/$\alpha$-dextrinase breaks isomaltose into $2$ glucose; trehalase breaks trehalose into $2$ glucose.

Why is $\alpha$-limit dextrin non-digestible by $\alpha$-amylase, and what enzyme degrades it?

$\alpha$-limit dextrin contains $\alpha\text{-1,6}$ linkages that cannot be cleaved by $\alpha$-amylase. It is digested into simple sugars by $\alpha$-dextrinase.

Which transport proteins transport glucose, galactose, and fructose across intestinal epithelial cells into the blood?

Glucose and galactose enter via secondary active transport by the sodium-glucose linked transporter (SGLT); fructose diffuses across via GLUT5. GLUT2 releases all monosaccharides into the bloodstream.

How are insoluble lipids prepared and hydrolyzed during digestion?

Stomach grinding converts lipids into an emulsion. Bile salts (synthesized from cholesterol in the liver and secreted by the gallbladder) enhance emulsification. Pancreatic lipases then break down triacylglycerols into free fatty acids and monoacylglycerol.

What role do micelles play in lipid absorption?

Micelles are spherical structures formed by small lipids in aqueous solutions that carry free fatty acids and monoacylglycerol to the plasma membrane of intestinal epithelial cells for absorption.

How are triacylglycerols processed inside intestinal epithelial cells for transport into the lymph system?

Fatty acids and monoacylglycerol enter cells via FATP, are transported by FABP to the smooth ER (SER) to resynthesize triacylglycerols, and combine with apoB-48, phospholipids, and cholesterol to form chylomicrons ($98\%$ triacylglycerols) released into lymph.

What enzyme in rattlesnake venom digests victim cell membranes?

Phospholipidases, which digest cell membranes at the bite site and disrupt red blood cell membranes.

What standard free energy threshold defines a "high energy compound" in catabolic reactions?

Molecules with phosphoryl groups that have a standard free energy of hydrolysis $\Delta G^{\circ'} \le -26\,kJ/mol$.

What are the standard free energy values ($\Delta G^{\circ'}$) for the hydrolysis of ATP to ADP and ATP to AMP?

For $ATP + H_2O \rightleftharpoons ADP + P_i$, $\Delta G^{\circ'} = -30\,kJ/mol$ ($-7.3\,kcal/mol$). For $ATP + H_2O \rightleftharpoons AMP + PP_i$, $\Delta G^{\circ'} = -45.6\,kJ/mol$ ($-10.9\,kcal/mol$).

What three structural factors make the hydrolysis of ATP exergonic?

1. Relief of charge repulsion among negative charges on ATP. 2. Resonance stabilization of released inorganic phosphate ($P_i$). 3. Ionization forming products ($ADP^{3-} + HPO_4^{2-} + H^+$) that are more stable than ATP.

Which biological divalent cation coordinates with phosphate groups of ATP and ADP in biological reactions?

$Mg^{2+}$, forming $MgATP^{2-}$ and $MgADP^{-}$.

Which high-energy compounds mentioned in the notes have a higher phosphoryl-transfer potential than ATP?

1,3 biphosphoglycerate (1,3 BPG), phosphoenolpyruvate (PEP), and creatine phosphate.

What cellular processes consume ATP, and what processes regenerate ATP according to the ATP-ADP cycle?

ATP consumption powers motion, active transport, biosynthesis, and signal amplification. ATP regeneration is driven by oxidation of fuel molecules and photosynthesis.