a&p2: GI phys (slides 11-27)

% Water content of saliva

99%

Enzyme in saliva that begins carbohydrate digestion

α‑amylase

Function of lysozyme in saliva

Destroys bacterial peptidoglycan (natural antibacterial)

Function of haptocorrin

Binds and protects vitamin B12 from stomach acid

Which macronutrient saliva begins digesting

Carbohydrates

Which nutrients require digestion before absorption

Carbohydrates and proteins

Which nutrients require no digestion, only absorption

Vitamins, minerals, water

Main carbohydrate polysaccharide

Starch

Main carbohydrate disaccharides

Sucrose, lactose, maltose

Main carbohydrate monosaccharides

Glucose, galactose, fructose

Where α‑amylase performs partial digestion

Mouth

Product of α‑amylase digestion of starch

Maltose

Role of stomach and esophagus in carbohydrate digestion

No role

Where complete carbohydrate digestion occurs

Small intestine brush border

Enzymes responsible for final carbohydrate digestion

Brush border glucosidases and disaccharidases

Where carbohydrate absorption occurs

Small intestine

Which structure contains brush border enzymes

Microvilli

What sucrose is broken into

Glucose and fructose

What lactose is broken into

Glucose and galactose

What maltose is broken into

Two glucose molecules

Why carbohydrate digestion stops in the stomach

Acid inactivates α‑amylase

Primary site of monosaccharide absorption

Small intestine

Which enzyme class completes carbohydrate digestion

Disaccharidases

Which organ produces salivary α‑amylase

Salivary glands

Purpose of saliva in digestion

Lubrication and initial carbohydrate breakdown

What enzyme breaks maltose into two glucose molecules

Maltase

What enzyme breaks lactose into glucose and galactose

Lactase

What enzyme breaks sucrose into glucose and fructose

Sucrase

What is the substrate of maltase

Maltose

What is the substrate of lactase

Lactose

What is the substrate of sucrase

Sucrose

What are the products of maltase

Glucose + glucose

What are the products of lactase

Glucose + galactose

What are the products of sucrase

Glucose + fructose

Where are disaccharidases located

Brush border of the small intestine

Where does final carbohydrate digestion occur

Brush border/microvilli

Which transporter absorbs glucose from the lumen

SGLT‑1

Which transporter absorbs galactose from the lumen

SGLT‑1

Which transporter absorbs fructose from the lumen

GLUT‑5

Which ion powers SGLT‑1

Na⁺

Which transporter moves all monosaccharides into the blood

GLUT‑2

Where is GLUT‑2 located

Basolateral membrane

Where is SGLT‑1 located

Apical membrane

Where is GLUT‑5 located

Apical membrane

Which monosaccharides use SGLT‑1

Glucose and galactose

Which monosaccharide uses facilitated diffusion

Fructose

Which transporter uses facilitated diffusion

GLUT‑5

Which transporter uses secondary active transport

SGLT‑1

Which pump maintains the sodium gradient for SGLT‑1

Na⁺/K⁺‑ATPase

Where does monosaccharide absorption occur

Duodenum/jejunum

What happens to monosaccharides after entering the enterocyte

Transported into blood via GLUT‑2

What stimulates incretin release

Glucose inside the small intestine

Which hormones are classified as incretins

GIP and GLP

Which cell releases GIP

K‑cell of the duodenum

Which cell releases GLP

L‑cell of the ileum

Where GIP is produced

Duodenum

Where GLP is produced

Ileum

What GIP stands for

Gastric inhibitory peptide

What GLP stands for

Glucagon‑like peptide

What incretins do to insulin secretion

Increase insulin release from β‑cells

What incretins do to glucagon secretion

Decrease glucagon release from α‑cells

How incretins affect gastric emptying

Delay gastric emptying by modulating the pyloric sphincter

Which hormone increases PYY release

Incretins

What PYY does

Acts as a satiety hormone

Which incretin effect helps lower post‑meal blood glucose

Increased insulin + decreased glucagon

Which part of the intestine detects glucose for incretin release

Small intestine

What hormone is high during fasting/pre‑prandial state

Glucagon

What glucagon does during fasting

Increases blood sugar to maintain homeostasis

What happens to blood sugar post‑prandially

Blood sugar decreases as glucose enters cells

What process lowers blood sugar after a meal

Increased permeabilization of glucose into cells

What DPP‑4 stands for

Dipeptidyl‑peptidase‑4

What DPP‑4 does to incretins

Breaks down/inhibits incretins

Where DPP‑4 is released from

Endothelial cells of blood vessels (paracrine secretion)

What incretins normally do to insulin

Increase insulin release

What incretins normally do to glucagon

Decrease glucagon release

What happens when DPP‑4 breaks down incretins

Less insulin, more glucagon

What class of drug inhibits DPP‑4

DPP‑4 inhibitor

Example of a DPP‑4 inhibitor drug

Sitagliptin

Which type of diabetes DPP‑4 inhibitors treat

Type 2 diabetes mellitus

Why DPP‑4 inhibitors do NOT treat type 1 diabetes

Type 1 lacks β‑cells to produce insulin

What incretin‑preserving drugs ultimately increase

Insulin levels

What incretin‑preserving drugs ultimately decrease

Glucagon levels

Why preserving incretins helps after meals

Enhances insulin response and lowers blood glucose

Which cell secretes stomach acid

Parietal (oxyntic) cell

Which pump secretes H⁺ into the stomach lumen

H⁺/K⁺‑ATPase

Which ion is exchanged for H⁺ at the apical membrane of the parietal cell

K⁺

Which channel allows Cl⁻ to exit into the stomach lumen

CFTR

Which transporter moves Cl⁻ into the cell from the blood

Cl⁻ ABC transporter

Which antiporter exchanges HCO₃⁻ for Cl⁻ on the basolateral side

Band III / AE1

What happens to HCO₃⁻ after leaving the parietal cell

Enters blood (alkaline tide)

Which hormone binds the CCK2 receptor

Gastrin

Which ligand binds the H₂ receptor

Histamine

Which ligand binds the M3 receptor

Acetylcholine (ACh)

Which ligand binds the EP3 receptor

Prostaglandin E₂ (PGE₂)

Which ligand binds the somatostatin receptor

Somatostatin

Which receptors activate the PLC → PKC pathway

CCK2 and M3

Which receptor activates the cAMP → PKA pathway

H₂ receptor

Which receptors inhibit acid secretion

EP3 receptor and somatostatin receptor

What PKA and PKC do to proton pumps

Phosphorylate and mobilize them to the apical membrane

What “potentiation” means in acid secretion

Synergistic boosting of HCl by gastrin, histamine, and ACh