Shared Flashcard Set


Digestion/Absorption of Carbs, Proteins and Lipids

Additional Biology Flashcards




What are examples of Monosacharides and Diasaccharides?
Remember, they serve fuel storage, cell signaling and cell structure.

1) Monosacharides
- Glucose
- Fructose
- Galactose

2) Disaccharides
- Sucrose (glucose + fructose)- table sugar
- Lactose (glucose + galactose)- milk sugar
- Maltose (glucose + glucose)- digestion product of starches
What are the 2 major complex CHO found in modern western diets?
1) Amylose- alpha 1,4 links of glucose in a straight chain.

2) Amylopectin- alpha 1,4 straight chains with a-1,6 linked branch points
What are the functions of soluble and insoluble dietary fiber, respectively, in GI absorption/motility?
1) Soluble forms like pectin and oat bran aid water absorption, delay of sugar absorption and binding bile salts and cholesterol

2) Insoluble forms like cellulose speed GI transit time.
What are the 3 major enzymes involved in carbohydrate digestion?
**Small intestine (jejunum particularly) is most important site

**Stomach has no pertinent role

1) Salivary a-amylase
- Breaks down internal alpha 1,4 links

2) Pancreatic a-amylase
- Breaks down alpha 1,4 (amylase) and alpha 1,6 (amylopectin)
- Duodenal release of secretin and CCK stimulate exocrine pancreas to produce HCO3- and alpha-amylase, respectively.

3) Brush border disaccharidases/oligosaccharidases
-Glucoamylase, Lactase and Isomaltase/Sucrase
- intestinal villi brush border proteins of glycocalyx produced as pro-enzymes that are cleaved by trypsin and then produce monomers of CHO.
What do each of the following enzymes do?

1) Isomaltase/Sucrase
2) Glucoamylase
3) Lactase
All of brush border enzymes that are secreted as pro-enzymes and activated by trypsin cleavage, producing monosaccharides from disaccharides.

1) Double headed where one domain hydrolyzes sucrose (fructose and glucose) and the other gets isomaltose (2 glucose)

2) Hydrolyzes a-1,4 on maltose to make 2 glucose

3) Beta galactosidase that hydrolyzes b-1,4 on lactose to galactose and glucose
How do each of the following proteins function in CHO absorption?

1) Sodium-dependent glucose transporter (SGLT1)
2) Fructose Transporter (GLUT5)
3) Sodium-independent Glucose transporter (GLUT2)
Absorption of monosaccharides in vicinity of villus

1) SGLT1 (Brush border of intestine and kidney)
- Co-transports 2Na and D-glucose (D-galactose) powered by Na+ gradient (Na/K ATPase)
- Concentrate glucose 10,000 fold

2) GLUT5 (brush border and basolateral)
- brush border for fructose

3) GLUT2 (basolateral membrane)
- Transports glucose/galactose/fructose out of enterocytes and into portal circulation
- High capacity low affinity
How are CHO distributed?
1) Monosaccharides exit enterocytes (Glut2 and Glut5) and diffuse into fenestrated capillaries of villus lamina propria

2) Enter liver via portal vein, where it is stored as glycogen (insulin and glucagon dependent) or converted to TG
What is the basis of the "Atkin's diet"?
Eat foods with low "glycemic index," that are slowly digested and absorbed (low carb).
1) What happens to amino groups that are broken off from protein during degradation?

2) What happens to the remaining carbon skeleton?
Remember, 40% turnover in GI each day because of caustic environment. Gets hit hard in malnutrition!

1) Processed to urea or bound to Glutamine, because NH4 is toxic to brain.

2) 3 ways
- Oxidation for energy,
- Storage as glycogen
- Synthesis of fatty acids for storage in adipose tissue
What conditions produce a positive or negative nitrogen balance?
Nitrogen usually is in steady state, where most is excreted bound to urea.

Positive balance means more protein is made and Negative means degradation exceeds synthesis.

1) Positive
- Growth
- Pregnancy
- Lactation
- Recovery from metabolic stress

2) Negative
- Uncontrolled DM
- Injury
- Surgery
- Infection, sepsis
True or false,

Recommended protein intake increases with age.
False! The opposite is true!

Increase it during pregnancy, though.
What factors determine "biological value" of protein?
essential AA content and digestibility

Essential AA

Any help in learning these little molecules proves truly valuable

Arginine, Histidine, Isoleucine, leucine, Threonine, Lysine, Methionine, Phenylalanine, Tryptophan , Valine

**Ariginine is "conditional" because it is non-essential if intestine and kidney are normal.

**to be useful, source must have all essential AA!**
How is protein digested/absorbed (enzymes, locations, mechanism)?
Remember, more protein is digested/absorbed each day than is taken in orally!

1) Stomach
- Acid pH uncoils 4 and 3 structure
- Pepsinogen (Chief cells) activated by HCl (Parietal cells)
- HCO3- from mucous cells prevents self digestion

2) Pancreas
- Proenzymes emptied in duodenum that must encounter enterokinase (intestinal brush border enzyme that cleaves trypsinogen to trypsin, which cleaves other pancreatic enzymes).

3) Small intestine
- Brush border glycocalyx enzymes hydrolyze oligopeptides
- Brush border and basolateral membrane peptidases, amino acid transporters and di and tri-peptide transporters

4) Portal Vein and Liver
- Assimilated AA are carried away by veins to hepatic protal vein and absorbed first by liver transporters.

- Liver makes plasma proteins and deaminates AA to ammonia (becomes urea or combines with glutamine)
What is the role of enterokinase in protein metabolism?
Released from brush border glycocalyx and cleaves pancreatic trypsinogen to trypsin in Duodenum.

Trypsin can then activate other pancreatic enzymes.

Why is the most common cause of death during an epidemic of starvation bacterial pneumonia?
- After 8-16h of fasting, glycogen stores in liver and muscle are mostly used up. Lipolysis can occur, but you can't get glucose from lipid and amino acids begin to be converted to glucose via gluconeogenesis.

- The first organs to manifest inadequate protein (<50% of normal) are liver and immune system, so people are immunocompromised.
How do you assess protein status in a nutritional evaluation?

hint; 3 areas
Liver proteins, Immune function and Lean body mass

1) Liver
- Albumin (LONG-TERM shits because of 20d half-life)
- Transferrin (half life of 8.8d, but increased in iron deficiency)
- Pre-albumin/Transtheyretin (24-48h half life, reflecting RECENT changes)

2) Immune function
- Total lymphocyte count and delayed hyersensitivity to allergens.

3) Lean body mass
- 24h urinary creatinine (should be 23 for m and 18 for f)
How does lipid digestion take place (enzymes, locations, mechanism)?
1) Gastric (not-essential if pancreas works)
- Titurition produces fine emulsion
- Gastric lipase (Chief cells) functions at pH 4-5.5 and produces free FA and 2,3-diglyceride
- Acidic stomach protonates FFA (incomplete!)

2) Intestinal
- Acidic chyme neutralized in duodenum by HCO3- from pancreas, biliary ducts and Brunner's glands (duodenal)

- FFA become ionized (lose hydrogen) and stimulate CCK release, leading to gallbladder contraction and bile release into small intestine

- CCK triggers further release of pancreatic enzymes through sphincter of Oddi: pancreatic lipase (pH sensitive), colipase, phospholipase A2 and cholesterol esterase.
What organ should you think of if you see the clinical symptom "Steatorrhea?"

**Gastric lipid digestion is non-essential, but pancreatic IS**

- If pancreas is impaired, you lose HCO3- secretion into duodenum, so protonated free fatty acids from stomach cannot be ionized, chyme cannot be neutralized and pancreatic enzymes like lipase are inactivated by low pH.

- Protonated lipids cannot be absorbed and they are excreted in feces.
What are the major enzymes involved in lipid digestion that are released by the pancreas?
Enter duodenum through sphincter of Oddi

1) Pancreatic lipase (acid-sensitive)

2) CO-lipase
- prevents inhibition of lipase by bile acids (also released through sphincter) by binding to both and locking them on the surface of the lipid droplet

3) Phospholipase A2
- Cleaves fatty acid from clcyerol

4) Cholesterol esterase (requires bile salts)
- Cleaves esters of cholesterol, vit A,D and E and total cleavage of TGA.
What is the role of bile salts in lipid absorption?
**Critical to assimilation of lipids and fat-soluble vitamins (ADEK)**

1) Released through sphincter of Oddi into duodenum, where they solubilize end products of digestion that are in mixed micelles by providing hydrophobic outer face for micelle, allowing presentation to aqueous environment of brush border for UPTAKE.

2) Lipid products diffuse across apical membrane of enterocytes, are re-esterified into TGA and cholesterol

4) Bile salts remain behind in lumen until terminal ileum, when they are transyctosed by specific receptor and enter portal circulation to be recycled and re-used by the liver**
How are lipid products that are taken up by enterocytes of the small intestine transported to other sites of the body?
1) Chylomicrons assembled in enterocyte with inner TGA core and out hydrophilic shell (phospholipids, free cholesterol and apoB48)

2) Chylomicrons carried in lymph to thoracic duct and into right atrium. Once in systemic circulation, they gain ApoE (Remnant recepetor binding and clearance by liver) and Apo CII (cofactor for LPL) from HDL.