4th Unit / Ch 15 Metabolism of Dietary Lipids Flashcards
What general name is given to the enzymes that degrade dietary fat (TAGs) in the mouth,
stomach, and small intestine, as shown?
Lipases degrade dietary fat ( TAGs ), a major source of our calories.
Where in the body does the degradation of dietary TAGs containing LCFAs occur primarily?
What are the two products?
What enzyme catalyzes the process?
What additional protein
is needed?
Degradation of dietary TAGs containing LCFA s occurs in the lumen of the small intestine. The products are two FFAs and one 2-MAG, which has a FA at C-2. Pancreatic lipase is the catalyst. The protein colipase is needed to stabilize the lipase at the lipid–aqueous interface.
What is the function of cholesterol esterase ?
What are its products?
Cholesterol esterase removes the FA from CEs, producing cholesterol and FFAs.
Pancreatic lipase concentration is low in neonates. How are they able to digest milk fat?
Acid lipases in the mouth ( lingual lipase ) and the stomach ( gastric lipase ) allow neonates
to digest milk fat (their primary source of calories) that is rich in MCFAs and SCFAs.
What are the functions of the hormones CCK and secretin in digestion?
CCK stimulates the release of bile from the gallbladder and enzymes from the pancreas. It slows release of gastric
contents by decreasing stomach motility.
Secretin causes the gallbladder to release a HCO 3 -rich solution that raises pH. [ Note: Dietary lipids themselves cause
hormone release from the gut endocrine cells.]
What is the role of emulsification in lipid digestion? How is it accomplished?
Emulsification increases the surface area of the lipid droplet formed in the polar aqueous environment
( hydrophobic effect ) by mechanical mixing ( peristalsis ) and the detergent-like properties of amphipathic BSs .
How and where are dietary lipids absorbed?
The FFAs, unesterified cholesterol, and 2-MAG from lipid digestion (along with BSs and fat-soluble vitamins) form
mixed micelles, the contents of which are taken up at the brush border of intestinal mucosal cells.
Why might individuals with cysticfi brosis ( CF ) be given supplemental pancreatic enzymes prior to eating?
With CF , the CFTR protein (a Cl- channel on epithelial cells) is defective, decreasing Cl- release and increasing
Na+ and H2O uptake by cells. Cell surface H2O depletion thickens secretions that clog the pancreatic ducts and hinder
enzymes from reaching the intestine ( pancreatic insufficiency ), thereby impeding digestion. Supplementation with
pancreatic enzymes prior to eating promotes digestion.
What LP particle shown transports dietary lipids through blood?
CMs (**Chylomicrons)** , formed in intestinal cells and secreted into the lymphatic system, are the LP particles that transport dietary lipids (and fat-soluble vitamins) through the blood.
What lipids are found in the core of the particle? What surface protein is characteristic of the particle?
Within the intestinal cells, FAs are activated and esterifi ed to the cholesterol and 2-MAG products of digestion, reforming the nonpolar TAGs and CEs that get packaged into CMs. Apolipoprotein ( apo )
B-48 is the characteristic surface protein of CMs.
[Note: PLs are also found on the surface.]
Why might fecal fat be measured if lipid malabsorption is suspected?
Fecal fat will be increased with defects in lipid digestion (such as in CF ) or absorption because dietary fat
is primarily excreted rather than absorbed with such defects. Steatorrhea (loose, fatty, and foul-smelling
feces) results.
What tissues (denoted by a red question mark)
are the primary sites for the degradation of
TAGs carried by CMs?
Muscle and adipose tissues are the primary sites
for degradation of TAGs carried by CMs.
What enzyme (denoted by a green question mark) degrades the TAGs?
Lipo Protein Lipase (LPL) , located on the endothelial surface of capillaries
in muscle and adipose tissue, degrades
the TAGs. LPL requires activation by Apolipoprotein C2 (apo CII)
located on CM surfaces.
-The FA products are taken in by muscles
(for energy) and adipocytes (for storage) and
are transported on serum albumin, taken up,
and used by the liver. The glycerol is picked
up by liver and phosphorylated to glycerol 3-P,
which can be used in hepatic TAG synthesis,
for example.
Why might TAGs rich in MCFAs be used in the
treatment of disorders of lipid digestion and/or
absorption or of CM metabolism?
TAGs rich in MCFAs might be used in the
treatment of disorders of lipid digestion (e.g.,
pancreatitis ) because they are (1) rapidly
degraded by lingual and gastric lipases , thereby
eliminating the need for pancreatic lipase and
(2) taken up by enterocytes without the aid of
mixed micelles . Additionally, they are released
from enterocytes directly into the blood and do
not require incorporation into CMs. Coconut oil
contains a high concentration of TAGs rich in
MCFAs and is used in medical nutrition therapy
for these disorders.
