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58 Cards in this Set

  • Front
  • Back
major fat in human diet; major storage lipid in plants/animals that we eat; consist of 3 fatty acids esterified to a glycerol backbone
triacylglycerols
amphipatic compounds (both hydrophilic/hydrophobic) synthesized in liver & secreted by gallbladder into intestinal lumen to emulsify fats in the intestine
bile salts
gut hormone secreted by intestinal cells when stomach content enters the intestine; stimulates contraction of gallbladder, release of bile acids & secretion of pancreatic enzymes
cholecystokinin
enzymes involved in limited digestion (due to low solubility of substrate) of triacylglycerols in mouth & stomach
lingual & gastric lipase
major enzyme produced in the pancreas that digests triacylglycerols
pancreatic lipase
peptide hormone released by small intestine in response to acidic materials entering the duodenum responsible for signalling the liver, pancreas & certain intestinal cells to secrete bicarbonate
secretin
enzyme produced only in salivary glands & acinar cells of pancreas that digests dietary starch
amylase
% of calories in typical U.S. diet that currently comes from fat
38%
According to current recommendations, fat should provide no more than ____ of the total calories in a diet.
30%
conditions related to increased serum amylase levels
pancreatitis & mumps (salivary gland lesions)
degradation products from breakdown of triacylglycerols
free fatty acids & 2-monoacylglycerol
major significant difference between fatty-acid composition of cow's milk & human milk
cow's milk: mostly short- & medium-chain fatty acids

human milk: mostly long-chain, polyunsaturated fatty acids (palmitic, oleic & linoleic acids) → important in brain development

NOTE: lingual/gastric lipases most active in infants compensate for low concentrations of pancreatic lipase & bile salts; human mammary gland also produces lipases that enter the milk
compound that raises the pH of the contents of the intestinal lumen into a range optimal for action of all digestive enzymes (pH ~6)
bicarbonate
substance derived from hemoglobin that is degraded to bilirubin & excreted by the liver in bile
heme
How do gallstones form specifically in patients with hemolytic anemia?
increased red blood cell destruction → greater amount of heme degraded by liver & spleen into large quantities of bilirubin → liver is overwhelmed (cannot conjugate bilirubin & convert it into water-soluble bilirubin diglucoronide) → greater % of bilirubin entering hepatic biliary ducts is in less water-soluble form → precipitation as gallstones rich in calcium bilirubinate in gallbladder

- smaller stones may leave gallbladder thru cystic duct → common bile duct → small intestine → excretion in stool

- larger stones may become entrapped in lumen of common bile duct → obstruction of bile flow (cholectasis) → ductal spasm → pain
Why are serum levels of pancreatic amylase & lipase elevated in patients with acute/chronic pancreatitis?
Enzymes escape from inflamed exocrine cells of pancreas → surrounding pancreatic veins → bloodstream

NOTE: inflammatory pancreatic process can result from toxic effect of acute/chronic excessive alcohol ingestion
fat-laden stools caused by malabsoprtion of dietary fats (due to lack of pancreatic secretions or insufficient production/secretion of bile salts)
steatorrhea
enzymes produced by pancreas that remove fatty acids from cholesterol esters (cholesterol esterified to fatty acids)
esterases
enzyme released by pancreas in its zymogen form & activated by trypsin that digests phospholipids to a free fatty acid & a lysophospholipid
phospholipase A2
compounds that act as detergents, binding to globules of dietary fat as they are broken up by peristaltic action of intestinal muscle & emulsifying them
bile salts
digestion of triacylglycerols in the intestinal lumen
(diagram)
enzyme that binds to dietary fat & lipase, relieving the bile salt inhibition & allowing triglyceride to enter the active site of lipase
colipase
tiny microdroplets emulsified by bile salts that package dietary lipids (fatty acids, 2-monoacylglycerols, cholesterol lysophospholipids, fat-soluble vitamins) produced by digestion for transport to intestinal epithelial cells & absorption

NOTE: bile salts are not absorbed, but left behind in lumen of gut
micelles
types of fatty acids that do not require bile salts for their absorption
(absorbed directly into intestinal epithelial cells → portal blood → transported to liver bound to albumin)
short- & medium-chain fatty acids (C4-C12)
concentration of bile salts necessary in lumen fir bile salt micelles to form
5-15mm = critical micelle concentration (CMC)

[below CMC → bile salts are soluble / above CMC → micelles form
% of bile salts recirculated when they reach the ileum

NOTE: bile salts are recycled & used multiple times in fat digestion
(diagram)
greater than 95%
fat-soluble vitamins
A, D, E, K
What could lead to a fat-soluble vitamin deficiency?
prolonged obstruction of the common duct that carries exocrine secretions from the pancreas & gallbladder into the intestine

(fat-soluble vitamins are absorbed from micelles along with long-chain faty acids & 2-monoacylglycerols)
soluble lipoprotein particles that do not coalesce in aqueous solutions
chylomicrons
protein constituents of lipoproteins
apoproteins
artificial fat substitute designed to allow individuals to obtain the taste & food consistency of fat without the calories from fat

- passes thru intestine intact & is eliminated by feces

- imparts a sweet taste (sucrose portion)

- passes thru digestive system unimpeded → can carry essential fat-soluble vitamins with it
Olestra
enzyme involved in the resynthesis of triacylglycerols
fatty acyl coenzyme A (CoA)
difference in triacylglycerol synthesis in intestinal cells vs. liver & adipose cells
in intestinal cells: 2-monoacylglycerol serves as intermediate

in liver & adipose cells: phosphatidic acid serves as intermediate
major apoprotein associated with chylomicrons as they leave the intestinal cells
B-48
resynthesis of triacylgycerols in intestinal epithelial cells
(diagram)
apoprotein synthesized in the liver that serves as major protein of very-low-density lipoprotein (VLDL)
B-100
Lipids (triacylglycerols) are synthesized in the ________.
smooth endoplasmic reticulum (sER)
Proteins are synthesized in the _______.
rough endoplasmic reticulum (rER)
organelles in which lipoproteins are assembled
ER & Golgi complex
process by which nascent chylomicrons are secreted by intestinal epithelial cells into chyle of lymphatic system
exocytosis
Nascent chylomicrons begin to enter the blood within _______ after the start of a meal & continue to enter as the meas is digested & absorbed.
1-2 hours
Chylomicrons transform from "nascent" to "mature" when ________.
they accept proteins from HDL within the lymph & blood
Why are chylomicrons the least dense of the blood lipoproteins?
due to their high triacylglycerol content
2 apoproteins acquired by chylomicrons from HDL
apoprotein CII (apoCII) & apoprotein E (apoE)
formation & secretion of nascent chylomicrons
(diagram)
fate of chylomicrons
(diagram)
the major component of chylomicrons
triglycerides
How are apoproteins B-48 & B-100 similar?
they are synthesized/encoded from the same gene

[primary transcript of gene undergoes RNA editing in intestine → a stop codon causes the 48% difference in size between both apoproteins]
apoprotein recognized by membrane receptors (on liver cells), allowing lipoproteins to enter cells by endocytosis for subsequent digestion by lysosomes
apoE
apoprotein that acts as an activator of lipoprotein lipase (LPL)
apoCII
enzyme on capillary endothelial cells (primarily within muscle & adipose tissue) that digests triacylglycerols of chylomicrons & VLDL in blood
lipoprotein lipase (LPL)
portion of chylomicron that remains in blood after LPL action

- binds o receptors on hepatocytes → apoE recognition → endocytosis → lysosome fusion with endocytotic vesicles → degradation by lysosomal enzymes
chylomicron remnant
products of lysosomal digestion of chylomicron remnants that can be reused by the cell
fatty acids, amino acids, glycerol, cholesterol, phosphate
complex polysaccharide (component of proteoglycans) used as an anticoagulant because it binds to antithrombin III (ATIII), which binds factors necessary for clotting & inhibits them from working
heparin

[LPL is bound to capillary endothelium thru binding to proteoglycans → heparin can bind to LPL & dislodge it from capillary wall - LPL is bound to capillary endothelium thru binding to proteoglycans → loss of LPL activity & increase of triglyceride content in blood]
fate of fatty acids & glycerol produced from triglyceride in chylomicron digested by LPL
fatty acids → enter adjacent organs for energy production (muscle) or fat storage (adipocytes)

glycerol → metabolized in liver (for possible use in fed state)
soluble protein that complexes with fatty acids to make them soluble in blood
albumin
hormone that stimulates the synthesis & secretion of adipose LPL, so that after a meal, when triglyceride levels increase in circulation, LPL is upregulated to facilitate hydrolysis of fatty acids from triglyceride
insulin
Km of LPL synthesized in adipose cells vs. muscle cells
adipose cells → higher Km → adipose LPL is more active after a meal, when chylomicron levels are elevated in blood to facilitate hydrolysis of fatty acids from triglycerides

muscle cells → low Km → muscle cells can obtain fatty acids from blood lipoproteins when needed for energy (even if lipoprotein concentration is low)