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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
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triacylglycerols
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amphipatic compounds (both hydrophilic/hydrophobic) synthesized in liver & secreted by gallbladder into intestinal lumen to emulsify fats in the intestine
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bile salts
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gut hormone secreted by intestinal cells when stomach content enters the intestine; stimulates contraction of gallbladder, release of bile acids & secretion of pancreatic enzymes
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cholecystokinin
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enzymes involved in limited digestion (due to low solubility of substrate) of triacylglycerols in mouth & stomach
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lingual & gastric lipase
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major enzyme produced in the pancreas that digests triacylglycerols
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pancreatic lipase
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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
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secretin
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enzyme produced only in salivary glands & acinar cells of pancreas that digests dietary starch
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amylase
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% of calories in typical U.S. diet that currently comes from fat
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38%
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According to current recommendations, fat should provide no more than ____ of the total calories in a diet.
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30%
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conditions related to increased serum amylase levels
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pancreatitis & mumps (salivary gland lesions)
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degradation products from breakdown of triacylglycerols
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free fatty acids & 2-monoacylglycerol
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major significant difference between fatty-acid composition of cow's milk & human milk
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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 |
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compound that raises the pH of the contents of the intestinal lumen into a range optimal for action of all digestive enzymes (pH ~6)
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bicarbonate
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substance derived from hemoglobin that is degraded to bilirubin & excreted by the liver in bile
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heme
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How do gallstones form specifically in patients with hemolytic anemia?
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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 |
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Why are serum levels of pancreatic amylase & lipase elevated in patients with acute/chronic pancreatitis?
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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 |
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fat-laden stools caused by malabsoprtion of dietary fats (due to lack of pancreatic secretions or insufficient production/secretion of bile salts)
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steatorrhea
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enzymes produced by pancreas that remove fatty acids from cholesterol esters (cholesterol esterified to fatty acids)
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esterases
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enzyme released by pancreas in its zymogen form & activated by trypsin that digests phospholipids to a free fatty acid & a lysophospholipid
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phospholipase A2
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compounds that act as detergents, binding to globules of dietary fat as they are broken up by peristaltic action of intestinal muscle & emulsifying them
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bile salts
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digestion of triacylglycerols in the intestinal lumen
(diagram) |
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enzyme that binds to dietary fat & lipase, relieving the bile salt inhibition & allowing triglyceride to enter the active site of lipase
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colipase
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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
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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)
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concentration of bile salts necessary in lumen fir bile salt micelles to form
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5-15mm = critical micelle concentration (CMC)
[below CMC → bile salts are soluble / above CMC → micelles form |
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% of bile salts recirculated when they reach the ileum
NOTE: bile salts are recycled & used multiple times in fat digestion (diagram) |
greater than 95%
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fat-soluble vitamins
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A, D, E, K
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What could lead to a fat-soluble vitamin deficiency?
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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) |
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soluble lipoprotein particles that do not coalesce in aqueous solutions
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chylomicrons
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protein constituents of lipoproteins
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apoproteins
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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
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enzyme involved in the resynthesis of triacylglycerols
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fatty acyl coenzyme A (CoA)
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difference in triacylglycerol synthesis in intestinal cells vs. liver & adipose cells
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in intestinal cells: 2-monoacylglycerol serves as intermediate
in liver & adipose cells: phosphatidic acid serves as intermediate |
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major apoprotein associated with chylomicrons as they leave the intestinal cells
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B-48
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resynthesis of triacylgycerols in intestinal epithelial cells
(diagram) |
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apoprotein synthesized in the liver that serves as major protein of very-low-density lipoprotein (VLDL)
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B-100
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Lipids (triacylglycerols) are synthesized in the ________.
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smooth endoplasmic reticulum (sER)
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Proteins are synthesized in the _______.
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rough endoplasmic reticulum (rER)
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organelles in which lipoproteins are assembled
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ER & Golgi complex
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process by which nascent chylomicrons are secreted by intestinal epithelial cells into chyle of lymphatic system
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exocytosis
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Nascent chylomicrons begin to enter the blood within _______ after the start of a meal & continue to enter as the meas is digested & absorbed.
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1-2 hours
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Chylomicrons transform from "nascent" to "mature" when ________.
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they accept proteins from HDL within the lymph & blood
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Why are chylomicrons the least dense of the blood lipoproteins?
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due to their high triacylglycerol content
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2 apoproteins acquired by chylomicrons from HDL
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apoprotein CII (apoCII) & apoprotein E (apoE)
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formation & secretion of nascent chylomicrons
(diagram) |
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fate of chylomicrons
(diagram) |
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the major component of chylomicrons
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triglycerides
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How are apoproteins B-48 & B-100 similar?
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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] |
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apoprotein recognized by membrane receptors (on liver cells), allowing lipoproteins to enter cells by endocytosis for subsequent digestion by lysosomes
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apoE
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apoprotein that acts as an activator of lipoprotein lipase (LPL)
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apoCII
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enzyme on capillary endothelial cells (primarily within muscle & adipose tissue) that digests triacylglycerols of chylomicrons & VLDL in blood
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lipoprotein lipase (LPL)
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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
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products of lysosomal digestion of chylomicron remnants that can be reused by the cell
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fatty acids, amino acids, glycerol, cholesterol, phosphate
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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
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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] |
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fate of fatty acids & glycerol produced from triglyceride in chylomicron digested by LPL
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fatty acids → enter adjacent organs for energy production (muscle) or fat storage (adipocytes)
glycerol → metabolized in liver (for possible use in fed state) |
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soluble protein that complexes with fatty acids to make them soluble in blood
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albumin
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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
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insulin
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Km of LPL synthesized in adipose cells vs. muscle cells
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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) |