Flashcards in Intro to lipids Deck (42):
1
lipids
-hydrophobic organic molecules that can be extracted from cells by non-polar solvents
-associated with each other, excluding water
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2 classes of lipids
-fatty acids
-isoprenoids
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fatty acids
-amphipathic, micelle forming, soaps
-energy storage (fat dep to cushion organs and insulate)
-membranes (electrical insulation) including phospholipids and sphingolipids
-signals
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isoprenoids
-bile acids/ salts
-membranes
-signals
-cofactors
-fat soluble vitamins
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fatty acid nomenclature
-carboxyl carbon = 1
-FA symbol: # before colon = total length of chain
-at neutral pH, FA's are charged and act as soaps
-# after colon = number of double bonds
-superscript is the double bond start point, it then reaches to the subsequent carbon
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stearic acid
18:0
-zero after colon representation full saturation
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palmitic acid
16:0
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alpha, beta, and omega
-alpha = first C after the carboxyl
-beta = second C after the carboxyl
-omega = last C of the chain
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omega number
number of carbons from the terminal methyl to the nearest double bond
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linoleic acid
-18:2
-9,12
-omega 6
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arachidonic acid
-20:4
-5,8,11,14
-omega 6
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linoleic and linolenic deficiency
-these are essential FA's
-symptoms: scaly dermatitis, alopecia (hair loss), thrombocytopenia (low platelet count), and cognitive development in children
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triacylglycerols (TAGs)
-dietary and storage fats
-effectively formed by dehydration reactions between 3 FA's and glycerol
-fully hydrophobic
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TAG nomenclature
-change the FA suffix from "-ic acid" to "-oyl"
-list by position before glycerol
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what determines the physical properties of FA containing compounds
-melting point
-this is what will determine if they are solids or liquids at RT
-determines if membranes formed from FA containing compounds are fluid or semi crystalline
-MP increases with length
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effects of tran saturation
-allows the FA's to pack more closely together
-natural foods have cis double bonds
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leptin
-released by adipose tissue
-suppresses food intake by altering the hormones released by the hypothalamus
-leptin KO's are extremely obese
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ghrelin
hunger hormone
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percentage of fat in the typical US diet
-35-40% of caloric intake
-triglycerides are the major source
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bile acids made from cholesterol in the liver are...
-converted to bile salts
-conjugated with glycine or taurine
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gall stones
-imbalance of cholesterol, bile salt and phospholipid secretion
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pancreatic lipases can not access hydrophobic fat droplets until
-emulsification happens
-gall bladder relases bile salts and phospholipids which get cleaved by pancreativ lipases
-these amphipathic molecules surround the TAG droplet and eventualy peristalsis makes them smaller
-these droplets with surrounding bile salts are called micelles
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micelles form at
-critical micelle concentrationconcentration
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hydrolysis of TAGs by pancreatic lipases
-TAG to diacylglycerol to monoacylglycerol
-full hydrolysis is not necessary, since the two hidroxyl groups on 2-MAG make is sufficiently soluble in water
-pancreatic lipase doesnt recognize olestra (FAs in ester linkages to hydroxyl groups on sucrose
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pancreatitis
-deep recurrent moderate to severe abdominal, back, or epigastric pain exacerbated y alcohol
-nausea and vomiting
-steatorrhea in chronic cases
-elevated serum kipases and serum amylase
-300,000 cases a year, 20,000 die
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steatorrhea
-lipid digestion disorders other than pancreatitis can cause this
-can be due to probelms with emulsification (biliary obstruction), lipolysis (pancreatic disease), or absorption by intestinal epithelia (celiac)
-causes intestinal discomfort, loss of essential FAs and fat soluble vitamins
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micelles facilitate absorption
-free FAs and 2-MAG at CMC are passively absorbed by intestinal epithelia
-this reduces their concentration to below the CMC, and micelles break down to restore the CMC
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bile salt recylcing
95% done through enterohepatic circulation
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how to get FA's out of the epithelial cell
-resynthesize the TAG without CoA
-with CoA, the FA can not leave the epithelial cell
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absorbing cholesterol esters
-hydrolysis of cholesterol esters to allow absorption
-resynthesis of CEs to drive absorption and prepare for transport
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peristalsis in lipid metabolism
-turns TAG droplets into micelles
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Critical micelle concentration
FA's can solubilize up until a threshold concentraiton
-above this concentration, they must form micelles in the gut
-as free fatty acids are removed from the gut via absorption, FA's will break away from the micelle to maintain equilibrium
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hydrolysis of TAGs by pancreatic lipase
-removes two FAs from TAG resulting in two free FA's and 2-monoacyl glycerol
-full hydrolysis is not necessary as the two hydroxyl groups on 2-MAG make it sufficiently water woluble
-pancreatic lipase does no recognize olestra (FA's in ester linkages to hydroxyl groups on sucrose)
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biliary obstruction
-dietary fat (TAG) can not be emulsified
-leads to steatorrhea
-bile salts can not be realeased through the bile duct from the gall bladder
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pancreatic disease
-emulsified TAG's can not be lipolysed
-problem with the release of pancreatic lipase
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celiac disease
-low intestinal surface area
-inhibits lipolysed lipids (FA's) from being absorbed into the intestinal epithelium
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chylomicron formation
-FA's, 2MAG, and cholesterol are inside the intestinal epithelium, they are re converted back into TAG's and CE's in between the bilayer of the ER using TAG synthase and ACAT
-Once in TAG and CE form,, they bud into the ER lumen and ApoB48 is addedto the membrane, creating a nascent chylomicron
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MTP
-loads chylomicrons with lipid and TG
-the chylomicron is then sent to the golgi for manufacturing and secretion
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chylomicron release
-nascent chylomicrons are transported from the ER to the golgi
-vesicles from the golgi fuse with the cell mem, releasing nascent chylomicrons into lymphatic system through lacteals
-ApoC2 and E are transferred from HDL, forming a mature chylomircon in the lymph
-chylomicrons then enter the blood through the thoracic duct
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lacteal
lymphatic capillary that absorbs dietary fats in the villi of the small intestine
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ApoC2
activates lipoprotein lipase on blood vessel inner surface (adipose and other tissue)
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