Intro to lipids Flashcards
lipids
- hydrophobic organic molecules that can be extracted from cells by non-polar solvents
- associated with each other, excluding water
2 classes of lipids
- fatty acids
- isoprenoids
fatty acids
- amphipathic, micelle forming, soaps
- energy storage (fat dep to cushion organs and insulate)
- membranes (electrical insulation) including phospholipids and sphingolipids
- signals
isoprenoids
- bile acids/ salts
- membranes
- signals
- cofactors
- fat soluble vitamins
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
stearic acid
18: 0
- zero after colon representation full saturation
palmitic acid
16:0
alpha, beta, and omega
- alpha = first C after the carboxyl
- beta = second C after the carboxyl
- omega = last C of the chain
omega number
number of carbons from the terminal methyl to the nearest double bond
linoleic acid
- 18:2
- 9,12
- omega 6
arachidonic acid
- 20:4
- 5,8,11,14
- omega 6
linoleic and linolenic deficiency
- these are essential FA’s
- symptoms: scaly dermatitis, alopecia (hair loss), thrombocytopenia (low platelet count), and cognitive development in children
triacylglycerols (TAGs)
- dietary and storage fats
- effectively formed by dehydration reactions between 3 FA’s and glycerol
- fully hydrophobic
TAG nomenclature
- change the FA suffix from “-ic acid” to “-oyl”
- list by position before glycerol
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
effects of tran saturation
- allows the FA’s to pack more closely together
- natural foods have cis double bonds
leptin
- released by adipose tissue
- suppresses food intake by altering the hormones released by the hypothalamus
- leptin KO’s are extremely obese
ghrelin
hunger hormone
percentage of fat in the typical US diet
- 35-40% of caloric intake
- triglycerides are the major source
bile acids made from cholesterol in the liver are…
- converted to bile salts
- conjugated with glycine or taurine
gall stones
-imbalance of cholesterol, bile salt and phospholipid secretion
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
micelles form at
-critical micelle concentrationconcentration
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
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
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
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
bile salt recylcing
95% done through enterohepatic circulation
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
absorbing cholesterol esters
- hydrolysis of cholesterol esters to allow absorption
- resynthesis of CEs to drive absorption and prepare for transport
peristalsis in lipid metabolism
-turns TAG droplets into micelles
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
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)
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
pancreatic disease
- emulsified TAG’s can not be lipolysed
- problem with the release of pancreatic lipase
celiac disease
- low intestinal surface area
- inhibits lipolysed lipids (FA’s) from being absorbed into the intestinal epithelium
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
MTP
- loads chylomicrons with lipid and TG
- the chylomicron is then sent to the golgi for manufacturing and secretion
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
lacteal
lymphatic capillary that absorbs dietary fats in the villi of the small intestine
ApoC2
activates lipoprotein lipase on blood vessel inner surface (adipose and other tissue)
ApoE and ApoB48
bind LDL receptor related protein (LRP) and allow chylomicron remnants to be internalized by the liver
