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Flashcards in Metabolism of Fats Deck (66):

How much fat do we normally get in our diets?



what % of our total dietary energy intake is fat?



where does the fat in our diet come from?

milk and milk products, cheese, cream, butter,
margarines, cooking oils,
lard, meat fats, eggs,
cereal grains, nuts, fat-rich fish and fruit (avocado), etc


what is taken in with the fat

fat-soluble vitamins
A, D, E, K


what fatty acids come as part of the fat we take in?

the essential omega-6 and omega-3 fatty acids linoleic acid (C18:2 D9,12)
and linolenic acid (C18:3 D9,12,15) respectively


what is the main strucure that the main fats in cooking oils, butter, margarine, meat fat, cereal and nut oils all have in common

TAG or
TRIACYLGLYCEROL (triglyceride) in which three fatty
acids are ester bonded to glycerol.


what is a simpler form of TAG

Simpler forms with one or two acyl chains esterified to glycerol


what are the other lipids that get taken into the intestine in our food
along with the triacylglycerol

Phospholipids from cell membranes
Cholesterol esters from animal
cell fat stores
Cholesterol from animal
cell membranes


what is the problem with fat digestion, absorption
and transport

Fat (triacylglycerol, TAG) is immiscible with water!


TAG has to be digested in an aqueous environment, the intestine. What is the SOLUTION

emulsification into small droplets (1-100m) and their stabilisation by bile salts and amphipathic lipids for enzyme action


TAG has to be transported round the body in the blood, also an aqueous environment, What is the solution?

coat TAG-rich particles with protective proteins and amphipathic lipids


what are the basics of fat digestion. to include the emulsification bile salts lipases and bile salts again

Emulsification in mouth and stomach at 37oC liquifies and emulsifies the bulk lipid phase into small (1-100m) droplets. This increases the surface area of TAG droplets for enzyme attack.

Bile salts from gallbladder and amphipathic lipids coat small emulsion particles preventing them re-aggregating into bulk TAG phase

Lipases degrade TAG

Bile salts solubilise products of lipase digestion into micelles (nm size) to facilitate uptake into enterocytes in jejunum region.


what the 3 sources of lipid-degrading enzymes

Lingual lipase
Gastric lipase
Pancreatic triglyceride lipase


what are the Pancreatic triglyceride lipases

bile salt-activated
lipase, pancreatic lipase related protein 2,
phospholipases, cholesterol esterases


what are the Gastric lipases

lipase cleaves 15-20% of dietary TAG fatty acids. Especially important in neonate for milk TAG digestion. Churning action of stomach at 37oC emulsifies bulk TAG phase-very important!


what are the lingual lipases

from Ebner’s glands on
dorsal surface of tongue, activity continued
in stomach


The churning action of the stomach at 37oC emulsifies the
bulk TAG phase into small droplets 1-100 microns or less in
diameter. These have a much larger surface area for lipase
enzymes to act on. What prevents the small TAG particles from re-aggregating
into a bulk fat phase in the duodenum where mixing is not so active?

The particles become coated with bile salts and more amphipathic phospholipids and cholesterol. The more polar surface prevents small emulsion droplets from re-aggregating yet allows lipase action to degrade the TAG


Steps of lipid absorption

Breakdown of products of lipid digestion + amphipathic bile salts = micelles
Micelles travel to apical brush border of intestinal Epithelial Cells (Ecs) and release products for digestion
Once inside intestinal Ecs lipid products are re-esterified with FFA = PLs, CEs, TAGs
Re-esterified lipids + apo(lipo)proteins = chylomicrons
Chylomicrons migrate to basolateral membrane of the ECs of the small intestine and exocytosis occurs into the lacteals, the thoracic duct and ultimately the blood


Lipid absorption, re-esterification, and incorporation into chylomicrons in the small intestine.

Mixed micelles release their contents that enter intestinal epithelial cells. Bile salts are recirculated from the ileum to the liver via the enterohepatic circulation. C cholesterol, CE cholesterol ester, FFA free fatty acid, MG 2-monoacylglycerol, LL lysolecithin, PL phospholipid, TG triglyceride, VA vitamin A, VD vitamin D, VE vitamin E, VK vitamin K


You are asked to see Mr. Stephenson, a 49-year-old man with chronic pancreatitis secondary to alcohol abuse. While eliciting his GI review of symptoms, you note that he complains of greasy, diarrheal bowel movements.


Excessive alcohol consumption is the most common cause of chronic pancreatitis and a very frequent cause of pancreatic insufficiency.
Patients who suffer from chronic pancreatitis produce insufficient amounts of lipase which is crucial for the digestion of lipids.
Malabsorption of lipids results in the excretion of greasy stools or steatorrhea.


true or false, Bile is continuously formed by the liver and secreted to the gallbladder where it is stored and concentrated.



what are bile acids and what do they do

Bile acids are the
breakdown products
of cholesterol
They are conjugated
to glycine and taurine
making one end more
polar and are present
in bile as the sodium
and potassium salts.

They are powerful


where are primary bile salts fromed and give examples

Cholic and chenodeoxycholic acids (and the corresponding
taurocholic acid, etc) are primary bile acids made by the liver


where are secondary bile salts fromed and give examples

are formed by bacterial action in the intestine and are secondary bile acids.


structure and consequential function of bile acids

Bile acids have a planar
structure with all polar
groups on one face and
non-polar groups on the
other face. So they are amphipathic, aggregate
into nm size micelles and
are good detergents.


how is some cholesterol excreted daily?

There is an enterohepatic
circulation of bile acids
with some being lost each day
in the faeces.


when is CCK Cholecystokinin released from the duodenal mucosa?

when food enters
the intestine


what does Cholecystokinin CCK do?

CCK in the blood stimulates
the gallbladder to release bile by contraction
of the gallbladder and relaxation of the
sphincter of Oddi which is normally closed
to prevent bile and hepatic secretions
flowing into the intestine until required.


what is cholelithiasis

stones in gallbladder



stones in ducts of biliary tree


Cholesterol stones

70-80% cholesterol


Pigment stones

bile pigments (bilirubin, billiverdin)


who is more at risk of kidney stones?

Caucasians, females, low fibre, high
cholesterol, starchy diet, overweight


true or false Most TAG is degraded to 1-monoacylglycerol with only a little glycerol being formed depending on how long food remains in the duodenum

Most TAG is degraded to 2-monoacylglycerol with only a little glycerol being formed depending on how long food remains in the duodenum


true or false Micelles of bile salts solubilise the fatty acids and 2-MAG from TAG degradation as well as lyso-lipids from phospholipid digestion and cholesterol. The mixed micelles transport
lipid digestion products to the
microvilli of erythrocyctes

Micelles of bile salts solubilise the fatty acids and 2-MAG from TAG degradation as well as lyso-lipids from phospholipid digestion and cholesterol. The mixed micelles transport
lipid digestion products to the
microvilli of enterocytes


what transport the products of fat digestion
across the unstirred water layer at the enterocyte surface

bile salt micellells


what woyld happen to 2MAG absportion with out bile salts

Without bile salts fatty
acids and 2-MAG are absorbed much more slowly.


what do bile salt micelles deliever?

products of fat digestion
across an unstirred water layer to the enterocyte
membrane where they are taken up by carrier-mediated and/or passive diffusion mechanisms


true or false, bile salts are not absorbed. They are transported to the ileum for reabsorption and recycling.



what happens to fatty acids and 2-MAG

they are reassembled into TAG,
some protein is added and the TAG is secreted as chylomicrons


wha tis the size of chylomicrons

75-1000nm in diameter


are Glycerol and short
chain fatty acids (C4-10)
are water-soluble and can they pass
through enterocytes
directly into the blood?



where are absorbed products of fat digestio reassembled into TAG

in the endoplasmic reticulum of enterocytes.


what is added as
the TAG droplet passes from the
endoplasmic reticulum to the Golgi
where glycosylation of proteins

Phospholipid and protein


how do chylomicrons enter the circulation and why

Chylomicrons are too big (up to 1m)
to pass into capillaries so enter the
circulation via the thoracic lymph duct


how does TAG
accummulate in the enterocytes.

Blocking protein synthesis
stops chylomicron release


Cholesterol, cholesterol ester
and fat-soluble vitamins are added
to the chylomicrons which move in
vesicles to the plasma membrane via what process



what is the structure of High density lipoproteins

disc-like shape


how do the rather similar struture of very low density liproptein differ

vary in the apoproteins
on the particle surface.


how do Chylomicrons transport dietary fat from intestine to tissues

via plasma


Chylomicrons transport dietary fat from intestine to tissues via plasma, what do other liproteins do?

circulate fat between tissues in the plasma


how does the colour of plasma change during and after eating a fatty meal?

After ingesting a fatty meal the plasma goes opaque with chylomicrons but
clears again in one to two hours as the chylomicrons are metabolised


importance of Omega 3 fatty acid

control blood clotting
build cell membrane s in the brain
normal growth and develoment
roles in bp, rheumatoid arthritis and depression


importance of Omega 6 fatty acid

brain function, normal growth and development


Fat (triacylglycerol, TAG) summary

is a major dietary component contributing to energy needs, also brings in fat-soluble vitamins and essential fatty acids


Chylomicrons summary

in the blood are stabilised by amphipathic apoproteins on their surface, phospholipids and some cholesterol and are only present in the blood after a meal (cleared in a couple of hours)


TAG summary

in chylomicrons is removed by lipoprotein lipase in capillaries in extrahepatic tissues: remaining TAG is taken up by liver for metabolism and recirculation


Enterocytes summary

reassemble 1-MAG and fatty acids back into TAG which is then secreted into lymphatics as big particles called chylomicrons - entering blood at thoracic duct


Digestion of fats presents problems due to

the fact that TAG is water-immiscible


Bile salt micelles summary

solubilise 1-MAG and fatty acids and transport them to enterocytes in duodenum and jejunum. 95% of bile salts are later reabsorbed in the ileum


Emulsification (mechanical disruption into tiny droplets) of fats occurs in

the stomach


Pancreatic TAG lipase summary

is the major enzyme digesting TAG mainly to 1-MAG (1-monoacylglycerol) plus two fatty acids (depends on transit time)


Fat emulsion particles summary

are stabilised in the duodenum by bile salts and other amphipathic lipid giving a large surface area for lipase enzymes to act on


Bile salts summary

derived from cholesterol metabolism are stored in gall bladder until needed


Actions of pancreatic lipase, bile salts and colipase in fat digestion.

(a) Pancreatic
lipases break down triglycerides. (b) Bile salts coat lipid droplet and displace lipases. (c)
Addition of colipases anchor lipases to bile salt-coated fat droplet (Adapted from American


What happens in the Emulsification of dietary fat.

Fat from the stomach is emulsified with bile salts and
lecithin (BL; small rectangles) in the duodenum. Bile salts are converted from bile acids
(BA) synthesized in the liver. The emulsified fat is digested by several lipases secreted from the
pancreas. Pancreatic lipase (PL) hydrolyzes triacylglycerols (TAG) to 2-monoacylglycerol (2MG)
plus free fatty acids (FFA) in the presence of colipase (CL). CL is also secreted from the pancreas
but in an inactive procolipase (proCL) form that is activated by the action of trypsin (not shown).
Cholesterol ester (CE) is de-esterified by cholesterol ester hydrolase (CEH) to cholesterol plus
FFA. Phospholipids (PH) are hydrolyzed by phospholipase A2 (PLA) to lysolecithin (LL) and
FFA. Like CL, PLA is activated from its inactive “pro” form (pPLA) by trypsin