Metabolism of Fats Flashcards
(66 cards)
How much fat do we normally get in our diets?
100-150g
what % of our total dietary energy intake is fat?
40%
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.
Why?
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.
true
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
detergents.
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.
