Stockham & Scott Chapter 16 Lipids AKG Flashcards
What are the measured lipid components in blood:
Cholesterol and Triglycerides, which are transported in serum via lipoproteins
List examples of sterols:
Cholesterol
Bile acids
Steroid hormones
Vitamin D
Fatty acids can circulate outside of lipoproteins, bound to albumin. T/F
True
Prostaglandins are what type of lipid?
Fatty acids
Give examples of terpenes (type of lipid):
Vitamins A, E, and K
List lipoproteins from lowest to highest protein content (and from highest to lowest triglyceride content)
- Chylomicrons
- VLDL
- IDL
- LDL
- HDL
Which lipoprotein has the highest cholesterol content and is the main lipoprotein in dogs:
HDL (considered the ‘good’ cholesterol in humans)
_____ are specific components of lipoproteins that influence their structure, serve as cofactors for enzymes, and act as ligands.
Apolipoproteins
HDL express which class of apolipoproteins?
A, C, E, D (all except B)
Chylomicrons express which class of apolipoproteins?
A, B, C, E (all except D)
VLDL & IDL express which class of apolipoproteins?
B, C, E (all except for A & D)
What makes lipoproteins containing apolipoprotein C-II special?
It allows them to bind to LPL on endothelial cells, and cleave fatty acids from triglyceride molecules. FAs then enter the cells (e.g., adipocytes, myocytes). This process repeats until TG is depleted.
This lipoprotein delivers cholesterol produced in the liver to other cells/tissues.
LDL
This lipoprotein scavenges excess cholesterol from cells and delivers it to the liver.
HDL
This lipoprotein is rich in triglycerides, transports TG from GIT to tissues, and is produced by enterocytes.
chylomicrons
This lipoprotein is rich in triglycerides, produced in the liver from NEFAs liberated by fat breakdown, and transports TGs from liver to tissues.
VLDL
This lipoprotein is rich in cholesterol, is produced from VLDL, transports cholesterol to tissues, and is taken up by LDL receptors.
LDL
This lipoprotein is rich in cholesterol, produced in the liver, and transports cholesterol from tissue to the liver.
HDL
This apoplipoprotein is a co-factor for LPL.
C-II
_____ is found on the luminal surface of endothelial cells, mediates removal of TGs from chylomicrons, VLDL, and IDL into tissues, and promotes binding of LDL to its receptor a.
Lipoprotein lipase
Lipoprotein lipase needs _____ to travel from inner- to outer- membrane leaflet on endothelial cells so they can come into contact with plasma lipoproteins.
Insulin
Increased LPL activity leads to _____ plasma TG and choelsterol.
decreased
IV ____ promotes release of LPL from endothelial cells and is aka “lipemia clearing factor”
heparin
LPL activity is enhanced by…
Insulin Thyroxine Heparin
What is the rate limiting enzyme in cholesterol production?
3-hydroxy-3-methylgluatryl-coenzyme A reductase
Free cholesterol is toxic, so there are two enzymes that esterify it:
- Plasma LCAT 2. Cellular acylcholesterol acyltransferase
LDL expresses what class of apolipoproteins?
B
How do cholesterol esters enter cells?
Receptor-mediated endocytosis of lipoprotein fragments
Ddx for hypercholesterolemia
- Increased production in liver
- Nephrotic syndrome
- PLN
- Incrased production in enterocytes
- Post-prandial hyperlipidemia
- Decreased lipolysis or intravascular processing of lipoproteins
- Hypothyroidism
- Nephrotic syndrome or PLN
- Lipoprotein lipase deficiency
- Other unknown mechnisms:
- Acute pancreatitis
- Obstructive cholestasis
- DM
- Excess GCs
- Hypercholesterolemia in briards
- Idiopathic hyperlipidemia in miniature schnauzers
Ddx for high HDL
- Decrease or absent cholesterol ester transfer activity (transfers cholesterol from HDL to LDL
High HDL ___ susceptibility to athrogenesis.
decreases
Chylomicron formation peaks ____ after eating, and is cleared ____ after eating.
2-6 hours
8-16 hours
Postprandial hyperlipidemia increases TG and cholesterol. T/F
True - but not always cholesterol
List ddx for primary or familial hyperlipoproteinemia (congenital defects in lipoprotein metabolism )
- Idiopathic hyperlipidemia of miniature schnauzers
- Increase in both TG and cholesterol
- Hyperlipidemia in a Brittany dog
- increase in TG, but NOT cholesterol
- Primary hyperchylomicronemia in cats: type III LPL deficiency
- Increase in TG but NOT cholesterol
- Hypercholesterolemia in briards
- Normal TG, but HIGH cholesterol
List ddx for secondary hyperlipoproteinemia (acquired disorder from damaged cells or abnormal hormonal activity)
- Acute pancreatitis
- Obstructive cholestasis
- Diabetes mellitus
- Hypothyroidism
- Hyperadrenocorticism in dogs
- Nephrotic syndrome and PLN
- Equine hyperlipemia
Pancreatitis can cause obstructive cholestasis. T/F
True
Obstructive cholestasis can cause increases in cholesterol and triglycerides. T/F
False - it may cause hypercholesterolemia but should NOT increase plasma triglyceride content
Mechanisms for hypercholesterolemia d/t obstructive cholestasis
- Decreaed biliary excretion
- In mice, increased bile acid synthesis induces increased synthesis of cholesterol
- Defective uptake of LDL (found increased LDL levels in dogs experimentally)
This disease process is associated with unique lipoproteins that have cathodal electrophoretic migrations (lipoprotein X1, X2, X3).
Obstructive choelstasis
Unclear why they form, but may be due to interaction between plasma lipids and bile acids, or due to decrease in LCAT activity
Lipoproteins X1, X2, X3 are found in patients with obstructive cholestasis. Their lipid content is mostly of ____ and non-esterified ____. Their protein content is mostly of ____ within the core apoplipoprotein ___ on the surface.
phospholipids
cholesterol
albumin
apoplipoprotein C
Mechanisms of hyperlipoproteinemia due to diabetes mellitus
- Decrease in insulin –> defective LPL activity –> decreased clearance of circulating lipoproteins
- Increase in hormone sensitivite lipase activity in adipocytes (due to the fact that cells can’t utilize circulating glucose) –> mobilization of bod lipids –> influx of free FAs into liver –> FA oxidation leads to excess acetyl-coA –> promotes TG, cholesterol, and ketone production
- Increased synthesis of HDL in intestinal mucosa
Approximately 90% of dogs with Cushing’s disease have fasting hypercholesterolemia +/- hypertriglyceridiemia. T/F
True
Mechanisms of hyperlipoproteinemia d/t hyperadrenocorticism in dogs
- Indirect effect: increased GC activity can lead to DM or steroid hepatopathy
- Direct effects:
- GC stimulates VLDL synthesis
- GC liberates FAs from adipose tissue –> influx of FFAs into liver –> acetylcoA –> stimulates production of TG and cholesterol –> increase in VLDL
- GCs antgonize actions of insulin –> decreased LPL activity –> decreased clearance of circulating lipoproteins
Mechanisms for hypercholesterolemia d/t nephrotic syndrome and PLN
- Exact mech. unknown, but many are at play
- Thought that there is loss of a protein needed for LPL binding to endothelial cells or for normal LPL activity; or loss of proteins/enzymes needed in lipid metabolism
- Good evidence to support defective lipolysis of lipoproteins that contain lipoprotein B (chylomicrons, VLDL, IDL, and LDL - all liporpoteins except HDL)
Equine hyperlipemia is a primary disorder due to congenital defects. T/F
False - it is a secondary disroder (NOT familial) and thought to be secondary to metabolic disorders that alter lipoprotein metabolism:
- Anorexia (physiologic or pathologic mobilization of FAs from adipocytes –> stimulates VLDL synthesis)
- Obesity
- Lactation –> increase in progesterone –> stimualtes GH –> insulin receptor and post-receptor defects –> insuline resistance
- Renal failure
- Endotoxemia
- Other states creating neg. energy balance
Ddx for hypocholesterolemia:
- Decreased production: PSS, PLE
- Hypoadrenocorticism
- Cortisol influences lipoprotein metabolism, complete mechanisms unknown
What are the interferences when measuring cholesterol? Are they negative or positive?
Negative interferences include: high bilirubin and high ascorbic acid
*can add ascorbic oxidase to mitigate effects hypercholesterolemia on other measurands
In a ____ sample, majority of TGs are within lipoproteins that were produced in the liver.
In a _____ sample, majority of the TGs are within chylomicrons assembled in enterocytes.
Fasting
Post-prandial
More correct name for triglyceride:
Triacylglycerol
(three fatty acids “triacyl” and “glycerol” backbone)
Method of TG measurement
Lipase liberates glycerol –> measure glycerol with coupled rxns via spectrophotometry
Please label the different bands and their associated lipoproteins, starting from origin and moving towards the anode.

- Chylomicron
- Beta-lipoprotein –> LDL
- Pre beta-lipoprotein –> VLDL
- alpha lipoprotein –> HDL
*alpha - a for being closest to anode
Lipoprotein electrophoresis is a qualitative method that can be used to detect dyslipoproteinemic patterns.
Increases in alpha-bands in dogs indicates ______
Increases in beta-bands in dogs indicates _____
Hypercholesterolemia (alpha bands)
Hypertriglyceridemia (beta bands)
Lipoprotein electrophoresis is a reliable method for measuring lipoproteins. T/F
False - recommended to use in combination with density fractionation or to simply monitor response to therapy becuase it doesn’t correctly label bands - not all lipoproteins of the same class have the same density)
NEFAs and glycerol from hydrolysis of _______ in adipose tissue, liver, and mammary tissue.
Hydrolysis is mediated by lipase. Lipase is stimualted by _____ and ____ and inhibited by _____.
triacylglycerol
Epinephrine and glucagon
Insulin
NEFAs are measured via enzymatic colorimetric assay, which detects ________, but does NOT detect _______.
Detects medium and long-chain fatty acids
Does not detect volatile FAs (e.g., propionic acid, butyric acid)
Increased NEFAs are a sign of ______ in cattle.
negative energy balance
Ddx for increased NEFAs:
- DM
- Hepatic lipidosis
- Over-feeding
- Obesity
- Food deprivation
- Post-exercise
NEFAs are measured mostly in ruminants before feeding and ____ days before calving.
2-14 days
Pre-parturient cows with increased _____ correlate with post-parturient Ketosis, displaced abomasums, and fatty liver.
NEFAs
Standing plasma test for chylomicrons is a test that puts a sample of plasma in the fridge for 16 hours, and confirms presence of chylomicrons is there is a cream top, but this is an unreliable test. What other tools are better to measure chylomicrons?
Ultracentrifugation and lipoprotein electrophoresis