A membrane lipid is a compound, which belongs to a group of which form the double-layered surfaces of all cells. Lipid metabolism is the synthesis and degradation of lipids in cells where fat are broken down for energy. Take up the gi lipid metab & membrane lipids MCQ's below to see how well you understood the course.
Their synthesis in the liver is increased after a meal containing cholesterol and cholesterol esters
They both contain CoA
When the LDLR is up-regulated, HMG-CoA reductase is switched on.
HMG-CoA reductase is activated when the LDLR is down-regulated and the cell requires cholesterol
Both HMG-CoA reductase and the LDLR are synthesized in response to high levels of intracellular cholesterol
Increasing the conversion of cholesterol to bile acids
Inhibiting the formation of HMG-CoA
Preventing the reabsorption of bile acids from the intestine
Inhibiting the formation of mevalonate
Inhibiting the absorption of cholesterol from the diet
Plasmalogens
Phosphatidylinositol
Cardiolipin
Platelet activating factor
Phosphatidylcholine
Tay-Sachs
Fabry
Krabbes
Neimann-Pick
Faber
HMG-CoA red uctase is activated due to low levels of thyroid hormones
Low density lipoprotein receptors are upregulated in these patients
Large amounts of cholic acid are reabsorbed from the intestine which feeds back to 7-a-hydroxylase resulting in inactivation of the enzyme
High levels of thyroid hormones increase the synthesis of cholesterol
Thyroid hormones are necessary for the activation of 7a-hydroxylase
Carnitine
Vitamin E
Riboflavin
Niacin
Thiamine
Complete absence of medium chain acyl-CoA dehydrogenase
Deficiency in one of the enzymes in the ketone body synthetic pathway
Carnitine deficiency
A low fat, high carbohydrate diet
Decreased production of insulin
Skeletal muscle
Spleen
Liver
Heart
Brain
Increased synthesis of fatty acids in adipose tissue due to excess free fatty acids released from adipose tissue
Decreased gluconeogenesis due to lack of activation of pyruvate carboxylase
Decreased levels of free fatty acids and undetectable ketone bodies in the plasma due to inactivation of LPL
Increased synthesis and recycling of fatty acids by the liver leading to increased adipose tissue storage of fats
Increased beta-oxidation due to increased activity of hormone sensitive lipase with subsequent increase in ketone bodies in plasma
Activation of fatty acid synthetase
To act as a precursor for addition of one carbon units
Activation of acetyl-CoA carboxylase
To add the activated carbon dioxide in the formation of malonyl-CoA
Activation of carnitine acyl transferase
Glyceraldehyde-1, 3-bisphosphate to 3-phosphoglycerate
Glucose-6-phosphate to ribulose-5-phosphate
Glucose-6-phosphate to fructose-6-phosphate
Citrate to malate
Pyruvate to lactate
Glucose
Triglycerides
P-hydroxybutarate
Acetyl-CoA
Glycogen
Fabrys
Tay-Sachs
Nieman-Pick
Gauchers
Krabbes
Lysosome
Peroxisome
Mitochondrion
Endoplasmic reticulum
Plasma membrane
Apo All
Apo Al
Apo CII
Apo AIV
Apo E
Linolenic acid
Linoleic acid
Arachidonic acid
Ecosapentanoic acid
Palmitic acid
Phosphatidylserine
Cardiolipin
Phosphatidyl inositol
Dipalmitoylphosphatidylcholine
Platelet activating factor
Fabrys
Sandhoff-Jatzkewitz
Krabbes
Gauchers
Neimann-Pick
Cardiolipin
Ceramide
Sphingomyelin
Dipalmitoyl phosphatidylcholine
Ganglioside
Thromboxane synthase
Prostaglandin E dehydrogenase
Lipoxygenase
Cyclooxygenase
Prostacyclin synthase
Cardiolipin
Phosphatidylinositol
Plasmalogens
Dipalmitoylphophatidylcholine
Platelet activating factor
They are involved in the activation of choline, ethanolamine and diacylglycerol (DAG)
They provide the energy to convert choline to ethanolamine
They are involved in the phosphorylation of choline and ethanolamine
They are recognition molecules for phospholipid transferases
They are important in signal transduction
The patient can go into cardiac arrest because of lack of fatty acids for ATP production.
A plasma sample taken 45 minutes after a meal would reveal high levels of triglycerides due to lack of function of adipose tissue lipoprotein lipase
Coma could result because of lack of fatty acids as fuel for the brain
The patient would present with low levels of plasma ketone bodies due to lack of uptake of fatty acids in liver
A plasma sample would reveal both low levels of triglycerides and glucose
Essential amino acid deficiency
Type 1 glycogen storage disease
Acute alcohol toxicity
Carnitine acyltranferase deficiency
Elevated insulin levels, which cause the hypoglycemia and increase fatty acid mobilization from adipose tissue
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