As a doctor you come across a patient (patient x) that has a defect in lipid met
ID: 98476 • Letter: A
Question
As a doctor you come across a patient (patient x) that has a defect in lipid metabolism. To ascertain the cause of this disorder, you add epinephrine to adipocytes obtained from Patient X and also to adipocytes obtained from a control patient and subsequently measure fatty acid release. Compared to the control patient, fatty acid release from Patient X’s cells is significantly lower. Why could have caused this difference between patients?
A mutation in protein kinase A (PKA) results in enhanced ABHD5 phosphorylation, resulting in inhibition of triglyceride hydrolysis
A mutation in lipoprotein lipase causes the enzyme to lose its ability to hydrolyze monoacylglycerols
A mutation in hormone sensitive lipase (HSL) results in reduced phosphorylation by PKA and slower diacylglycerol and subsequent monoacylglycerol hydrolysis
A mutation in the catalytic site of pancreatic lipase results in reduced triglyceride hydrolysis and fatty acid release
A mutation in acyl-CoA synthetase reduces fatty acid oxidation, leading to the inhibition of fatty acid release
a.A mutation in protein kinase A (PKA) results in enhanced ABHD5 phosphorylation, resulting in inhibition of triglyceride hydrolysis
b.A mutation in lipoprotein lipase causes the enzyme to lose its ability to hydrolyze monoacylglycerols
c.A mutation in hormone sensitive lipase (HSL) results in reduced phosphorylation by PKA and slower diacylglycerol and subsequent monoacylglycerol hydrolysis
d.A mutation in the catalytic site of pancreatic lipase results in reduced triglyceride hydrolysis and fatty acid release
e.A mutation in acyl-CoA synthetase reduces fatty acid oxidation, leading to the inhibition of fatty acid release
Explanation / Answer
The correct answer for this question is option D i.e a mutation in the catalytic site of pancreatic lipase results in reduced triglyceride hydrolysis and fatty acid release.Pancreatic lipase is the enzyme which break downs the bond between glycerol and fatty acid to release them
Let's see all the options one by one why they can't be the right answer for this question.
Option A states that a mutation in protein kinase A results in enhanced ABHD5 phosphorylation, resulting in inhibition of triglyceride hydrolysis . This option is wrong because PKA actually activates the enzyme which will ultimately phosphorylate ABHD5. So, if there is mutation in PKA, it will decrease the phosphorylation instead of enhancing it.
Option B states that a mutation in lipoprotein lipase causes the emzyme to lose its ability to hydrolyze monoacylglycerides. This option is wrong because a lipoprotein lipase hydrolyses the triglycerides into monoacylglycerides.
Option C states that a mutation in hormone sensitive lipase (HSL) results in reduced phosphorylation by PKA and slower diacylglycerol and subsequent monoglycerol hydrolysis. This option is wrong because PKA phosphorylates the HSL and HSL then hydrolyses diacylglycerol into monoacylglycerol. Monoglycerol is then hydrolysed to glycerol and fatty acid by MGL enzyme which is actually active even in the absence of hormonal stimulation.
Option E states that a mutation in acyl CoA synthetase reduces the fatty acid oxidation, leading to inhibition of fattty acid release . This option is wrong because fatty acid oxidation using acyl-CoA does not result into fatty acid release. It releases Fatty acyl CoA which finallly goes to citic acid cycle.
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