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Old 08-29-2012
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Arrow Belindalmm Daily Questions: Biochemistry #5

A 7-year-old boy is brought to the physician by his mother because of digestive problems. His mother says that he often experiences severe abdominal cramps after eating a high-fat meal. Diagnosis of a genetic defect resulting in a deficiency of lipoprotein lipase is made. Which of the following substances is most likely increased in this patient's plasma following a fatty meal?

A. Alumin-bound free fatty acids
B. chylomicrons
C. HDL
D. LDL
E. Unesterified fatty acids
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B. Chylomicrons
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B....abetalipoproteinemia
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Default my answer :)

B. chylomicrons
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Default Abetalipoproteininema

there is deficiency of apoB 100 and 48
So there would not be any formation of chylomicrons (as they require apoB-48)
or LDL and HDL
E. Unesterified fatty acids
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Chylomicrons Type I hypercholestrolemia.. S/s of recurrent ac. Pancreatitis
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i'll go with B) chylomicrons
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Default Answer is Chylomicrons.

Lipoprotein lipase is required for degradation of both Chylomicrons and VLDL. The role that lipoprotein lipase taking on is to release triglycerol within the core of Chylomicrons and VLDL into adipose tissue and liver, respectively. Thus, any defects in lipoprotein lipase will hinder triglycerol reabsorption into adipose tissue after a fatty meal, leading to fatty stool and abdominal cramp.
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Quote:
Originally Posted by koolkiller88 View Post
there is deficiency of apoB 100 and 48
So there would not be any formation of chylomicrons (as they require apoB-48)
or LDL and HDL
E. Unesterified fatty acids
You are right that formation of Chylomicrons and VLDL requires apoB 48 and apoB 100, but lipoprotein lipase is not participating in this synthesis process since apo B 48&100 and lipoprotein lipase are totally two different concepts. Since the formation of Chylomicrons is not hindered, the fatty acids are esterified.
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Quote:
Originally Posted by belindalimm View Post
Lipoprotein lipase is required for degradation of both Chylomicrons and VLDL. The role that lipoprotein lipase taking on is to release triglycerol within the core of Chylomicrons and VLDL into adipose tissue and liver, respectively. Thus, any defects in lipoprotein lipase will hinder triglycerol reabsorption into adipose tissue after a fatty meal, leading to fatty stool and abdominal cramp.
So diagnosis would be Abetalipoproteinemia right?
If yes,
According to kaplan
Abetalipoproteinemia patients have low to absent serum apoB-100 and apoB-48. Serum triglycerides may be near zero and cholestrol extremely low.
because chylomicron levels are very low, fat accumulate in intertinal enterocytes, Essential fatty acids and vit. A and E are not absorbed. Symptoms can be-
steatorrhea
Cerebellar ataxia
pigmentry degeneration in retina
acanthocytes
possible night blindness.
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Quote:
Originally Posted by koolkiller88 View Post
So diagnosis would be Abetalipoproteinemia right?
If yes,
According to kaplan
Abetalipoproteinemia patients have low to absent serum apoB-100 and apoB-48. Serum triglycerides may be near zero and cholestrol extremely low.
because chylomicron levels are very low, fat accumulate in intertinal enterocytes, Essential fatty acids and vit. A and E are not absorbed. Symptoms can be-
steatorrhea
Cerebellar ataxia
pigmentry degeneration in retina
acanthocytes
possible night blindness.
I don't think the diagnosis is abetalipoproteinemia since there is no deficiency or absence in apoB 48 and apoB 100. What do you think?
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Nothing in the stem even suggests that there's a problem with apob 48 nor 100. The question clearly refers to lipase deficiency only.
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Quote:
Originally Posted by belindalimm View Post
I don't think the diagnosis is abetalipoproteinemia since there is no deficiency or absence in apoB 48 and apoB 100. What do you think?
Not abetaliporpeteinemia... The question says lpl deficiency... Had It Been abeta... It would have shown symptoms other than abdominal cramps .... Like those stated in d above post..
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yes, the question clearly states lipoprotein lipase deficiency....it's type 1 hyperlipoproteinemia(hyperchylomicronemia)
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Quote:
Originally Posted by belindalimm View Post
I don't think the diagnosis is abetalipoproteinemia since there is no deficiency or absence in apoB 48 and apoB 100. What do you think?
Ya i didn't paid attention on lipoprotein lipase def. diagnosis.

but i need to confirm my presumption:
In Abetalipopretienimea we have ataixa, thory RBC (because of vit. E is not getting absorbed) and night blindness (because vit A is not getting absorbed)

but can be have these symptoms in lipoprotein lipase def.?
(as in this def. also chylomicrons are getting absorbed but not getting metabolised, just getting stored)
any comments-
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Quote:
Originally Posted by koolkiller88 View Post
Ya i didn't paid attention on lipoprotein lipase def. diagnosis.

but i need to confirm my presumption:
In Abetalipopretienimea we have ataixa, thory RBC (because of vit. E is not getting absorbed) and night blindness (because vit A is not getting absorbed)

but can be have these symptoms in lipoprotein lipase def.?
(as in this def. also chylomicrons are getting absorbed but not getting metabolised, just getting stored)
any comments-
I do agree with you that in lipoprotein lipase deficiency there still exists Vitamin A and E malabsorption because of stearorrhea. But I doubt if Chylomicrons gonna get absorbed. Chylomicrons are the fatty acids carrier in blood stream from peripheral tissue to liver, so I just regard them as shuttle which won't or less be absorbed in liver and other tissue(but they do get metabolized in liver). As long as there is plenty of apo B48, apo C and apo E, Chylomicrons would turn over and over, just to reach a stable concentration stage in blood. There is cholesterol and tryglycerides stored in liver, muscular cells, heart and adipose tissue, not the Chylomicrons get stored.

What do you think? Welcome any of your comments.
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