Can someone help me with this question :)
Maybe because there is more flux of FFA to the liver as an alternative fuel..
But what s the reason for this all?
This is an interesting question because according to the literature not all patients with GSD type III develop a hyperlipidemia. I am not aware of a kinetic study looking into the details of lipoprotein metabolism in these patients but it is possible that the reason is a overproduction of VLDL.
Definitely an interesting question. Where is the AGL enzyme localized in hepatocytes? BRENDA says it is localized to the sarcoplasmic reticulum in rat skeletal muscle. If AGL is localized to ER in hepatocytes, perhaps the enzyme is involved in supplying glycosyl units for glycosylation of secretory pathway proteins. This might fit with Dr. Hoffmann's suggestion of VLDL overproduction. Is it known whether the hyperlipidemia of GSD III is Chylos or VLDL or LDL or HDL?
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