Control of chylomicron export from the intestine
| Autor: | C. M. Mansbach, Shahzad Siddiqi |
|---|---|
| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Physiology Endoplasmic Reticulum 03 medical and health sciences symbols.namesake Physiology (medical) Chylomicrons Animals Humans Intestinal Mucosa Transcellular Transport Vesicles Hepatology biology Triglyceride transport Endoplasmic reticulum Vesicle Gastroenterology food and beverages SAR1B Golgi apparatus Protein Transport 030104 developmental biology Biochemistry biology.protein symbols Phosphorylation lipids (amino acids peptides and proteins) Chylomicron |
| Zdroj: | American Journal of Physiology-Gastrointestinal and Liver Physiology. 310:G659-G668 |
| ISSN: | 1522-1547 0193-1857 |
| DOI: | 10.1152/ajpgi.00228.2015 |
| Popis: | The control of chylomicron output by the intestine is a complex process whose outlines have only recently come into focus. In this review we will cover aspects of chylomicron formation and prechylomicron vesicle generation that elucidate potential control points. Substrate (dietary fatty acids and monoacylglycerols) availability is directly related to the output rate of chylomicrons. These substrates must be converted to triacylglycerol before packaging in prechylomicrons by a series of endoplasmic reticulum (ER)-localized acylating enzymes that rapidly convert fatty acids and monoacylglycerols to triacylglycerol. The packaging of the prechylomicron with triacylglycerol is controlled by the microsomal triglyceride transport protein, another potential limiting step. The prechylomicrons, once loaded with triacylglycerol, are ready to be incorporated into the prechylomicron transport vesicle that transports the prechylomicron from the ER to the Golgi. Control of this exit step from the ER, the rate-limiting step in the transcellular movement of the triacylglycerol, is a multistep process involving the activation of PKCζ, the phosphorylation of Sar1b, releasing the liver fatty acid binding protein from a heteroquatromeric complex, which enables it to bind to the ER and organize the prechylomicron transport vesicle budding complex. We propose that control of PKCζ activation is the major physiological regulator of chylomicron output. |
| Databáze: | OpenAIRE |
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