Cellular Lipid Metabolism by Sven-Olof Olofsson, Pontus Boström, Jens Lagerstedt (auth.),

By Sven-Olof Olofsson, Pontus Boström, Jens Lagerstedt (auth.), Christian Ehnholm (eds.)

For years lipids have interested mobile biologists and biochemists as a result of their profound results on phone functionality. "Cellular Lipid Metabolism" highlights new options and up to date findings, but additionally experiences very important discoveries made some time past. amazing overseas specialists give a contribution thirteen chapters at the genetics, molecular and mobile biology of lipids. providing analyses on the molecular point they exhibit the foundations during which mobile lipid metabolism capabilities. extra, a number of fascinating observations that can't but be defined are pointed out, stimulating the readers to destiny reports. This e-book offers a useful resource of knowledge for biomedical researchers in strength metabolism, vascular biology, endocrinology and lipidology.

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Additional studies are required to determine how and where in the cell the primordial lipid droplets are formed. Of key importance is the identification of a link between the accumulation of lipid droplets and the development of insulin resistance, but further research is required to clarify the precise mechanism and proteins involved. We propose that these investigations may identify targets that could be modulated to reduce the accumulation of lipid droplets and hence reverse the associated complications.

Serum 24(S)-OHC concentration apparently reflects the rate of cholesterol turnover in the brain, and it has been suggested as a new diagnostic indicator of diseases affecting the CNS. Hepatic cholesterol-7a-hydroxylase (encoded by CYP7A1) carries out the initial enzymatic step in the major, so-called neutral pathway of bile acid synthesis (reviewed by Björkhem and Eggertsen 2001) . 7 a -OHC is thus produced in relatively large quantities in the liver and part of it leaks into the circulation, where it is one of the most abundant oxysterols.

4 The assembly and secretion of VLDL. ApoB100 is co-translationally lipidated in the ER by the transfer protein MTP to form a partially assembled primordial particle (pre-VLDL; I). If apoB100 is not co-translationally lipidated, it is retracted to the cytosol and sorted to proteasomal degradation (II). Pre-VLDL is either retained and degraded, or further lipidated to form a small triglyceride-poor form of VLDL (VLDL2; III). VLDL2 reaches the Golgi apparatus (IV) where it can either be secreted (V) or converted to the large triglyceride-rich form, VLDL1, by a bulk addition of triglycerides (VI).

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