BioFiles Volume 5, Number 7 — Lipid Metabolism

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The human body regulates cellular lipid concentrations by location and time, and deregulation is associated with a variety of human diseases. In addition to disorders due to inborn errors of lipid metabolism, diseases like cardiovascular disease, diabetes, cancer, infections, and neurodegenerative diseases are frequently lipid related. A key feature of diabetes, obesity, and atherosclerosis is excessive lipid accumulation in cells. Excess energy is stored as triacylglycerols for later use when nutrients are scarce. These triacylglycerols, along with the precursors to membrane lipids, are stored in cytoplasmic lipid droplets in eukaryotic cells. Host-pathogen interactions in lipid metabolism are also of interest in infectious disease research since pathogenic microorganisms can use the host's lipids as a carbon and energy source, which provides an advantage to the pathogen in persistence, virulence, and overcoming host immune responses. Major drug classes like the statins and cyclooxygenase (COX) inhibitors target enzymes involved in lipid metabolism. Increased concentrations of lysophosphatidylcholines and decreased concentrations of antioxidative ether phospholipids in serum have been associated with acquired obesity. Detailed analysis of the local concentrations of lipids, their precursors, and metabolites as a function of time will aid the understanding of their roles in the vital functions of cells.

Next to adipose tissue, the central nervous system has the highest cellular lipid concentration. Injuries and disorders of the CNS may be influenced by changes in lipid metabolism. The accumulation of LDL-derived lipids in the arterial wall results in atherosclerosis and is a risk factor for stroke. Lipid metabolism is altered by tumor necrosis factor-a (TNF-a) and interleukin-1 (IL-1), which stimulate production of eicosanoids, ceramide, and reactive oxygen species. Reactive oxygen species that exceed the cell's capability for detoxification result in oxidative stress yielding oxidized phospholipids that are metabolized to 4-hydroxynonenal, 4-oxo-2-nonenal, and acrolein. Neurodegenerative diseases, CNS injuries, and brain traumas can be influenced by lipid oxidation because of the high lipid content and oxygen consumption of the brain. Sphingomyelin accumulation results from acidic sphingomyelinase deficiency in Niemann-Pick disease A and B, while cholesterol accumulation occurs in Niemann- Pick disease C due to mutations in either the NPC1 or NPC2 genes. Cholesterol is an important regulator of lipid organization and a precursor for neurosteroid biosynthesis. The gene encoding the apolipoprotein E4 variant of the principal cholesterol carrier protein in the brain (the E4 allele of APOE ) is a significant risk factor for Alzheimer's disease. Lipid peroxidation due to phospholipase activation may contribute in part to Parkinson's disease.

Description Product No.
N-Acetyl-D-sphingosine A7191-1MG
A7191-5MG
Acrolein 01679-10ML
Cholesterol C8667-500MG
C8667-1G
C8667-5G
C8667-25G
C8667-100G
Cholesterol 20808-100G-R
20808-1KG-R
Galactocerebrosides from bovine brain C4905-10MG
C4905-25MG
L-α-Glycerophosphorylcholine G5291-10MG
G5291-50MG
G5291-100MG
N-Hexanoyl- D -sphingosine H6524-1MG
H6524-5MG
HNE-DMA H9538-2MG
H9538-5MG
D-α-Hydroxyglutaric acid disodium salt H8378-25MG
H8378-100MG
H8378-250MG
Malondialdehyde tetrabutylammonium salt 63287-1G-F
63287-5G-F
N-Palmitoyl- D - sphingomyelin semisynthetic from bovine brain sphingomyelin P6778-1MG
P6778-10MG
N-Octanoyl-D-sphingosine O1882-5MG
Sphingomyelin S7004-5MG
S7004-10MG
S7004-50MG
S7004-100MG
S7004-500MG
Sphingomyelin S0756-50MG
S0756-100MG
S0756-500MG
Trisodium (2 RS ,3 RS )-2- methylcitrate 59464-10MG
59464-50MG

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