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Lipid droplets have been found to participate in lipid
metabolism, protein degradation, ER stress, protein glycosylation and pathogen
infection. If lipid droplets are not of the right composition or size or if
they do not form correctly, these could possibly cause an increase in pathogen
infection, or a decrease in protein degradation and glycosylation. There could
also be problems with proteins on the surfaces of the lipid droplets that alter
cell signaling if the lipid droplets are not formed normally.1 These
proteins are also involved with lipid metabolism and if altered they could
cause lipid storage disorders or lipid metabolism disorders such as Tay-Sachs
disease or Gaucher disease.2 Lipid droplets are also a reservoir for
cholesterol and problems with lipid droplets could lead to issues with membrane
formation and maintenance. If there is not enough cholesterol in the lipid
bilayer there will not be enough stability in the membrane. It will be too
fluid without cholesterol and there would be little regulation of the
phospholipids.3 If temperatures are low, cholesterol will prevent
the membrane from becoming stiff. If there is not enough cholesterol when
temperatures are low, the passage of water molecules, ions and other molecules
into the bilayer that are necessary for cell function might be altered.4
On the contrary, if there is are too many lipid droplets and an accumulation of
cholesterol, arterial hardening, heart disease or even strokes can occur.1
During ER stress, lipids are needed to provide energy to accommodate for this
stress and if there are not enough lipids, the body will turn to break down
proteins in the blood. This will increase H concentration in the blood and
could possibly lead to acidosis.5 Droplet formation is also
important as lipid droplets have enzymes that are required to maintain ER
structure. Some of these enzymes are important in regulating membrane fusion
and connecting ER tubules.1

            Raft
domains are important part of membranes as they function in regulating
transport through membranes, cell signaling and many other functions. Researchers
found that ABCA1, ABCG1, and ABCG4 lipid transporters disrupt raft domains.
This can cause an efflux of cholesterol from the plasma membrane which will
disrupt membrane transport (especially endocytosis) and cellular signaling. When
cellular signaling is disrupted, there will be a decrease in the immune system
response. These transporters were also found to suppress inflammatory
responses, decrease platelet production and regulate t cell proliferation. Regulation
of t cell proliferation will help fight against infections but keep essential
cells from being destroyed. They have also been found to decrease cholera toxin
binding to GM1 which will prevent against the destruction of nerve cells. ABCA1
and ABCG4 also inhibit cell death of macrophages and remove excess cholesterol
in macrophages. It is essential to maintain macrophage composition so that they
can maintain normal function and fight off foreign molecules. ABCA1 is also found
to regulate cholesterol levels by removing it from non-domain rafts as well.
ABCA1 is also useful as it removes 7-ketocholesterol to prevent it from accumulating
and becoming toxic in the central nervous system. A decrease in sphingomyelin
levels might also mediate the role of ABCA1 and ABCG1 which could cause atherosclerosis.6

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