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Triglyceride uptake into tissue

Increased synthesis of lipid or uptake. Increased synthesis of lipid may be the cause of fatty liver after hydrazine administration as this compound increases the activity of the enzyme involved in the synthesis of diglycerides. Hydrazine also depletes ATP and, however, inhibits protein synthesis. Large doses of ethanol will cause fatty liver in humans, and it is believed that this is partly due to an increase in fatty acid synthesis. This is a result of an increase in the NADH/NAD"1" ratio and therefore of the synthesis of triglycerides. Changes in the mobilization of lipids in tissues followed by uptake into the liver can also be another cause of steatosis. [Pg.225]

Metformin is the only biguanide available in the United States. It enhances insulin sensitivity of both hepatic and peripheral (muscle) tissues. This allows for increased uptake of glucose into these insulin-sensitive tissues. Metformin consistently reduces A1C levels by 1.5% to 2%, FPG levels by 60 to 80 mg/dL, and retains the ability to reduce FPG levels when they are very high (>300 mg/dL). It reduces plasma triglycerides and low-density lipoprotein (LDL) cholesterol by 8% to 15% and modestly increases high-density lipoprotein (HDL) cholesterol (2%). It does not induce hypoglycemia when used alone. [Pg.231]

Lipase Inhibitor Orlistat (Xenical, Roche) is prescribed for the treatment of obesity. It inhibits the gastrointestinal lipase enzymes by binding to the lipase through the serine site and inactivates the enzyme. Fat in the form of triglycerides cannot be hydrolyzed by the lipase and converted to free fatty acids and monoglycerides. Thus, there is no uptake of fat molecules into the cell tissue. [Pg.36]

The LDL particle (10% triglyceride content) is finally taken up into the liver and other tissues by the LDL receptor. The LDL receptor is a six-domain transmembrane protein whose synthesis is under negative feedback regulation, such that when intracellular cholesterol levels are raised, new LDL receptors are not formed, thereby preventing the uptake of further cholesterol from plasma LDL. LDL also inhibits HMG-CoA reductase and hence cholesterol synthesis by negative feedback inhibition. Absence of the LDL receptor leads to hypercholesterol-aemia and atherosclerosis, as there is a decrease in the rate at which LDLs are removed from the plasma. [Pg.37]


See other pages where Triglyceride uptake into tissue is mentioned: [Pg.885]    [Pg.395]    [Pg.383]    [Pg.396]    [Pg.152]    [Pg.153]    [Pg.131]    [Pg.19]    [Pg.494]    [Pg.137]    [Pg.133]    [Pg.500]    [Pg.494]    [Pg.383]    [Pg.313]    [Pg.2]    [Pg.28]    [Pg.166]    [Pg.158]    [Pg.232]    [Pg.702]    [Pg.304]    [Pg.352]    [Pg.739]    [Pg.185]    [Pg.184]    [Pg.169]    [Pg.50]    [Pg.58]    [Pg.88]    [Pg.91]    [Pg.150]    [Pg.519]    [Pg.18]    [Pg.185]    [Pg.64]    [Pg.177]    [Pg.68]    [Pg.363]    [Pg.42]   
See also in sourсe #XX -- [ Pg.368 , Pg.381 ]




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Tissue uptake

Triglycerides, tissue uptake

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