Triacylglycerol Metabolism In Adipocytes

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chylomicrons and VLDL are progressively degrades

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in the CAPILLARY BEDS of tissues such as muscles and adipose tissue, through the triacylglycerol hydrolyzing enzyme lipoprotein lipase. This process is facillitated by APOC2 from circulating HDL.

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The fatty acids released

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can either travel along with serum albumin or be taken up by the cells at the site of lipolysis.

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In the fed state

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chylomicrons and VLDL are a source of fatty acids for adipocyte triglyceride synthesis.

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AFter be taken up by adipocytes, the free fatty acids are acivated to fatty acyl CoA and

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they then synthesize triglycerides in a similar manner as the liver.

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Adipocytes do not express glycerol kinase

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so all the glycerol-3-phosphate comes from DHAP dihydroxyacetonephosphate from glycolysis.

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Fasted State

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FA are mobilized from adipocyte triglyceride droplets through the action of HORMONE SENSITIVE LIPASE. Lipolysis is a hallmark feature of the fasted state.

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Activating hormones of HSL.

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are epi-activity, glucagon----starvation, ACTH---stress

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low insulin to glucagon ratio

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leads to the activation of adenylate cyclase in the adipocyte increasing cAMP

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cAMP----to PKA-----phosphoryaltes and activates

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HSL

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HSL

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hydrolyzes fatty acids from triacylglycerols and diacylglycerols.

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the new free fatty acids hydrolyzed by HSL

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are transported bound to serum albumin to various tissues for use via B-oxidation to yield ATP in muslce and ketones bodies in the liver.

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The glycerol released during lypolysis

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can be converted to glucose in the liver after phosph. by glycerol kinase.

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HSL

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is down regulated by INSULIN by lowering cAMP levels and activating a lipase phosphatase. INhibts adenylate cyclase