Kmara
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Hi, I'm new to this forum and have just started reviewing Bioch, trying to focus on clinical aspects. Please help me clarify my q:
Why TAG synthesis in adipose tissue of alcoholics isn't increased whereas liver produces TAG in excess?
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| skylark
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TAG synthesis in asipose is not at all important in humans. The liver does the job.
So whenever the need for TAG, the liver produces them. In alcoholics the energy is more than sufficent to drive this process even though other pathways are turned down. Unless you starve a person for a long period of time, you won't get to demonstrate any TAG production in the fat cells.
That's what i remember. But I have to review all these things again as well..... hope this helps you though 
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| Kmara
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Thanks a lot skylark. Actually the other day I was reviewing the mechanisms of fatty liver formation in chronic alcoholics and since increased TAG synthesis in hepatocytes, along with impairment of VLDL release from them, is one of the main reasons for that I thought to myself what happens with TAG synthesis in adipocytes, just to contrast and compare to consolidate my reviewing.
Here is what I came to: Alcohol increases NADH which leads to greater conversion of DHAP to glycerol phosphate in liver, but the same pathway to produce TAGs is used by fat cells.(Lippincott’s Illustrated Review). Increased NADH production also prevents gluconeogenesis by shunting pyruvate and OAA to lactate and malate leading to a low-energy state and thus a high glucagon/insulin ratio. Since glucose level is low and also adipocytes need insulin to get glucose, insignificant amount of DHAP is available to be converted into glycerol phosphate. Moreover increased glucagon level causes releasing of free FAs from fat cells and high NADH halts their oxidation. So liver gets reachly supplied with FAs and glycerol phosphate – building blocks for TAGs synthesis.
Please correct me if my reasoning is wrong. And I guess my initial question wasn’t worded quite appropriately.
Best regards
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