21.) According to the discussion, does PPAR activation lead only to increased fa

Question

21.) According to the discussion, does PPAR activation lead only to increased fatty acid oxidation, or is there also a reduction in glucose catabolism as well? Justify your answer.

DISCUSSION In endurance sport competitions such cycling, marathon runs, race walking, and cross-country skiing, "hitting the wall' is a dra- matic demonstration of sudden and complete exhaustion. It is thought to be due to the depletion of liver and muscle glycogen and can be averted by training that promotes mitochondrial biogenesis, increased type I fibers, and enhanced FA burning.

Explanation / Answer

Ans 19): The drug GW has not promoted changes in muscle subtype or biogenesis (increased number) of mitochondria unlike the changes in endurance sport athletes

Explanation: The drug GW-501,516, GW1516, GSK-516, or commonly called as Cardarine or Endurobol synthesized in 1990 is a PPAR-delta receptor agonist (GW binds to PPAR-delta receptor and promotes fatty acid consumption) which changes the body fuel preference to fatty acids than the glucose. When glucose levels depletes (to 70mg/deci liter) in long endurance sport the metabolism shifts to fatty acid consumption as fuel rather than glucose or glycogen consumption (it protects the brain because its sole source of energy is glucose). In athletes involved in long endurance sports/activity PPAR-delta naturally gets expressed and helps them in consuming fatty acid rather than glucose for their long endurance activity, hence they can remain psychologically active. This is a natural mechanism of the body, But GW drug can make this happen without involving in long endurance sport. However this drug found to induce cancer, hence banned now.

What is PPAR-delta: Peroxisome proliferator-activated receptor delta or also called as NR1C2 expression leads to proliferation of peroxisome which in turn leads to increased catabolism of long chain fatty acids and branched chain fatty acids

Ans 21.): From the discussion PPAR activation lead to increased fatty acid oxidation and reduction in glucose catabolism. PPAR upregulated many fatty acid metabolizing genes and mitochondrial activity genes for increased mitochondrial function without increasing the number of mitochondria. It upregulated antioxidant and glutathione synthesis genes to protect from increased mitochondrial activity and free radical formation. It down regulated most of the glycolytic pathway and reduced glucose catabolism (preserving glucose for brain functio) genes but upregulated gluconeogenesis pathway in muscle cells (aiding in maintaining glucose levels above 70mg/deci liter for proper brain function). Overall PPAR found to be a master regulator of many catabolic genes.

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