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Excidium28
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Estrogen and Lipolysis
The female hormone estrogen may have a positive effect on resting and exercise fat metabolism. Although there appears to be a connection between estrogen and increased fat metabolism, the mechanisms are not fully understood. Research has also suggested that estrogen may aid in the mobilization of fat from adipose tissue. Although the mechanisms, again, are not fully understood, several theories have been proposed.
Estrogen has been found to inhibit the hormone LPL (Ashley, Kramer, and Bishop 2000). Remember that LPL is responsible for the breakdown of TG in the bloodstream and storing them in adipose tissue whenever they are not needed as fuel for active tissues. Estrogen has also been shown to enhance epinephrine production. A higher concentration of epinephrine increases the activity of HSL, the hormone responsible for adipose tissue lipolysis.
Estrogen has also been reported to stimulate the production of growth hormone (GH). Growth hormone inhibits the uptake of glucose (carbohydrate) by active tissues and increases the mobilization of FFA from adipose tissue. GH works by inhibiting insulin production from the pancreas and stimulating HSL (Ashley, Kramer, and Bishop 2000). Insulin is the main hormone that promotes glucose transport into muscle cells to be used as energy, and it is a potent inhibitor of HSL. Estrogen may enhance fat metabolism by increasing the production of GH and inhibiting the production of insulin. In turn, this would decrease glucose metabolism and increase FFA utilization (Ashley, Kramer, and Bishop 2000).
Another factor that could promote a higher fat metabolism in women is an increase in blood flow to adipose tissue, especially during exercise (Braun and Horton 2001). Estrogen has been shown to cause a vasodilation (widening) in blood vessels, but it is not known if this vasodilation is specific to adipose tissue perfusion (flow of blood into the tissue) or a general effect on the entire vasculature in the body. Estrogen also increases the production of the hormone nitric oxide (NO). NO, which is produced by cells that line the blood vessels, causes a relaxation of the smooth muscle that surrounds blood vessels, leading to vasodilation. If women maintained a higher blood flow to the adipose tissue, interaction between epinephrine and adipose tissue beta receptors would be increased. Additionally, this could enhance FFA transport from adipose tissue to active muscles during exercise.
The female hormone estrogen may have a positive effect on resting and exercise fat metabolism. Although there appears to be a connection between estrogen and increased fat metabolism, the mechanisms are not fully understood. Research has also suggested that estrogen may aid in the mobilization of fat from adipose tissue. Although the mechanisms, again, are not fully understood, several theories have been proposed.
Estrogen has been found to inhibit the hormone LPL (Ashley, Kramer, and Bishop 2000). Remember that LPL is responsible for the breakdown of TG in the bloodstream and storing them in adipose tissue whenever they are not needed as fuel for active tissues. Estrogen has also been shown to enhance epinephrine production. A higher concentration of epinephrine increases the activity of HSL, the hormone responsible for adipose tissue lipolysis.
Estrogen has also been reported to stimulate the production of growth hormone (GH). Growth hormone inhibits the uptake of glucose (carbohydrate) by active tissues and increases the mobilization of FFA from adipose tissue. GH works by inhibiting insulin production from the pancreas and stimulating HSL (Ashley, Kramer, and Bishop 2000). Insulin is the main hormone that promotes glucose transport into muscle cells to be used as energy, and it is a potent inhibitor of HSL. Estrogen may enhance fat metabolism by increasing the production of GH and inhibiting the production of insulin. In turn, this would decrease glucose metabolism and increase FFA utilization (Ashley, Kramer, and Bishop 2000).
Another factor that could promote a higher fat metabolism in women is an increase in blood flow to adipose tissue, especially during exercise (Braun and Horton 2001). Estrogen has been shown to cause a vasodilation (widening) in blood vessels, but it is not known if this vasodilation is specific to adipose tissue perfusion (flow of blood into the tissue) or a general effect on the entire vasculature in the body. Estrogen also increases the production of the hormone nitric oxide (NO). NO, which is produced by cells that line the blood vessels, causes a relaxation of the smooth muscle that surrounds blood vessels, leading to vasodilation. If women maintained a higher blood flow to the adipose tissue, interaction between epinephrine and adipose tissue beta receptors would be increased. Additionally, this could enhance FFA transport from adipose tissue to active muscles during exercise.
