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Has clen down-regulated your Beta receptors? By pass the receptors while activating thyroid hormones with cAMPHIBOLIC for synergymuscle.com.
FORSKOLIN FOR FAT LOSS
Normally when the body requires the use of stored fat for fuel, hormones such as epinephrine or norepinephrine bind to receptors on fat cells and initiate a signaling cascade that eventually results in the activation of an enzyme within the fat cell called hormone sensitive lipase (HSL). Fat is stored in the form of triglycerides, composed of fatty acid chains bound to a glycerol backbone. HSL frees up the fatty acids so they can leave the fat cell, enter the bloodstream, and travel to wherever they are needed for fuel, primarily working muscle.
Forskolin mimics the effects of the body's fat mobilizing hormones like epinephrine by entering fat cells and increasing levels of the enzyme adenylate cyclase, which in turn increases cyclic adenosine monophosphate (cAMP), an important compound involved in the signaling cascade described above. The increase in cAMP leads to activation of HSL, and fat is mobilized, ready to be used as fuel. Note as depicted in the illustration below that forskolin bypasses the hormonal receptor and enters the cell by traversing the cellular membrane. In the case of fat cells, epinephrine or a chemical analog of epinephrine such as clenbuterol or albuterol binds to these so-called beta adrenergic receptor sites and initiates the signaling cascade that ultimately results in fat release.
Prolonged use of these chemical agents however ultimately leads to a desensitization of the receptor, and a loss of drug effectiveness. With beta-receptors desensitization occurs primarily by a decrease in cell surface receptor number. This is important clinically because beta2 receptor agonists such as clenbuterol and albuterol are commonly used to treat asthma by binding to beta-receptors in lung tissue. They lead to the relaxation of bronchial smooth muscle and decrease airway resistance. Hence the widespread use of forskolin to treat airway constriction in allergies and asthma.
Note that since like beta agonists, forskolin too initiates the signaling cascade, but since it acts independently of beta receptors, even cells whose beta receptors have been severely downregulated by exposure to beta2 agonists are still responsive to forskolin (1). So a person who has been using clenbuterol or albuterol over an extended period might consider switching to a forskolin-based product, achieving the same net result of fat loss by bypassing the downregulated beta-receptors. Interestingly, beta2 receptors in tissue samples that had experienced this downregulation/desensitization (technically called tachyphylaxis) by continual exposure to salbutamol recovered sensitivity to the drug in vitro when exposed to forskolin (2) If this works in vivo it gives a person who wants to increase lipolysis several options for the combined or individual use of a beta agonist and forskolin.
FORSKOLIN AND THE THYROID
So far to summarize, we see that forskolin has the ability to activate Hormone Sensitive Lipase and release free fatty acids that can be used by the body for fuel. This lipolytic effect is obviously advantageous for a person seeking to lose fat. However, unless the fat mobilized by forskolin is actually burned for fuel, it will simply be redeposited as fat. One could obviously increase exercise levels to burn this mobilized fat, or go on a calorie restricted diet. These are certainly healthful approaches to weight loss, but forskolin itself can promote the burning of these liberated fats by virtue of its ability to elevate metabolic rate by stimulating the production of thyroid hormone.
Thyroid Stimulating Hormone, or TSH, is a hormone released by the pituitary gland that signals the thyroid gland to produce T4 and T3. Forskolin, when added to thyroid tissue in culture, mimics the effect of TSH and stimulates the production of thyroid hormone (3). Thyroid hormone is well known to increase metabolic rate by way of several mechanisms, and this increased metabolic rate will lead to the use of the mobilized fatty acids for fuel.
In addition to stimulating the secretion of primarily T4 from the thyroid, forskolin promotes the conversion of the relatively inactive T4 to its potent metabolite T3 via the action of type II deiodinase. Forskolin has been shown to induce the expression of type II deiodinase in peripheral tissue, especially skeletal muscle (4)
Thyroid hormone has been shown to be helpful in treating depressive disorders. Also, several studies have shown that patients suffering from depression have reduced levels of activity of cAMP signaling in the brain. (4) Forskolin administration to depressed and schizophrenic patients has resulted in marked improvement in symptoms in these subjects (5). On the other hand, enhanced cAMP signaling in bipolar patients may contribute to manic episodes (6). So while possibly benefiting people suffering from depression, forskolin could exacerbate the symptoms of bipolar disorder. One should obviously consult with a medical professional here before self-medicating with forskolin.
FORSKOLIN FOR FAT LOSS
Normally when the body requires the use of stored fat for fuel, hormones such as epinephrine or norepinephrine bind to receptors on fat cells and initiate a signaling cascade that eventually results in the activation of an enzyme within the fat cell called hormone sensitive lipase (HSL). Fat is stored in the form of triglycerides, composed of fatty acid chains bound to a glycerol backbone. HSL frees up the fatty acids so they can leave the fat cell, enter the bloodstream, and travel to wherever they are needed for fuel, primarily working muscle.
Forskolin mimics the effects of the body's fat mobilizing hormones like epinephrine by entering fat cells and increasing levels of the enzyme adenylate cyclase, which in turn increases cyclic adenosine monophosphate (cAMP), an important compound involved in the signaling cascade described above. The increase in cAMP leads to activation of HSL, and fat is mobilized, ready to be used as fuel. Note as depicted in the illustration below that forskolin bypasses the hormonal receptor and enters the cell by traversing the cellular membrane. In the case of fat cells, epinephrine or a chemical analog of epinephrine such as clenbuterol or albuterol binds to these so-called beta adrenergic receptor sites and initiates the signaling cascade that ultimately results in fat release.
Prolonged use of these chemical agents however ultimately leads to a desensitization of the receptor, and a loss of drug effectiveness. With beta-receptors desensitization occurs primarily by a decrease in cell surface receptor number. This is important clinically because beta2 receptor agonists such as clenbuterol and albuterol are commonly used to treat asthma by binding to beta-receptors in lung tissue. They lead to the relaxation of bronchial smooth muscle and decrease airway resistance. Hence the widespread use of forskolin to treat airway constriction in allergies and asthma.
Note that since like beta agonists, forskolin too initiates the signaling cascade, but since it acts independently of beta receptors, even cells whose beta receptors have been severely downregulated by exposure to beta2 agonists are still responsive to forskolin (1). So a person who has been using clenbuterol or albuterol over an extended period might consider switching to a forskolin-based product, achieving the same net result of fat loss by bypassing the downregulated beta-receptors. Interestingly, beta2 receptors in tissue samples that had experienced this downregulation/desensitization (technically called tachyphylaxis) by continual exposure to salbutamol recovered sensitivity to the drug in vitro when exposed to forskolin (2) If this works in vivo it gives a person who wants to increase lipolysis several options for the combined or individual use of a beta agonist and forskolin.
FORSKOLIN AND THE THYROID
So far to summarize, we see that forskolin has the ability to activate Hormone Sensitive Lipase and release free fatty acids that can be used by the body for fuel. This lipolytic effect is obviously advantageous for a person seeking to lose fat. However, unless the fat mobilized by forskolin is actually burned for fuel, it will simply be redeposited as fat. One could obviously increase exercise levels to burn this mobilized fat, or go on a calorie restricted diet. These are certainly healthful approaches to weight loss, but forskolin itself can promote the burning of these liberated fats by virtue of its ability to elevate metabolic rate by stimulating the production of thyroid hormone.
Thyroid Stimulating Hormone, or TSH, is a hormone released by the pituitary gland that signals the thyroid gland to produce T4 and T3. Forskolin, when added to thyroid tissue in culture, mimics the effect of TSH and stimulates the production of thyroid hormone (3). Thyroid hormone is well known to increase metabolic rate by way of several mechanisms, and this increased metabolic rate will lead to the use of the mobilized fatty acids for fuel.
In addition to stimulating the secretion of primarily T4 from the thyroid, forskolin promotes the conversion of the relatively inactive T4 to its potent metabolite T3 via the action of type II deiodinase. Forskolin has been shown to induce the expression of type II deiodinase in peripheral tissue, especially skeletal muscle (4)
Thyroid hormone has been shown to be helpful in treating depressive disorders. Also, several studies have shown that patients suffering from depression have reduced levels of activity of cAMP signaling in the brain. (4) Forskolin administration to depressed and schizophrenic patients has resulted in marked improvement in symptoms in these subjects (5). On the other hand, enhanced cAMP signaling in bipolar patients may contribute to manic episodes (6). So while possibly benefiting people suffering from depression, forskolin could exacerbate the symptoms of bipolar disorder. One should obviously consult with a medical professional here before self-medicating with forskolin.