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amentoflavone like caffeine?

manny27

Newbie Brother
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someone PLEASE explain to me how amentoflavone is like caffeine? it causes "concentration-dependent increase in Ca2+" what the heck does that mean? lol someone speak my language please:p
 
Ca 2+ = positive calcium ion bros...but it's not exactly the way you're thinking....amentoflavone is kind of pushed as caffeine alternative to some degree...
 
Muscle cells need calcium to contract. The more calcium available to the muscle, the greater the potential force of the contraction.both caffeine n
amentoflavone help shuttle calcium to the muscles
 
here's all the info you need on it...



Amentoflavone

Mood/CNS effects

There are a whole host of studies examining the effects of Amentoflavone on various neurological endpoints. Without going into each one individually, research highlights will be presented.
Amentoflavone interacts with the GABA-A receptor by acting as a negative modulator. This would produce a central stimulant effect by inducing wakefulness/alertness. Amentoflavone uptake into the CNS is limited by P-glycoprotein, an efflux pump that pumps specific compounds back outside of the CNS. There are numerous ways to overcome the P-glycoprotein transporter; a very well-documented one is by consuming grapefruit or its constituents.
In addition, amentoflavone has demonstrated antidepressant and anxiolytic (anti-anxiety) effects in vivo by interacting with not only the GABA-A receptor, but also the serotonin and alpha-adrenergic receptors. In fact, of all the tested constituents of St. John’s Wort (a known antidepressant/anti-anxiety plant), amentoflavone displayed the strongest anxiolytic activity.

Summary: CNS stimulant, anxiolytic, anti-depressant




Fatty Acid Synthase Inhibition

Fatty acid synthase, as the name implies, is responsible for the endogenous synthesis of fatty acids in humans. It is currently a drug target for metabolic syndrome. In at least three separate trials, amentoflavone has demonstrated the ability to inhibit fatty acid synthase, and thus fat production.

Summary: Reduced fatty acid synthesis



Phosphodiesterase (PDE) Inhibition

PDE is the enzyme responsible for breaking down cAMP/cGMP. cAMP/cGMP promote smooth muscle relaxation (vasodilation; this is how PDE5 inhibitors help with erectile dysfunction) and lipolysis. Indeed, Forskolin has documented lipolytic activity by increasing cAMP levels via increased cAMP production. PDE inhibition, as with amentoflavone, hits the opposite side of the coin: reduced cAMP breakdown. By increasing cAMP levels, amentoflavone can synergize with adrenergic agonists (i.e. b-agonists) because second messenger pathways follow the rule of amplification.
Amentoflavone inhibits a broad array of PDE isoforms, and it is the most potent inhibitor out of all tested flavonoids in Ginkgo biloba. Further, of all tested constituents of Allanblackia monticola, Amentoflavone was the strongest vasodilator, inhibiting norepinephrine-induced vasoconstriction by a whopping 35%.
Summary: Increased lipolysis (fat loss) and increased vasodilation


Muscular Strength and Endurance

One well-documented mechanism of increasing exercise performance is vasodilation, which helps supply (oxygen; waste removal) meet the demand of exercising muscle tissue (hypoxia; metabolic waste accumulation). Amentoflavone has a well-documented effect on vasodilation as described above.
In addition to this, Amentoflavone provides a relatively unique mechanism for increasing power output: increased Ca2+ release from the sarcoplasmic reticulum. By increasing intracellular Ca2+ downstream of the signal for muscle contraction, binding to troponin-C is increased and the force of muscular contraction, on a cell-by-cell basis, also increases.
Caffeine acts via a similar mechanism to increase strength output, and researchers found that not only does Amentoflavone likely bind to the caffeine-binding site, but it does so with 20 times greater potency than caffeine.

Summary: Improved strength (Ca2+ release) and improved endurance (vasodilation)


Insulin Sensitivity/GDA - PTP1B inhibition

PTP1B is an enzyme involved in insulin signaling, and inhibition of PTP1B is being investigated as a possible treatment for obesity and diabetes. PTP1B inhibition will chiefly improve insulin sensitivity by augmenting insulin’s actions within the cell at a lower circulating level of insulin. This is a fairly novel approach to improving insulin sensitivity and will continue to be investigated.

Summary: Improved insulin sensitivity




Dyslipidemia

Amentoflavone has been shown in vivo to reduce circulating lipids (LDL/TG), making it of further benefit to obesity/diabetes/metabolic syndrome.

Summary: Reduced lipids
 
here's all the info you need on it...



Amentoflavone

Mood/CNS effects

There are a whole host of studies examining the effects of Amentoflavone on various neurological endpoints. Without going into each one individually, research highlights will be presented.
Amentoflavone interacts with the GABA-A receptor by acting as a negative modulator. This would produce a central stimulant effect by inducing wakefulness/alertness. Amentoflavone uptake into the CNS is limited by P-glycoprotein, an efflux pump that pumps specific compounds back outside of the CNS. There are numerous ways to overcome the P-glycoprotein transporter; a very well-documented one is by consuming grapefruit or its constituents.
In addition, amentoflavone has demonstrated antidepressant and anxiolytic (anti-anxiety) effects in vivo by interacting with not only the GABA-A receptor, but also the serotonin and alpha-adrenergic receptors. In fact, of all the tested constituents of St. John’s Wort (a known antidepressant/anti-anxiety plant), amentoflavone displayed the strongest anxiolytic activity.

Summary: CNS stimulant, anxiolytic, anti-depressant




Fatty Acid Synthase Inhibition

Fatty acid synthase, as the name implies, is responsible for the endogenous synthesis of fatty acids in humans. It is currently a drug target for metabolic syndrome. In at least three separate trials, amentoflavone has demonstrated the ability to inhibit fatty acid synthase, and thus fat production.

Summary: Reduced fatty acid synthesis



Phosphodiesterase (PDE) Inhibition

PDE is the enzyme responsible for breaking down cAMP/cGMP. cAMP/cGMP promote smooth muscle relaxation (vasodilation; this is how PDE5 inhibitors help with erectile dysfunction) and lipolysis. Indeed, Forskolin has documented lipolytic activity by increasing cAMP levels via increased cAMP production. PDE inhibition, as with amentoflavone, hits the opposite side of the coin: reduced cAMP breakdown. By increasing cAMP levels, amentoflavone can synergize with adrenergic agonists (i.e. b-agonists) because second messenger pathways follow the rule of amplification.
Amentoflavone inhibits a broad array of PDE isoforms, and it is the most potent inhibitor out of all tested flavonoids in Ginkgo biloba. Further, of all tested constituents of Allanblackia monticola, Amentoflavone was the strongest vasodilator, inhibiting norepinephrine-induced vasoconstriction by a whopping 35%.
Summary: Increased lipolysis (fat loss) and increased vasodilation


Muscular Strength and Endurance

One well-documented mechanism of increasing exercise performance is vasodilation, which helps supply (oxygen; waste removal) meet the demand of exercising muscle tissue (hypoxia; metabolic waste accumulation). Amentoflavone has a well-documented effect on vasodilation as described above.
In addition to this, Amentoflavone provides a relatively unique mechanism for increasing power output: increased Ca2+ release from the sarcoplasmic reticulum. By increasing intracellular Ca2+ downstream of the signal for muscle contraction, binding to troponin-C is increased and the force of muscular contraction, on a cell-by-cell basis, also increases.
Caffeine acts via a similar mechanism to increase strength output, and researchers found that not only does Amentoflavone likely bind to the caffeine-binding site, but it does so with 20 times greater potency than caffeine.

Summary: Improved strength (Ca2+ release) and improved endurance (vasodilation)


Insulin Sensitivity/GDA - PTP1B inhibition

PTP1B is an enzyme involved in insulin signaling, and inhibition of PTP1B is being investigated as a possible treatment for obesity and diabetes. PTP1B inhibition will chiefly improve insulin sensitivity by augmenting insulin’s actions within the cell at a lower circulating level of insulin. This is a fairly novel approach to improving insulin sensitivity and will continue to be investigated.

Summary: Improved insulin sensitivity




Dyslipidemia

Amentoflavone has been shown in vivo to reduce circulating lipids (LDL/TG), making it of further benefit to obesity/diabetes/metabolic syndrome.

Summary: Reduced lipids

Nice... Learned something new
 
here's all the info you need on it...



Amentoflavone

Mood/CNS effects

There are a whole host of studies examining the effects of Amentoflavone on various neurological endpoints. Without going into each one individually, research highlights will be presented.
Amentoflavone interacts with the GABA-A receptor by acting as a negative modulator. This would produce a central stimulant effect by inducing wakefulness/alertness. Amentoflavone uptake into the CNS is limited by P-glycoprotein, an efflux pump that pumps specific compounds back outside of the CNS. There are numerous ways to overcome the P-glycoprotein transporter; a very well-documented one is by consuming grapefruit or its constituents.
In addition, amentoflavone has demonstrated antidepressant and anxiolytic (anti-anxiety) effects in vivo by interacting with not only the GABA-A receptor, but also the serotonin and alpha-adrenergic receptors. In fact, of all the tested constituents of St. John’s Wort (a known antidepressant/anti-anxiety plant), amentoflavone displayed the strongest anxiolytic activity.

Summary: CNS stimulant, anxiolytic, anti-depressant




Fatty Acid Synthase Inhibition

Fatty acid synthase, as the name implies, is responsible for the endogenous synthesis of fatty acids in humans. It is currently a drug target for metabolic syndrome. In at least three separate trials, amentoflavone has demonstrated the ability to inhibit fatty acid synthase, and thus fat production.

Summary: Reduced fatty acid synthesis



Phosphodiesterase (PDE) Inhibition

PDE is the enzyme responsible for breaking down cAMP/cGMP. cAMP/cGMP promote smooth muscle relaxation (vasodilation; this is how PDE5 inhibitors help with erectile dysfunction) and lipolysis. Indeed, Forskolin has documented lipolytic activity by increasing cAMP levels via increased cAMP production. PDE inhibition, as with amentoflavone, hits the opposite side of the coin: reduced cAMP breakdown. By increasing cAMP levels, amentoflavone can synergize with adrenergic agonists (i.e. b-agonists) because second messenger pathways follow the rule of amplification.
Amentoflavone inhibits a broad array of PDE isoforms, and it is the most potent inhibitor out of all tested flavonoids in Ginkgo biloba. Further, of all tested constituents of Allanblackia monticola, Amentoflavone was the strongest vasodilator, inhibiting norepinephrine-induced vasoconstriction by a whopping 35%.
Summary: Increased lipolysis (fat loss) and increased vasodilation


Muscular Strength and Endurance

One well-documented mechanism of increasing exercise performance is vasodilation, which helps supply (oxygen; waste removal) meet the demand of exercising muscle tissue (hypoxia; metabolic waste accumulation). Amentoflavone has a well-documented effect on vasodilation as described above.
In addition to this, Amentoflavone provides a relatively unique mechanism for increasing power output: increased Ca2+ release from the sarcoplasmic reticulum. By increasing intracellular Ca2+ downstream of the signal for muscle contraction, binding to troponin-C is increased and the force of muscular contraction, on a cell-by-cell basis, also increases.
Caffeine acts via a similar mechanism to increase strength output, and researchers found that not only does Amentoflavone likely bind to the caffeine-binding site, but it does so with 20 times greater potency than caffeine.

Summary: Improved strength (Ca2+ release) and improved endurance (vasodilation)


Insulin Sensitivity/GDA - PTP1B inhibition

PTP1B is an enzyme involved in insulin signaling, and inhibition of PTP1B is being investigated as a possible treatment for obesity and diabetes. PTP1B inhibition will chiefly improve insulin sensitivity by augmenting insulin’s actions within the cell at a lower circulating level of insulin. This is a fairly novel approach to improving insulin sensitivity and will continue to be investigated.

Summary: Improved insulin sensitivity




Dyslipidemia

Amentoflavone has been shown in vivo to reduce circulating lipids (LDL/TG), making it of further benefit to obesity/diabetes/metabolic syndrome.

Summary: Reduced lipids

x2x2x2x

stick with this.
 
here's all the info you need on it...



Amentoflavone

Mood/CNS effects

There are a whole host of studies examining the effects of Amentoflavone on various neurological endpoints. Without going into each one individually, research highlights will be presented.
Amentoflavone interacts with the GABA-A receptor by acting as a negative modulator. This would produce a central stimulant effect by inducing wakefulness/alertness. Amentoflavone uptake into the CNS is limited by P-glycoprotein, an efflux pump that pumps specific compounds back outside of the CNS. There are numerous ways to overcome the P-glycoprotein transporter; a very well-documented one is by consuming grapefruit or its constituents.
In addition, amentoflavone has demonstrated antidepressant and anxiolytic (anti-anxiety) effects in vivo by interacting with not only the GABA-A receptor, but also the serotonin and alpha-adrenergic receptors. In fact, of all the tested constituents of St. John’s Wort (a known antidepressant/anti-anxiety plant), amentoflavone displayed the strongest anxiolytic activity.

Summary: CNS stimulant, anxiolytic, anti-depressant




Fatty Acid Synthase Inhibition

Fatty acid synthase, as the name implies, is responsible for the endogenous synthesis of fatty acids in humans. It is currently a drug target for metabolic syndrome. In at least three separate trials, amentoflavone has demonstrated the ability to inhibit fatty acid synthase, and thus fat production.

Summary: Reduced fatty acid synthesis



Phosphodiesterase (PDE) Inhibition

PDE is the enzyme responsible for breaking down cAMP/cGMP. cAMP/cGMP promote smooth muscle relaxation (vasodilation; this is how PDE5 inhibitors help with erectile dysfunction) and lipolysis. Indeed, Forskolin has documented lipolytic activity by increasing cAMP levels via increased cAMP production. PDE inhibition, as with amentoflavone, hits the opposite side of the coin: reduced cAMP breakdown. By increasing cAMP levels, amentoflavone can synergize with adrenergic agonists (i.e. b-agonists) because second messenger pathways follow the rule of amplification.
Amentoflavone inhibits a broad array of PDE isoforms, and it is the most potent inhibitor out of all tested flavonoids in Ginkgo biloba. Further, of all tested constituents of Allanblackia monticola, Amentoflavone was the strongest vasodilator, inhibiting norepinephrine-induced vasoconstriction by a whopping 35%.
Summary: Increased lipolysis (fat loss) and increased vasodilation


Muscular Strength and Endurance

One well-documented mechanism of increasing exercise performance is vasodilation, which helps supply (oxygen; waste removal) meet the demand of exercising muscle tissue (hypoxia; metabolic waste accumulation). Amentoflavone has a well-documented effect on vasodilation as described above.
In addition to this, Amentoflavone provides a relatively unique mechanism for increasing power output: increased Ca2+ release from the sarcoplasmic reticulum. By increasing intracellular Ca2+ downstream of the signal for muscle contraction, binding to troponin-C is increased and the force of muscular contraction, on a cell-by-cell basis, also increases.
Caffeine acts via a similar mechanism to increase strength output, and researchers found that not only does Amentoflavone likely bind to the caffeine-binding site, but it does so with 20 times greater potency than caffeine.

Summary: Improved strength (Ca2+ release) and improved endurance (vasodilation)


Insulin Sensitivity/GDA - PTP1B inhibition

PTP1B is an enzyme involved in insulin signaling, and inhibition of PTP1B is being investigated as a possible treatment for obesity and diabetes. PTP1B inhibition will chiefly improve insulin sensitivity by augmenting insulin’s actions within the cell at a lower circulating level of insulin. This is a fairly novel approach to improving insulin sensitivity and will continue to be investigated.

Summary: Improved insulin sensitivity




Dyslipidemia

Amentoflavone has been shown in vivo to reduce circulating lipids (LDL/TG), making it of further benefit to obesity/diabetes/metabolic syndrome.

Summary: Reduced lipids

and there you have it... Lol
 
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