Berberiini auttaa

Berberiini on luontaistuote, jota myydään tabletteina apteekissa, luontaistuotekaupoissa ja muuallakin, esim. Tarjoustalossa. Itse ostin kokeeksi pienen pakkauksen (60 tbl 20 euroa) apteekista ja sen jälkeen isot pakkaukset Tarjoustalosta (120 tbl 25 euroa).

Berberiiniä otetaan 1-3 tbl päivässä ja se tasoittaa verensokereita ja rasva-arvoja. Se sopii reseptilääkkeidenkin kanssa käytettäväksi. Se ei ole laihdutuslääke, mutta minulla sen vaikutus on ollut tosi positiivinen. Syön 2 tablettia päivässä ja kaksi ekaa viikkoa oli aina nälkä jo tunti ennen ateriaa ja sitten tuo oire katosi ja ylimääräiset ahmimiskohtauksetkin muuttuivat päivittäisistä enintään kerran viikossa iskeviksi. Ja kun alan ahmia, pystyn jopa lopettamaan kesken ennen kuin ruoka loppuu. Selkeä muutos :)

Mitä enemmän insuliinia, sitä matalampi verensokeri ja isompi nälkä. Insuliini auttaa sokerin verestä käyttöön sinne, missä sitä tarvitaan. Insuliini ei siis vähennä nälkää.

Berberiini ei voi salvata lihasten kasvua, sillä silloin sen pitäisi estää lihaksia saamasta ravintoa verestä. Kerrot berberiinin laskeneen verensokeriasi eli toimineen insuliinin tavoin, joten miksi lihasten kohdalla tuo sokerin siirtäminen sinne missä sitä tarvitaan ei toimisikaan? Minne se sokeri katosi verestäsi? Vai tarkoitatko hypolla jotain muuta kuin verensokerin laskua alle normaaliarvojen?

kypsätäti kirjoitti:

Mitä enemmän insuliinia, sitä matalampi verensokeri ja isompi nälkä. Insuliini auttaa sokerin verestä käyttöön sinne, missä sitä tarvitaan. Insuliini ei siis vähennä nälkää.

Berberiini ei voi salvata lihasten kasvua, sillä silloin sen pitäisi estää lihaksia saamasta ravintoa verestä. Kerrot berberiinin laskeneen verensokeriasi eli toimineen insuliinin tavoin, joten miksi lihasten kohdalla tuo sokerin siirtäminen sinne missä sitä tarvitaan ei toimisikaan? Minne se sokeri katosi verestäsi? Vai tarkoitatko hypolla jotain muuta kuin verensokerin laskua alle normaaliarvojen?

Lue lisää

Se että insuliini kasvattaa nälkää terveillä ei pidä paikkansa ollenkaan.
Voit itse kokeilla vaikka heralla, joka on hyvin insuliinigeeninen.
Oletan ettet siis ole insuliinille resitentti tai tyypin 2 diabeetikko.
Ja tuohon lihaskasvuun:Berberine impairs muscle metabolism by two novel mechanisms. It impairs mitochonidrial function stimulating the expression of atrogin-1 without affecting phosphorylation of forkhead transcription factors. The increase in atrogin-1 not only stimulated protein degradation but also suppressed protein synthesis, causing muscle atrophy. There is evidence that an herbal compound, berberine, improves insulin-mediated glucose metabolism and enhances insulin sensitivity in mice (1–3). For example, Lee et al. (1) reported that administering berberine to insulin-resistant db/db mice led to a decrease in body fat and significant improvement in glucose tolerance. Because catabolic conditions associated with insulin resistance can lead to progressive muscle atrophy, we examined whether berberine improves muscle protein metabolism. This was of interest because successful inhibition of mechanisms causing loss of muscle mass in diabetic mice might be extended to other catabolic conditions that cause muscle atrophy (4–8). However, we found that berberine actually promoted muscle atrophy in both wild-type and db/db mice. This led us to examine potential mechanisms causing berberine-induced muscle atrophy.

Muscle atrophy induced by several catabolic conditions (e.g., cancer, cachexia, diabetes, chronic kidney disease, cardiac failure, sepsis) share a common group of biochemical and transcriptional adaptations (7–12). In atrophying muscles, there is a higher level of expression of the E3 ubiquitin ligase, atrogin-1/MAFbx, which has been closely linked to stimulation of muscle protein degradation by the ubiquitin-proteasome system (UPS) (13–17). The mechanism that increases atrogin-1 expression has been linked to defects in insulin/IGF-1 signaling, specifically, suppression of insulin receptor substrate (IRS)-1–associated phosphatidylinositol 3-kinase (PI3K) activity and a reduction in p-Akt (14–16). The decrease in p-Akt, in turn, reduces phosphorylation of the forkhead transcription factors (FoxOs) that can enter the nucleus to stimulate atrogin-1 expression. The focus on atrogin-1 in conditions stimulating muscle atrophy arises because atrogin-1 expression causes a proportional increase in muscle protein degradation (17).

Besides accelerated protein degradation causing muscle atrophy, a decrease in protein synthesis will cause loss of muscle protein. Mechanisms changing protein synthesis include impaired insulin/IGF-1 signaling, reducing PI3K and p-Akt activities (9). Another mechanism that can impair muscle protein synthesis was recently reported by Gwinn et al. (18). They found that a rise in p–AMP-activated protein kinase (AMPK) inhibits the activity of the mTOR complex I (TORC1). The mechanism for this response involved phosphorylation of raptor, a regulatory protein that is associated with mTOR. A third mechanism that could impair muscle protein synthesis is suggested by the recent report of Lagirand-Cantaloube et al. (19). They found that atrogin-1 will conjugate ubiquitin to eIF-3f, an essential factor regulating protein translation. Since atrogin-1 is exclusively expressed in muscle, it is possible that activation of atrogin-1 could reduce protein synthesis by stimulating eIF-3f degradation by the UPS. If this were the case, changes in protein degradation could be linked to changes in protein synthesis.

We evaluated how berberine-induced mechanisms would cause muscle atrophy in normal and db/db diabetic mice. Specifically, we measured changes in muscle protein turnover and evaluated the influence of atrogin-1 on these processes. We also evaluated the influence of mitochondria in berberine-induced muscle atrophy, because Turner et al. (2) reported that treating cultured muscle cells with berberine led to impaired mitochondrial function. We found that berberine increased p-AMPK in muscle. Therefore, we examined stimulation of mitochondrial function with peroxisome proliferator–activated receptor (PPAR) γ coactivator (PGC)-1α to determine whether it would correct abnormalities in muscle protein turnover.

http://diabetes.diabetesjournals.org/content/59/8/1879.full

tutkinut kirjoitti:

Se että insuliini kasvattaa nälkää terveillä ei pidä paikkansa ollenkaan.
Voit itse kokeilla vaikka heralla, joka on hyvin insuliinigeeninen.
Oletan ettet siis ole insuliinille resitentti tai tyypin 2 diabeetikko.
Ja tuohon lihaskasvuun:Berberine impairs muscle metabolism by two novel mechanisms. It impairs mitochonidrial function stimulating the expression of atrogin-1 without affecting phosphorylation of forkhead transcription factors. The increase in atrogin-1 not only stimulated protein degradation but also suppressed protein synthesis, causing muscle atrophy. There is evidence that an herbal compound, berberine, improves insulin-mediated glucose metabolism and enhances insulin sensitivity in mice (1–3). For example, Lee et al. (1) reported that administering berberine to insulin-resistant db/db mice led to a decrease in body fat and significant improvement in glucose tolerance. Because catabolic conditions associated with insulin resistance can lead to progressive muscle atrophy, we examined whether berberine improves muscle protein metabolism. This was of interest because successful inhibition of mechanisms causing loss of muscle mass in diabetic mice might be extended to other catabolic conditions that cause muscle atrophy (4–8). However, we found that berberine actually promoted muscle atrophy in both wild-type and db/db mice. This led us to examine potential mechanisms causing berberine-induced muscle atrophy.

Muscle atrophy induced by several catabolic conditions (e.g., cancer, cachexia, diabetes, chronic kidney disease, cardiac failure, sepsis) share a common group of biochemical and transcriptional adaptations (7–12). In atrophying muscles, there is a higher level of expression of the E3 ubiquitin ligase, atrogin-1/MAFbx, which has been closely linked to stimulation of muscle protein degradation by the ubiquitin-proteasome system (UPS) (13–17). The mechanism that increases atrogin-1 expression has been linked to defects in insulin/IGF-1 signaling, specifically, suppression of insulin receptor substrate (IRS)-1–associated phosphatidylinositol 3-kinase (PI3K) activity and a reduction in p-Akt (14–16). The decrease in p-Akt, in turn, reduces phosphorylation of the forkhead transcription factors (FoxOs) that can enter the nucleus to stimulate atrogin-1 expression. The focus on atrogin-1 in conditions stimulating muscle atrophy arises because atrogin-1 expression causes a proportional increase in muscle protein degradation (17).

Besides accelerated protein degradation causing muscle atrophy, a decrease in protein synthesis will cause loss of muscle protein. Mechanisms changing protein synthesis include impaired insulin/IGF-1 signaling, reducing PI3K and p-Akt activities (9). Another mechanism that can impair muscle protein synthesis was recently reported by Gwinn et al. (18). They found that a rise in p–AMP-activated protein kinase (AMPK) inhibits the activity of the mTOR complex I (TORC1). The mechanism for this response involved phosphorylation of raptor, a regulatory protein that is associated with mTOR. A third mechanism that could impair muscle protein synthesis is suggested by the recent report of Lagirand-Cantaloube et al. (19). They found that atrogin-1 will conjugate ubiquitin to eIF-3f, an essential factor regulating protein translation. Since atrogin-1 is exclusively expressed in muscle, it is possible that activation of atrogin-1 could reduce protein synthesis by stimulating eIF-3f degradation by the UPS. If this were the case, changes in protein degradation could be linked to changes in protein synthesis.

We evaluated how berberine-induced mechanisms would cause muscle atrophy in normal and db/db diabetic mice. Specifically, we measured changes in muscle protein turnover and evaluated the influence of atrogin-1 on these processes. We also evaluated the influence of mitochondria in berberine-induced muscle atrophy, because Turner et al. (2) reported that treating cultured muscle cells with berberine led to impaired mitochondrial function. We found that berberine increased p-AMPK in muscle. Therefore, we examined stimulation of mitochondrial function with peroxisome proliferator–activated receptor (PPAR) γ coactivator (PGC)-1α to determine whether it would correct abnormalities in muscle protein turnover.

http://diabetes.diabetesjournals.org/content/59/8/1879.full

Lue lisää

Ihmisillä ole todettu lihaskatoa berberiinistä. Sen sijaan ihmisillä on todettu rasvan katoamista elimistöstä sekä verensokerin, rasva-arvojen ja maksa-arvojen paranemista. Syön nyt kuudetta kuukautta lääkärin valvonnassa berberiiniä ja verikokeitten tulokset ovat parantuneet, rasvaa on poistunut ja lihasvoimatkin kasvaneet, kun painon pudottua jaksaa liikkua enemmän. Ja se paras vaikutus on ollut ahmintakohtausten merkittävä väheneminen ja siksi minusta berberiiniä kannattaa kokeilla, jos BED on ongelma.

Mainitsemassasi tutkimuksessa hiiriin pistettiin ruiskulla berberiiniä ja vastakkaisia tutkimustuloksia löytyy: Muscle atrophy is a characteristic of chronic diseases including diabetes. Surprisingly, berberine was reported to promote muscle atrophy in both wild-type and db/db mice through hampering mitochondrial function and stimulating the expression of atrogin-1, which promoted protein degradation and suppressed protein synthesis67. However, in another study, berberine improved muscle atrophy, increased glycogen storage and decreased triglycerides content in skeletal muscle of type 2 diabetic rats. Further experiments revealed that reduced expression of CDK9 and cyclin T1 in the muscle was reversed with berberine68. Berberine also increased PPARa/d expression and reduced PPARg expression in skeletal muscle similar as rosiglitazone or fenofibrate69. The controversial data may be due to diverse methods of administration. Muscle atrophy was induced by berberine injection. Oral administration of berberine led to improvement of muscle atrophy. The actual effects of berberine remain to be explored.

http://www.sciencedirect.com/science/article/pii/S2211383512000871

kypsätäti kirjoitti:

Ihmisillä ole todettu lihaskatoa berberiinistä. Sen sijaan ihmisillä on todettu rasvan katoamista elimistöstä sekä verensokerin, rasva-arvojen ja maksa-arvojen paranemista. Syön nyt kuudetta kuukautta lääkärin valvonnassa berberiiniä ja verikokeitten tulokset ovat parantuneet, rasvaa on poistunut ja lihasvoimatkin kasvaneet, kun painon pudottua jaksaa liikkua enemmän. Ja se paras vaikutus on ollut ahmintakohtausten merkittävä väheneminen ja siksi minusta berberiiniä kannattaa kokeilla, jos BED on ongelma.

Mainitsemassasi tutkimuksessa hiiriin pistettiin ruiskulla berberiiniä ja vastakkaisia tutkimustuloksia löytyy: Muscle atrophy is a characteristic of chronic diseases including diabetes. Surprisingly, berberine was reported to promote muscle atrophy in both wild-type and db/db mice through hampering mitochondrial function and stimulating the expression of atrogin-1, which promoted protein degradation and suppressed protein synthesis67. However, in another study, berberine improved muscle atrophy, increased glycogen storage and decreased triglycerides content in skeletal muscle of type 2 diabetic rats. Further experiments revealed that reduced expression of CDK9 and cyclin T1 in the muscle was reversed with berberine68. Berberine also increased PPARa/d expression and reduced PPARg expression in skeletal muscle similar as rosiglitazone or fenofibrate69. The controversial data may be due to diverse methods of administration. Muscle atrophy was induced by berberine injection. Oral administration of berberine led to improvement of muscle atrophy. The actual effects of berberine remain to be explored.

http://www.sciencedirect.com/science/article/pii/S2211383512000871

Lue lisää

Itselle ei sopinut ollenkaan, koska erään taudin takia olen insuliinille erittäin herkkä. Itsellä kävi päin vastoin kun lopetin berberiinin käytön.
Voimat kasvoivat, jaksaminen parani ja ummetus loppui.
Berberiiniä käyttäessä keho yritti minulla kovasti ketoosiin, koska se työnsi verensokerin soluihin niin voimakkaasti. Saman efektin saan rasvattomilla
maitotuotteilla, currylla, kanelilla tai syömällä pelkkää sian lihaa sisältävän aterian.