Berberine Prolongs Life Span and Stimulates Locomotor Activity of &amp;lt;i&amp;gt;Drosophila melanogaster&amp;lt;/i&amp;gt;

Navrotskaya, Valeriya; Oxenkrug, Gregory F.; Vorobyova, Lyudmila; Summergrad, Paul

doi:10.4236/ajps.2012.327123

Cited by 28 publications

(18 citation statements)

References 35 publications

(22 reference statements)

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“…Berberine improves IR in diabetic hamsters [106] and diabetic patients [107,108]. It is noteworthy that both berberine and minocycline prolonged life span and improved health span in Drosophila model [109,110]. Consistent with our hypothesis is observation that vitamin B6 supplementation dose-dependently decreased insulin levels and improved IR in KK-A(y) mice, an animal model of obese, type 2 diabetes [111,112].…”

Section: Other Conditions Associated With Insulin Resistancesupporting

confidence: 66%

Insulin Resistance and Dysregulation of Tryptophan–Kynurenine and Kynurenine–Nicotinamide Adenine Dinucleotide Metabolic Pathways

2013

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Insulin resistance (IR) underlines aging and aging-associated medical (diabetes, obesity, dyslipidemia, hypertension) and psychiatric (depression, cognitive decline) disorders (AAMPD). Molecular mechanisms of IR in genetically or metabolically predisposed individuals remain uncertain. Current review of literature and our data presents the evidences that dysregulation of tryptophan (TRP) – kynurenine (KYN) and KYN – nicotinamide adenine dinucleotide (NAD) metabolic pathways is one of the mechanisms of IR. First and rate-limiting step of TRP – KYN pathway is regulated by enzymes inducible by pro-inflammatory factors and/or stress hormones. The key enzymes of KYN – NAD pathway require pyridoxal-5-phosphate (P5P), an active form of vitamin B6, as a co-factor. Deficiency of P5P diverts KYN – NAD metabolism from production of NAD to the excessive formation of xanthurenic acid (XA). Human and experimental studies suggested that XA and some other KYN metabolites might impair production, release and biological activity of insulin. We propose that one of the mechanisms of IR is inflammation- and/or stress-induced up-regulation of TRP – KYN metabolism in combination with P5P deficiency-induced diversion of KYN – NAD metabolism towards formation of XA and other KYN derivatives affecting insulin activity. Monitoring of KYN/P5P status and formation of XA might help to identify subjects-at-risk for IR. Pharmacological regulation of the TRP – KYN and KYN – NAD pathways and maintaining of adequate vitamin B6 status might contribute to prevention and treatment of IR in conditions associated with inflammation/stress–induced excessive production of KYN and deficiency of vitamin B6, e.g., diabetes type 2, obesity, cardiovascular diseases, aging, menopause, pregnancy, and hepatitis C virus infection.

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Section: Other Conditions Associated With Insulin Resistancesupporting

confidence: 66%

Insulin Resistance and Dysregulation of Tryptophan–Kynurenine and Kynurenine–Nicotinamide Adenine Dinucleotide Metabolic Pathways

2013

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“…Berberine exerts therapeutic potential in diabetic hamsters [79] and diabetic patients [80,81]. It is noteworthy that both berberine and minocycline prolonged life span and improved health span in the Drosophila model [82, 83]. Consistent with our hypothesis, is observation that vitamin B6 supplementation dose-dependently decreased insulin levels and improved insulin resistance in KK-A(y) mice, an animal model of obese, type 2 diabetes [84, 85].…”

Section: Kynurenine/tryptophan Ratio Neopterin and P5p Levels In Depsupporting

confidence: 71%

Kynurenines And Vitamin B6: Link Between Diabetes And Depression.

Oxenkrug

Ratner

Summergrad

2013

JBD

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The increased association between depression and diabetes mellitus is generally acknowledged. Recent studies suggest that depression leads to diabetes. However, the underlying molecular mechanisms for this association remain unclear. Literature and our data indicate that inflammatory and/or stress factors in depression up-regulate tryptophan (TRP) conversion into kynurenine (KYN), a substrate for nicotinamide adenine dinucleotide (NAD) biosynthesis. Deficiency of vitamin B6, a co-factor of the key enzymes of KYN -NAD pathway, shunts KYN metabolism from formation of NAD towards production of xanthurenic (XA) and kynurenic (KYNA) acids. Human and experimental studies reveal that XA, KYNA and their metabolites interfere with production, release and biological activity of insulin. We propose that inflammation-and/or stress-induced up-regulation of TRP -KYN metabolism in combination with vitamin B6 deficiency is one of the mechanisms mediating increased risk of diabetes in depression.Consequently, monitoring formation of diabetogenic KYN derivatives might help to identify subjects-atrisk for the development of diabetes. Pharmacological down-regulation of the TRP -KYN -NAD pathway and maintenance of adequate vitamin B6 status might help to prevent the development of diabetes in depression and other conditions associated with inflammation/stress-induced excessive production of KYN and vitamin B6 deficiency, e.g., obesity, cardiovascular diseases, aging, menopause, pregnancy, and hepatitis C virus infection.Corresponding author: Oxenkrug Gregory F. goxenkrug@tuftsmedicalcenter.org Running title: Running title: kynurenines, B6, diabetes and depression Kynurenines and vitamin B6: link between diabetes and depression.

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“…Recently, it was reported that BBR could exhibit a lifespan-prolonged function by influencing the conversion of tryptophan into kynurenine in Drosophila [9]. Meanwhile, BBR was also proposed as a potential antiaging agent in oxidative DNA damage and could affect mitoxantrone-induced cellular senescence [10, 11].…”

Section: Introductionmentioning

confidence: 99%

The Preconditioning of Berberine Suppresses Hydrogen Peroxide-Induced Premature Senescence via Regulation of Sirtuin 1

Zhu

Yue

Guo

et al. 2017

Oxidative Medicine and Cellular Longevity

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With a long history of application in Chinese traditional medicine, berberine (BBR) was reported to exhibit healthspan-extending properties in some age-related diseases, such as type 2 diabetes and atherosclerosis. However, the antiaging mechanism of BBR is not completely clear. By means of hydrogen peroxide- (H2O2-) induced premature cellular senescence model, we found that a low-concentration preconditioning of BBR could resist premature senescence in human diploid fibroblasts (HDFs) measured by senescence-associated β-galactosidase (SA-β-gal), accompanied by a decrease in loss of mitochondrial membrane potential and production of intracellular reactive oxygen species (ROS). Moreover, the low-concentration preconditioning of BBR could make cells less susceptible to subsequent H2O2-induced cell cycle arrest and growth inhibition. Experimental results further showed that the low concentration of BBR could induce a slight increase of ROS and upregulate the expression level of sirtuin 1 (SIRT1), an important longevity regulator. H2O2-induced activation of checkpoint kinase 2 (Chk2) was significantly attenuated after the preconditioning of BBR. The present findings implied that the low-concentration preconditioning of BBR could have a mitohormetic effect against cellular senescence triggered by oxidative stress in some age-related diseases through the regulation of SIRT1.

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Berberine Prolongs Life Span and Stimulates Locomotor Activity of <i>Drosophila melanogaster</i>

Cited by 28 publications

References 35 publications

Insulin Resistance and Dysregulation of Tryptophan–Kynurenine and Kynurenine–Nicotinamide Adenine Dinucleotide Metabolic Pathways

Insulin Resistance and Dysregulation of Tryptophan–Kynurenine and Kynurenine–Nicotinamide Adenine Dinucleotide Metabolic Pathways

Kynurenines And Vitamin B6: Link Between Diabetes And Depression.

The Preconditioning of Berberine Suppresses Hydrogen Peroxide-Induced Premature Senescence via Regulation of Sirtuin 1

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