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Young-joon Surh - One of the best experts on this subject based on the ideXlab platform.

  • 6 Gingerol prevents uvb induced ros production and cox 2 expression in vitro and in vivo
    Free Radical Research, 2007
    Co-Authors: Kwangmin Na, Young-joon Surh
    Abstract:

    [6]-Gingerol, a naturally occurring plant phenol, is one of the major components of fresh ginger (Zingiber officinale Roscoe, Zingiberaceae) and has diverse pharmacologic effects. Here, we describe its novel anti-oxidant, anti-apoptotic, and anti-inflammatory activities in vitro and in vivo. In vitro, pre-treatment with [6]-Gingerol reduced UVB-induced intracellular reactive oxygen species levels, activation of caspase-3, -8, -9, and Fas expression. It also reduced UVB-induced expression and transactivation of COX-2. Translocation of NF-κB from cytosol to nucleus in HaCaT cells was inhibited by [6]-Gingerol via suppression of IκBα phosphorylation (ser-32). Examination by EMSAs and immunohistochemistry showed that topical application of [6]-Gingerol (30 μM) prior to UVB irradiation (5 kJ/m2) of hairless mice, also inhibited the induction of COX-2 mRNA and protein, as well as NF-κB translocation. These results suggest that [6]-Gingerol could be an effective therapeutic agent providing protection against UVB...

  • 6 Gingerol prevents uvb induced ros production and cox 2 expression in vitro and in vivo
    Free Radical Research, 2007
    Co-Authors: Jinkyoung Kim, Young-joon Surh, Younghwa Kim, Taeyoon Kim
    Abstract:

    [6]-Gingerol, a naturally occurring plant phenol, is one of the major components of fresh ginger (Zingiber officinale Roscoe, Zingiberaceae) and has diverse pharmacologic effects. Here, we describe its novel anti-oxidant, anti-apoptotic, and anti-inflammatory activities in vitro and in vivo. In vitro, pre-treatment with [6]-Gingerol reduced UVB-induced intracellular reactive oxygen species levels, activation of caspase-3, -8, -9, and Fas expression. It also reduced UVB-induced expression and transactivation of COX-2. Translocation of NF-kappaB from cytosol to nucleus in HaCaT cells was inhibited by [6]-Gingerol via suppression of IkappaBalpha phosphorylation (ser-32). Examination by EMSAs and immunohistochemistry showed that topical application of [6]-Gingerol (30 microM) prior to UVB irradiation (5 kJ/m(2)) of hairless mice, also inhibited the induction of COX-2 mRNA and protein, as well as NF-kappaB translocation. These results suggest that [6]-Gingerol could be an effective therapeutic agent providing protection against UVB-induced skin disorders.

  • 6 Gingerol inhibits cox 2 expression by blocking the activation of p38 map kinase and nf kappab in phorbol ester stimulated mouse skin
    Oncogene, 2005
    Co-Authors: Joydeb Kumar Kundu, Young Kee Shin, Jin Hong Park, Young-joon Surh
    Abstract:

    [6]-Gingerol inhibits COX-2 expression by blocking the activation of p38 MAP kinase and NF- κ B in phorbol ester-stimulated mouse skin

  • 6 Gingerol inhibits cox 2 expression by blocking the activation of p38 map kinase and nf kappab in phorbol ester stimulated mouse skin
    Oncogene, 2005
    Co-Authors: Sue Ok Kim, Joydeb Kumar Kundu, Young Kee Shin, Jin Hong Park, Taeyoon Kim, Myunghaing Cho, Young-joon Surh
    Abstract:

    [6]-Gingerol, a pungent ingredient of ginger (Zingiber officinale Roscoe, Zingiberaceae), has a wide array of pharmacologic effects. The present study was aimed at unraveling the molecular mechanisms underlying previously reported antitumor promoting effects of [6]-Gingerol in mouse skin in vivo. One of the well-recognized molecular targets for chemoprevention is cyclooxygenase-2 (COX-2) that is abnormally upregulated in many premalignant and malignant tissues and cells. In our present study, topical application of [6]-Gingerol inhibited COX-2 expression in mouse skin stimulated with a prototype tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA). Since the transcription factor nuclear factor-kappaB (NF-kappaB) is known to regulate COX-2 induction, we attempted to determine the effect of [6]-Gingerol on TPA-induced activation of NF-kappaB. Pretreatment with [6]-Gingerol resulted in a decrease in both TPA-induced DNA binding and transcriptional activities of NF-kappaB through suppression of IkappaBalpha degradation and p65 nuclear translocation. Phosphorylation of both IkappaBalpha and p65 was substantially blocked by [6]-Gingerol. In addition, [6]-Gingerol inhibited TPA-stimulated interaction of phospho-p65-(Ser-536) with cAMP response element binding protein-binding protein, a transcriptional coactivator of NF-kappaB. Moreover, [6]-Gingerol prevented TPA-induced phosphorylation and catalytic activity of p38 mitogen-activated protein (MAP) kinase that regulates COX-2 expression in mouse skin. The p38 MAP kinase inhibitor SB203580 attenuated NF-kappaB activation and subsequent COX-2 induction in TPA-treated mouse skin. Taken together, our data suggest that [6]-Gingerol inhibits TPA-induced COX-2 expression in mouse skin in vivo by blocking the p38 MAP kinase-NF-kappaB signaling pathway.

  • inhibitory effects of 6 Gingerol on pma induced cox 2 expression and activation of nf κb and p38 mapk in mouse skin
    Biofactors, 2004
    Co-Authors: Sue Ok Kim, Joydeb Kumar Kundu, Kyungsoo Chun, Young-joon Surh
    Abstract:

    [6]-Gingerol, a major pungent ingredient of ginger (Zingiber officinale Roscoe, Zingiberaceae), has a wide array of pharmacologic effects. Previous studies have demonstrated that [6]-Gingerol inhibits mouse skin tumor promotion and anchorage-independent growth of cultured mouse epidermal cells stimulated with epidermal growth factor. Cyclooxygenase-2 (COX-2), a key enzyme in the prostaglandin biosynthesis, has been recognized as a molecular target for many anti-inflammatory as well as chemopreventive agents. Topical application of [6]-Gingerol inhibited phorbol 12-myristate 13-acetate -induced COX-2 expression. One of the essential transcription factors responsible for COX-2 induction is NF-kappaB. [6]-Gingerol suppressed NF-kappaB DNA binding activity in mouse skin. In addition, [6]-Gingerol inhibited the phoshorylation of p38 mitogen-activated protein kinase which may account for its inactivation of NF-kappaB and suppression of COX-2 expression.

Joydeb Kumar Kundu - One of the best experts on this subject based on the ideXlab platform.

  • 6 Gingerol inhibits cox 2 expression by blocking the activation of p38 map kinase and nf kappab in phorbol ester stimulated mouse skin
    Oncogene, 2005
    Co-Authors: Joydeb Kumar Kundu, Young Kee Shin, Jin Hong Park, Young-joon Surh
    Abstract:

    [6]-Gingerol inhibits COX-2 expression by blocking the activation of p38 MAP kinase and NF- κ B in phorbol ester-stimulated mouse skin

  • 6 Gingerol inhibits cox 2 expression by blocking the activation of p38 map kinase and nf kappab in phorbol ester stimulated mouse skin
    Oncogene, 2005
    Co-Authors: Sue Ok Kim, Joydeb Kumar Kundu, Young Kee Shin, Jin Hong Park, Taeyoon Kim, Myunghaing Cho, Young-joon Surh
    Abstract:

    [6]-Gingerol, a pungent ingredient of ginger (Zingiber officinale Roscoe, Zingiberaceae), has a wide array of pharmacologic effects. The present study was aimed at unraveling the molecular mechanisms underlying previously reported antitumor promoting effects of [6]-Gingerol in mouse skin in vivo. One of the well-recognized molecular targets for chemoprevention is cyclooxygenase-2 (COX-2) that is abnormally upregulated in many premalignant and malignant tissues and cells. In our present study, topical application of [6]-Gingerol inhibited COX-2 expression in mouse skin stimulated with a prototype tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA). Since the transcription factor nuclear factor-kappaB (NF-kappaB) is known to regulate COX-2 induction, we attempted to determine the effect of [6]-Gingerol on TPA-induced activation of NF-kappaB. Pretreatment with [6]-Gingerol resulted in a decrease in both TPA-induced DNA binding and transcriptional activities of NF-kappaB through suppression of IkappaBalpha degradation and p65 nuclear translocation. Phosphorylation of both IkappaBalpha and p65 was substantially blocked by [6]-Gingerol. In addition, [6]-Gingerol inhibited TPA-stimulated interaction of phospho-p65-(Ser-536) with cAMP response element binding protein-binding protein, a transcriptional coactivator of NF-kappaB. Moreover, [6]-Gingerol prevented TPA-induced phosphorylation and catalytic activity of p38 mitogen-activated protein (MAP) kinase that regulates COX-2 expression in mouse skin. The p38 MAP kinase inhibitor SB203580 attenuated NF-kappaB activation and subsequent COX-2 induction in TPA-treated mouse skin. Taken together, our data suggest that [6]-Gingerol inhibits TPA-induced COX-2 expression in mouse skin in vivo by blocking the p38 MAP kinase-NF-kappaB signaling pathway.

  • inhibitory effects of 6 Gingerol on pma induced cox 2 expression and activation of nf κb and p38 mapk in mouse skin
    Biofactors, 2004
    Co-Authors: Sue Ok Kim, Joydeb Kumar Kundu, Kyungsoo Chun, Young-joon Surh
    Abstract:

    [6]-Gingerol, a major pungent ingredient of ginger (Zingiber officinale Roscoe, Zingiberaceae), has a wide array of pharmacologic effects. Previous studies have demonstrated that [6]-Gingerol inhibits mouse skin tumor promotion and anchorage-independent growth of cultured mouse epidermal cells stimulated with epidermal growth factor. Cyclooxygenase-2 (COX-2), a key enzyme in the prostaglandin biosynthesis, has been recognized as a molecular target for many anti-inflammatory as well as chemopreventive agents. Topical application of [6]-Gingerol inhibited phorbol 12-myristate 13-acetate -induced COX-2 expression. One of the essential transcription factors responsible for COX-2 induction is NF-kappaB. [6]-Gingerol suppressed NF-kappaB DNA binding activity in mouse skin. In addition, [6]-Gingerol inhibited the phoshorylation of p38 mitogen-activated protein kinase which may account for its inactivation of NF-kappaB and suppression of COX-2 expression.

Ishrat Aklima Muna - One of the best experts on this subject based on the ideXlab platform.

  • 6 Gingerol from zingiber officinale potentiates glp 1 mediated glucose stimulated insulin secretion pathway in pancreatic β cells and increases rab8 rab10 regulated membrane presentation of glut4 transporters in skeletal muscle to improve hyperglycemia in lepr db db type 2 diabetic mice
    BMC Complementary and Alternative Medicine, 2017
    Co-Authors: Mehdi Bin Samad, Md. Nurul Absar Bin Mohsin, Bodiul Alam Razu, Mohammad Tashnim Hossain, Sinayat Mahzabeen, Naziat Unnoor, Ishrat Aklima Muna
    Abstract:

    [6]-Gingerol, a major component of Zingiber officinale, was previously reported to ameliorate hyperglycemia in type 2 diabetic mice. Endocrine signaling is involved in insulin secretion and is perturbed in db/db Type-2 diabetic mice. [6]-Gingerol was reported to restore the disrupted endocrine signaling in rodents. In this current study on Leprdb/db diabetic mice, we investigated the involvement of endocrine pathway in the insulin secretagogue activity of [6]-Gingerol and the mechanism(s) through which [6]-Gingerol ameliorates hyperglycemia. Leprdb/db type 2 diabetic mice were orally administered a daily dose of [6]-Gingerol (200 mg/kg) for 28 days. We measured the plasma levels of different endocrine hormones in fasting and fed conditions. GLP-1 levels were modulated using pharmacological approaches, and cAMP/PKA pathway for insulin secretion was assessed by qRT-PCR and ELISA in isolated pancreatic islets. Total skeletal muscle and its membrane fractions were used to measure glycogen synthase 1 level and Glut4 expression and protein levels. 4-weeks treatment of [6]-Gingerol dramatically increased glucose-stimulated insulin secretion and improved glucose tolerance. Plasma GLP-1 was found to be significantly elevated in the treated mice. Pharmacological intervention of GLP-1 levels regulated the effect of [6]-Gingerol on insulin secretion. Mechanistically, [6]-Gingerol treatment upregulated and activated cAMP, PKA, and CREB in the pancreatic islets, which are critical components of GLP-1-mediated insulin secretion pathway. [6]-Gingerol upregulated both Rab27a GTPase and its effector protein Slp4-a expression in isolated islets, which regulates the exocytosis of insulin-containing dense-core granules. [6]-Gingerol treatment improved skeletal glycogen storage by increased glycogen synthase 1 activity. Additionally, GLUT4 transporters were highly abundant in the membrane of the skeletal myocytes, which could be explained by the increased expression of Rab8 and Rab10 GTPases that are responsible for GLUT4 vesicle fusion to the membrane. Collectively, our study reports that GLP-1 mediates the insulinotropic activity of [6]-Gingerol, and [6]-Gingerol treatment facilitates glucose disposal in skeletal muscles through increased activity of glycogen synthase 1 and enhanced cell surface presentation of GLUT4 transporters.

  • [6]-Gingerol, from Zingiber officinale, potentiates GLP-1 mediated glucose-stimulated insulin secretion pathway in pancreatic β-cells and increases RAB8/RAB10-regulated membrane presentation of GLUT4 transporters in skeletal muscle to improve hyperglycemia in Leprdb/db type 2 diabetic mice
    BMC, 2017
    Co-Authors: Mehdi Bin Samad, Md. Nurul Absar Bin Mohsin, Bodiul Alam Razu, Mohammad Tashnim Hossain, Sinayat Mahzabeen, Naziat Unnoor, Ishrat Aklima Muna, Farjana Akhter, Ashraf Ul Kabir, J. M. A. Hannan
    Abstract:

    Abstract Background [6]-Gingerol, a major component of Zingiber officinale, was previously reported to ameliorate hyperglycemia in type 2 diabetic mice. Endocrine signaling is involved in insulin secretion and is perturbed in db/db Type-2 diabetic mice. [6]-Gingerol was reported to restore the disrupted endocrine signaling in rodents. In this current study on Leprdb/db diabetic mice, we investigated the involvement of endocrine pathway in the insulin secretagogue activity of [6]-Gingerol and the mechanism(s) through which [6]-Gingerol ameliorates hyperglycemia. Methods Leprdb/db type 2 diabetic mice were orally administered a daily dose of [6]-Gingerol (200 mg/kg) for 28 days. We measured the plasma levels of different endocrine hormones in fasting and fed conditions. GLP-1 levels were modulated using pharmacological approaches, and cAMP/PKA pathway for insulin secretion was assessed by qRT-PCR and ELISA in isolated pancreatic islets. Total skeletal muscle and its membrane fractions were used to measure glycogen synthase 1 level and Glut4 expression and protein levels. Results 4-weeks treatment of [6]-Gingerol dramatically increased glucose-stimulated insulin secretion and improved glucose tolerance. Plasma GLP-1 was found to be significantly elevated in the treated mice. Pharmacological intervention of GLP-1 levels regulated the effect of [6]-Gingerol on insulin secretion. Mechanistically, [6]-Gingerol treatment upregulated and activated cAMP, PKA, and CREB in the pancreatic islets, which are critical components of GLP-1-mediated insulin secretion pathway. [6]-Gingerol upregulated both Rab27a GTPase and its effector protein Slp4-a expression in isolated islets, which regulates the exocytosis of insulin-containing dense-core granules. [6]-Gingerol treatment improved skeletal glycogen storage by increased glycogen synthase 1 activity. Additionally, GLUT4 transporters were highly abundant in the membrane of the skeletal myocytes, which could be explained by the increased expression of Rab8 and Rab10 GTPases that are responsible for GLUT4 vesicle fusion to the membrane. Conclusions Collectively, our study reports that GLP-1 mediates the insulinotropic activity of [6]-Gingerol, and [6]-Gingerol treatment facilitates glucose disposal in skeletal muscles through increased activity of glycogen synthase 1 and enhanced cell surface presentation of GLUT4 transporters

Lianwen Qi - One of the best experts on this subject based on the ideXlab platform.

  • simultaneous determination of 6 Gingerol 8 Gingerol 10 Gingerol and 6 shogaol in rat plasma by liquid chromatography mass spectrometry application to pharmacokinetics
    Journal of Chromatography B, 2009
    Co-Authors: Changyin Li, Ping Li, Lianwen Qi
    Abstract:

    Abstract A rapid high-performance liquid chromatography–mass spectrometry (HPLC–MS) method was developed and validated for simultaneous quantification of 6-Gingerol, 8-Gingerol, 10-Gingerol and 6-shogaol in rat plasma after oral administration of ginger oleoresin. Plasma samples extracted with a liquid–liquid extraction procedure were separated on an Agilent Zorbax StableBond-C 18 column (4.6 mm × 50 mm, 1.8 μm) and detected by MS with electrospray ionization interface in positive selective ion monitoring (SIM) mode. Calibration curves (1/ x 2 weighted) offered satisfactory linearity ( r 2  > 0.995) in a wide linear range (0.0104–13.0 μg/mL for 6-Gingerol, 0.00357–4.46 μg/mL for 8-Gingerol, 0.00920–11.5 μg/mL for 10-Gingerol and 0.00738–9.22 μg/mL for 6-shogaol). The lower limit of quantification (LLOQ) was in a range of 3.57–10.4 ng/mL. The analytes and internal standard can be baseline separated within 6 min. Inter- and intra-day assay variation was less than 15%. This developed method was successfully applied to pharmacokinetic studies of ginger oleoresin after oral administration to rats. Glucuronide of 6-Gingerol was determined after β-glucuronidase hydrolysis for more information, and the intestinal glucuronidation was further confirmed by comparison of plasma samples of hepatic portal vein and femoral vein.

  • Simultaneous determination of 6-Gingerol, 8-Gingerol, 10-Gingerol and 6-shogaol in rat plasma by liquid chromatography-mass spectrometry: Application to pharmacokinetics.
    Journal of chromatography. B Analytical technologies in the biomedical and life sciences, 2009
    Co-Authors: Changyin Li, Ping Li, Lianwen Qi
    Abstract:

    A rapid high-performance liquid chromatography-mass spectrometry (HPLC-MS) method was developed and validated for simultaneous quantification of 6-Gingerol, 8-Gingerol, 10-Gingerol and 6-shogaol in rat plasma after oral administration of ginger oleoresin. Plasma samples extracted with a liquid-liquid extraction procedure were separated on an Agilent Zorbax StableBond-C(18) column (4.6 mm x 50 mm, 1.8 microm) and detected by MS with electrospray ionization interface in positive selective ion monitoring (SIM) mode. Calibration curves (1/x(2) weighted) offered satisfactory linearity (r(2)>0.995) in a wide linear range (0.0104-13.0 microg/mL for 6-Gingerol, 0.00357-4.46 microg/mL for 8-Gingerol, 0.00920-11.5 microg/mL for 10-Gingerol and 0.00738-9.22 microg/mL for 6-shogaol). The lower limit of quantification (LLOQ) was in a range of 3.57-10.4 ng/mL. The analytes and internal standard can be baseline separated within 6 min. Inter- and intra-day assay variation was less than 15%. This developed method was successfully applied to pharmacokinetic studies of ginger oleoresin after oral administration to rats. Glucuronide of 6-Gingerol was determined after beta-glucuronidase hydrolysis for more information, and the intestinal glucuronidation was further confirmed by comparison of plasma samples of hepatic portal vein and femoral vein.

Mehdi Bin Samad - One of the best experts on this subject based on the ideXlab platform.

  • 6 Gingerol from zingiber officinale potentiates glp 1 mediated glucose stimulated insulin secretion pathway in pancreatic β cells and increases rab8 rab10 regulated membrane presentation of glut4 transporters in skeletal muscle to improve hyperglycemia in lepr db db type 2 diabetic mice
    BMC Complementary and Alternative Medicine, 2017
    Co-Authors: Mehdi Bin Samad, Md. Nurul Absar Bin Mohsin, Bodiul Alam Razu, Mohammad Tashnim Hossain, Sinayat Mahzabeen, Naziat Unnoor, Ishrat Aklima Muna
    Abstract:

    [6]-Gingerol, a major component of Zingiber officinale, was previously reported to ameliorate hyperglycemia in type 2 diabetic mice. Endocrine signaling is involved in insulin secretion and is perturbed in db/db Type-2 diabetic mice. [6]-Gingerol was reported to restore the disrupted endocrine signaling in rodents. In this current study on Leprdb/db diabetic mice, we investigated the involvement of endocrine pathway in the insulin secretagogue activity of [6]-Gingerol and the mechanism(s) through which [6]-Gingerol ameliorates hyperglycemia. Leprdb/db type 2 diabetic mice were orally administered a daily dose of [6]-Gingerol (200 mg/kg) for 28 days. We measured the plasma levels of different endocrine hormones in fasting and fed conditions. GLP-1 levels were modulated using pharmacological approaches, and cAMP/PKA pathway for insulin secretion was assessed by qRT-PCR and ELISA in isolated pancreatic islets. Total skeletal muscle and its membrane fractions were used to measure glycogen synthase 1 level and Glut4 expression and protein levels. 4-weeks treatment of [6]-Gingerol dramatically increased glucose-stimulated insulin secretion and improved glucose tolerance. Plasma GLP-1 was found to be significantly elevated in the treated mice. Pharmacological intervention of GLP-1 levels regulated the effect of [6]-Gingerol on insulin secretion. Mechanistically, [6]-Gingerol treatment upregulated and activated cAMP, PKA, and CREB in the pancreatic islets, which are critical components of GLP-1-mediated insulin secretion pathway. [6]-Gingerol upregulated both Rab27a GTPase and its effector protein Slp4-a expression in isolated islets, which regulates the exocytosis of insulin-containing dense-core granules. [6]-Gingerol treatment improved skeletal glycogen storage by increased glycogen synthase 1 activity. Additionally, GLUT4 transporters were highly abundant in the membrane of the skeletal myocytes, which could be explained by the increased expression of Rab8 and Rab10 GTPases that are responsible for GLUT4 vesicle fusion to the membrane. Collectively, our study reports that GLP-1 mediates the insulinotropic activity of [6]-Gingerol, and [6]-Gingerol treatment facilitates glucose disposal in skeletal muscles through increased activity of glycogen synthase 1 and enhanced cell surface presentation of GLUT4 transporters.

  • [6]-Gingerol, from Zingiber officinale, potentiates GLP-1 mediated glucose-stimulated insulin secretion pathway in pancreatic β-cells and increases RAB8/RAB10-regulated membrane presentation of GLUT4 transporters in skeletal muscle to improve hyperglycemia in Leprdb/db type 2 diabetic mice
    BMC, 2017
    Co-Authors: Mehdi Bin Samad, Md. Nurul Absar Bin Mohsin, Bodiul Alam Razu, Mohammad Tashnim Hossain, Sinayat Mahzabeen, Naziat Unnoor, Ishrat Aklima Muna, Farjana Akhter, Ashraf Ul Kabir, J. M. A. Hannan
    Abstract:

    Abstract Background [6]-Gingerol, a major component of Zingiber officinale, was previously reported to ameliorate hyperglycemia in type 2 diabetic mice. Endocrine signaling is involved in insulin secretion and is perturbed in db/db Type-2 diabetic mice. [6]-Gingerol was reported to restore the disrupted endocrine signaling in rodents. In this current study on Leprdb/db diabetic mice, we investigated the involvement of endocrine pathway in the insulin secretagogue activity of [6]-Gingerol and the mechanism(s) through which [6]-Gingerol ameliorates hyperglycemia. Methods Leprdb/db type 2 diabetic mice were orally administered a daily dose of [6]-Gingerol (200 mg/kg) for 28 days. We measured the plasma levels of different endocrine hormones in fasting and fed conditions. GLP-1 levels were modulated using pharmacological approaches, and cAMP/PKA pathway for insulin secretion was assessed by qRT-PCR and ELISA in isolated pancreatic islets. Total skeletal muscle and its membrane fractions were used to measure glycogen synthase 1 level and Glut4 expression and protein levels. Results 4-weeks treatment of [6]-Gingerol dramatically increased glucose-stimulated insulin secretion and improved glucose tolerance. Plasma GLP-1 was found to be significantly elevated in the treated mice. Pharmacological intervention of GLP-1 levels regulated the effect of [6]-Gingerol on insulin secretion. Mechanistically, [6]-Gingerol treatment upregulated and activated cAMP, PKA, and CREB in the pancreatic islets, which are critical components of GLP-1-mediated insulin secretion pathway. [6]-Gingerol upregulated both Rab27a GTPase and its effector protein Slp4-a expression in isolated islets, which regulates the exocytosis of insulin-containing dense-core granules. [6]-Gingerol treatment improved skeletal glycogen storage by increased glycogen synthase 1 activity. Additionally, GLUT4 transporters were highly abundant in the membrane of the skeletal myocytes, which could be explained by the increased expression of Rab8 and Rab10 GTPases that are responsible for GLUT4 vesicle fusion to the membrane. Conclusions Collectively, our study reports that GLP-1 mediates the insulinotropic activity of [6]-Gingerol, and [6]-Gingerol treatment facilitates glucose disposal in skeletal muscles through increased activity of glycogen synthase 1 and enhanced cell surface presentation of GLUT4 transporters