SPP Presents: GlycoMyx

[Geoforce]

It's hard to tell in that picture, but that girls arms are more pumped and vascular than they have ever been.

 

[Geoforce]

Flash sale going on right now on GlycoMyx at your favorite Planet guys. Many repeat users, see what all the fuss is about the perfect carb!

 

[MidwestBeast]

Flash sale going on right now on GlycoMyx at your favorite Planet guys. Many repeat users, see what all the fuss is about the perfect carb!

I'm gonna pull the trigger. I've got about a scoop left in my tub.

OM NOM NOM NOM

 

[bigguyn10ec]

I really would like to try this.

 

[dsade]

How are you all liking the effects of GlycoMyx?

J Nutr Biochem. 2012 Sep 17. pii: S0955-2863(12)00202-1. doi: 10.1016/j.jnutbio.2012.07.009. [Epub ahead of print]
[h=1]Purple sweet potato color attenuates hepatic insulin resistance via blocking oxidative stress and endoplasmic reticulum stress in high-fat-diet-treated mice.[/h]Zhang ZF, Lu J, Zheng YL, Wu DM, Hu B, Shan Q, Cheng W, Li MQ, Sun YY.
[h=3]Source[/h]Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, Jiangsu Province, P. R. China.

[h=3]Abstract[/h]Purple sweet potato color (PSPC), a class of naturally occurring anthocyanins, has been reported to possess a variety of health-promoting properties. Emerging evidence indicates that PSPC can suppress postprandial hyperglycemia via inhibition of α-glucosidases. However, the protective effects of PSPC on hepatic insulin resistance and the precise mechanisms underlying these protective effects have never been investigated. In this study, our data showed that PSPC effectively improved the fasting blood glucose level, glucose and insulin tolerance by suppressing reactive oxygen species (ROS) production and by restoring glutathione (GSH) content and antioxidant enzymes' activities. PSPC further prevented the oxidative-stress-mediated endoplasmic reticulum (ER) stress in the livers of high-fat-diet (HFD)-treated mice. Moreover, PSPC dramatically suppressed the c-Jun-N-terminal kinase 1 and I kappa B kinase β activation and nuclear factor-kappa B p65 nuclear translocation caused by oxidative and ER stress in the livers of HFD-treated mice. Ultimately, PSPC notably restored the impairment of the insulin receptor substrate-1/phosphoinositide 3 kinase/protein kinase B (Akt) insulin signaling in the livers of HFD-treated mice. In conclusion, our findings indicate that PSPC protected against HFD-induced hepatic insulin resistance via decreasing ROS level and blocking ROS-mediated ER stress.
Crown Copyright © 2012. Published by Elsevier Inc. All rights reserved

 

[MidwestBeast]

How are you all liking the effects of GlycoMyx?

J Nutr Biochem. 2012 Sep 17. pii: S0955-2863(12)00202-1. doi: 10.1016/j.jnutbio.2012.07.009. [Epub ahead of print]
Purple sweet potato color attenuates hepatic insulin resistance via blocking oxidative stress and endoplasmic reticulum stress in high-fat-diet-treated mice.

Zhang ZF, Lu J, Zheng YL, Wu DM, Hu B, Shan Q, Cheng W, Li MQ, Sun YY.
Source

Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, Jiangsu Province, P. R. China.

Abstract

Purple sweet potato color (PSPC), a class of naturally occurring anthocyanins, has been reported to possess a variety of health-promoting properties. Emerging evidence indicates that PSPC can suppress postprandial hyperglycemia via inhibition of α-glucosidases. However, the protective effects of PSPC on hepatic insulin resistance and the precise mechanisms underlying these protective effects have never been investigated. In this study, our data showed that PSPC effectively improved the fasting blood glucose level, glucose and insulin tolerance by suppressing reactive oxygen species (ROS) production and by restoring glutathione (GSH) content and antioxidant enzymes' activities. PSPC further prevented the oxidative-stress-mediated endoplasmic reticulum (ER) stress in the livers of high-fat-diet (HFD)-treated mice. Moreover, PSPC dramatically suppressed the c-Jun-N-terminal kinase 1 and I kappa B kinase β activation and nuclear factor-kappa B p65 nuclear translocation caused by oxidative and ER stress in the livers of HFD-treated mice. Ultimately, PSPC notably restored the impairment of the insulin receptor substrate-1/phosphoinositide 3 kinase/protein kinase B (Akt) insulin signaling in the livers of HFD-treated mice. In conclusion, our findings indicate that PSPC protected against HFD-induced hepatic insulin resistance via decreasing ROS level and blocking ROS-mediated ER stress.
Crown Copyright © 2012. Published by Elsevier Inc. All rights reserved