The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 19 No. 7 • December 2016


EGCG Suppresses Gluconeogenesis in Liver Cells, Protecting Against Major Pathway Leading to Excess Blood Sugar in Type 2 Diabetes

Failure of feedback mechanisms to inhibit gluconeogenesis (the conversion of amino acids to glucose) in the liver is a major reason for excess blood sugar in type 2 diabetes. (Eating is supposed to shut down gluconeogenesis, with glucose derived from food acting as a negative feedback signal.) The release of GLP-1 (glucagon like peptide 1) is involved in the feedback inhibition of eating to tell liver cells to stop gluconeogenesis. In a fairly recent paper (Collins, 2007), researchers were able to show in mouse liver cells that EGCG suppressed gluconeogenesis by activating 5’-AMP-activated protein kinase (AMPK), an important regulator of energy metabolism that responds to eating by (for one thing) suppressing gluconeogenesis. (The authors point out that the activation of AMPK is associated with EGCG-induced apoptosis in cancer cells, but that is another story.)

The results of this study suggest that EGCG could, as the authors note in their summary (last paragraph in the paper), point to a new therapeutic approach for the management of diabetes. (Collins, 2007)

Reference

  • Collins et al. Epigallocatechin-3-gallate (EGCG), a green tea polyphenol, suppresses J Biol Chem. 282(41):30143-9 (2007).

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