- Curcumin, the anti-inflammatory, anti-ageing and anti-cancer compound from turmeric, is well-known for it's anti-adipogenic / slimming activity and thereby it's usefulness in anti-cellulite creams
- Turmeric acts via various pathways to inhibit growth of fat cells and in a recent study yet one more fat accumulation inhibiting pathway has been discovered: turmeric inhibits glucose absorption by intestinal cells, by blocking the protein GLUT1
- This leads to blood sugar reduction and fat reduction and is in addition to turmeric's inhibiting effect on GLUT4, which blocks glucose absorption by fat cells
- The researchers state that due to the blockage of GLIT1 turmeric may also compromise cancer cells that depend on GLUT1 for glucose absorption
- Source: Curcumin directly inhibits the transport activity of GLUT1.
- Abstract: Curcumin, a major ingredient in turmeric, has a long history of medicinal applications in a wide array of maladies including treatment for diabetes and cancer. Seemingly counterintuitive to the documented hypoglycemic effects of curcumin, however, a recent report indicates that curcumin directly inhibits glucose uptake in adipocytes. The major glucose transporter in adipocytes is GLUT4. Therefore, this study investigates the effects of curcumin in cell lines where the major transporter is GLUT1. We report that curcumin has an immediate inhibitory effect on basal glucose uptake in L929 fibroblast cells with a maximum inhibition of 80% achieved at 75 μM curcumin. Curcumin also blocks activation of glucose uptake by azide, glucose deprivation, hydroxylamine, or phenylarsine oxide. Inhibition does not increase with exposure time and the inhibitory effects reverse within an hour. Inhibition does not appear to involve a reaction between curcumin and the thiol side chain of a cysteine residue since neither prior treatment of cells with iodoacetamide nor curcumin with cysteine alters curcumin's inhibitory effects. Curcumin is a mixed inhibitor reducing the Vmax of 2DG transport by about half with little effect on the Km. The inhibitory effects of curcumin are not additive to the effects of cytochalasin B and 75 μM curcumin actually reduces specific cytochalasin B binding by 80%. Taken together, the data suggest that curcumin binds directly to GLUT1 at a site that overlaps with the cytochalasin B binding site and thereby inhibits glucose transport. A direct inhibition of GLUT proteins in intestinal epithelial cells would likely reduce absorption of dietary glucose and contribute to a hypoglycemic effect of curcumin. Also, inhibition of GLUT1 activity might compromise cancer cells that overexpress GLUT1 and be another possible mechanism for the documented anticancer effects of curcumin.
< Back to curcumin