Turmeric inhibits conversion of amino acids into glucose

Gluconeogenesis is a useful process, but if muscle building is your hobby, you’d probably prefer it if it didn’t work so well. Gluconeogenesis is the process in which amino acids are converted into glucose. But fortunately there’s turmeric, and thanks to nutritionists at Auburn University we know that turmeric inhibits gluconeogenesis.


The active substance in turmeric is curcumin. Take 4-8 g of the stuff and about 0.5 – 1.7 micromoles of it will reach your blood. That’s not a lot. This is because enzymes easily convert curcumin [structural formula is top one here below] into dihydrocurcumin [second structural formula], tetrahydrocurcumin [formula 3], hexahydrocurcumin [formula 4] and hexahydrocurcuminol [formula 5].
Turmeric inhibits conversion of amino acids into glucose
What’s more, other enzymes attach sulphates and sugar groups to curcumin analogues so that the body gets rid of them quickly.

In their study [which by the way was not funded by the supplements industry] the researchers studied the effects of curcumin [Cur], its metabolite tetrahydrocurcumin [THC] and the C3 complex made by Sabinsa [C3] on liver cells. Curcumin preparations are being tested on diabetics because curcumin improves the glucose uptake of muscle cells. These researchers wanted to know whether curcumin also has effects in the liver, which may be useful for diabetics.

To do this the researchers looked at gluconeogenesis, a reaction in which molecules like pyruvate, lactate, glycerol and – yes – the amino acids alanine and glutamine are converted into glucose in the liver. The amino acids come from the muscles, mostly in the form of a conversion product from other amino acids.


‘The’ hormone involved in the conversion of amino acids into glucose is cortisol. That’s why strength athletes regard cortisol as a muscle growth enemy. And it’s why the researchers exposed their liver cells to the cortisol based synthetic hormone dexamethason.

Curcumin versis gluconeogenesis
The figures below show that dexamethason boosts the activity of the enzymes phosphoenol pyruvate carboxy kinase [PEPCK] and glucose6-phosphatase [G6Pase] in the liver cells. These are key enzymes in the process of gluconeogenesis. But when the researchers added Cur, THC and C3 to the liver cells, the activity decreased.


The metabolite THC [rather than Cur or C3] reduces the activity of G6Pase at concentrations a supplements taker could use. That means that the whole gluconeogenesis process goes more slowly. If the other curcumin metabolites have the same effect as THC, then you can expect curcumin supplementation to inhibit the conversion of amino acids into glucose.

Curcumin activates AMPK and suppresses gluconeogenic gene expression in hepatoma cells.


Curcumin, the bioactive component of curry spice turmeric, and its related structures possess potent anti-oxidant and anti-inflammatory properties. Several lines of evidence suggest that curcumin may play a beneficial role in animal models of diabetes, both by lowering blood glucose levels and by ameliorating the long-term complications of diabetes. However, current understanding of the mechanism of curcumin action is rudimentary and is limited to its anti-oxidant and anti-inflammatory effects. In this study we examine potential anti-diabetic mechanisms of curcumin, curcumin C3 complex), and tetrahydrocurcuminoids (THC). Curcuminoids did not exert a direct effect on receptor tyrosine kinase activity, 2-deoxy glucose uptake in L6-GLUT4myc cells, or intestinal glucose metabolism measured by DPP4/alpha-glucosidase inhibitory activity. We demonstrate that curcuminoids effectively suppressed dexamethasone-induced phosphoenol pyruvate carboxy kinase (PEPCK) and glucose6-phosphatase (G6Pase) in H4IIE rat hepatoma and Hep3B human hepatoma cells. Furthermore, curcuminoids increased the phosphorylation of AMP-activated protein kinase (AMPK) and its downstream target acetyl-CoA carboxylase (ACC) in H4IIE and Hep3B cells with 400 times (curcumin) to 100,000 times (THC) the potency of metformin. These results suggest that AMPK mediated suppression of hepatic gluconeogenesis may be a potential mechanism mediating glucose-lowering effects of curcuminoids.

PMID: 19665995 [PubMed – indexed for MEDLINE]

Source: http://www.ncbi.nlm.nih.gov/pubmed/19665995

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