Curcumin - Turmeric Weight Loss

Curcumin (/'k?rkju:m?n/) is a diarylheptanoid. It is the principal curcuminoid of turmeric, which is a member of the ginger family (Zingiberaceae). Turmeric's other two curcuminoids are desmethoxycurcumin and bis-desmethoxycurcumin. The curcuminoids are natural phenols that are responsible for the yellow color of turmeric. Curcumin can exist in several tautomeric forms, including a 1,3-diketo form and two equivalent enol forms. The enol form is more energetically stable in the solid phase and in solution.

Curcumin can be used for boron quantification in the curcumin method. It reacts with boric acid to form a red-color compound, rosocyanine.

Curcumin is a bright-yellow color and may be used as a food coloring. As a food additive, its E number is E100.

Adverse effects

Clinical studies in humans with high doses (2-12 grams) of curcumin have shown few side-effects, with some subjects reporting mild nausea or diarrhea. More recently, curcumin was found to alter iron metabolism by chelating iron and suppressing the protein hepcidin, potentially causing iron deficiency in susceptible patients.

Chemistry

Curcumin incorporates several functional groups. The aromatic ring systems, which are phenols, are connected by two ?,?-unsaturated carbonyl groups. The diketones form stable enols and are readily deprotonated to form enolates; the ?,?-unsaturated carbonyl group is a good Michael acceptor and undergoes nucleophilic addition. The structure was first identified in 1910 by J. Mi?ob?dzka, Stanis?aw Kostanecki and Wiktor Lampe.

Curcumin is used as an indicator for boron.

Biosynthesis

The biosynthetic route of curcumin has proven to be very difficult for researchers to determine. In 1973, Roughly and Whiting proposed two mechanisms for curcumin biosynthesis. The first mechanism involved a chain extension reaction by cinnamic acid and 5 malonyl-CoA molecules that eventually arylized into a curcuminoid. The second mechanism involved two cinnamate units coupled together by malonyl-CoA. Both mechanisms use cinnamic acid as their starting point, which is derived from the amino acid phenylalanine. This is noteworthy because plant biosyntheses employing cinnamic acid as a starting point are rare compared to the more common use of p-coumaric acid. Only a few identified compounds, such as anigorufone and pinosylvin, use cinnamic acid as their start molecule. An experimentally backed route was not presented until 2008. This proposed biosynthetic route follows both the first and second mechanisms suggested by Roughley and Whiting. However, the labeling data supported the first mechanism model in which 5 malonyl-CoA molecules react with cinnamic acid to form curcumin. However, the sequencing in which the functional groups, the alcohol and the methoxy, introduce themselves onto the curcuminoid seems to support more strongly the second proposed mechanism. Therefore, it was concluded the second pathway proposed by Roughly and Whiting was correct.

Pharmacodynamics

In vitro, curcumin has been shown to inhibit certain epigenetic enzymes (the histone deacetylases: HDAC1, HDAC3, and HDAC8) and transcriptional co-activator proteins (the p300 histone acetyltransferase). Curcumin also inhibits the arachidonate 5-lipoxygenase enzyme in vitro.

Pharmacokinetics

In Phase I clinical trials, dietary curcumin was shown to exhibit poor bioavailability, exhibited by rapid metabolism, low levels in plasma and tissues, and extensive rapid excretion. Potential factors that limit the bioavailability of curcumin include insolubility in water (more soluble in alkaline solutions) and poor absorption. Numerous approaches to increase curcumin bioavailability have been explored, including the use of absorption factors (such as piperine), liposomes, nanoparticles or a structural analogue.

Research

Therapeutic uses

A survey of the literature shows a number of potential effects under study and that daily doses over a 3-month period of up to 12 grams were safe. However, several studies of curcumin efficacy and safety revealed poor absorption and low bioavailability.

Clinical trials in humans are studying the effect of curcumin on various diseases, including multiple myeloma, pancreatic cancer, myelodysplastic syndromes, colon cancer, psoriasis, arthritis, major depressive disorder and Alzheimer's disease.

Diagnostic use

Preliminary research has found that curcuminoid binds to amyloid proteins associated with Alzheimer's disease. Because curcumin increases fluorescent activity after it binds to amyloid protein, curcumin is being studied as a possible identifier. Tests have detected amyloid proteins in human eyes, offering the possibility that simple eye exams could provide early detection of the disease.

References

External links

• Turmeric and curcumin, from Memorial Sloan-Kettering Cancer Center
• Turmeric and curcumin, from M.D. Anderson Cancer Center
• Turmeric, from the University of Maryland Medical Center

Interesting Informations

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