Curcumin, Cardiometabolic Health and Dementia

Abstract

Current research indicates curcumin [diferuloylmethane; a polyphenolic compound isolated from the rhizomes of the dietary spice turmeric (Curcuma longa)] exerts a beneficial effect on health which may be partly attributable to its anti-oxidative and anti-inflammatory properties. The aim of this review is to examine potential mechanisms of the actions of curcumin in both animal and human studies. Curcumin modulates relevant molecular target pathways to improve glucose and lipid metabolism, suppress inflammation, stimulate antioxidant enzymes, facilitate insulin signalling and reduce gut permeability. Curcumin also inhibits Aβ and tau accumulation in animal models and enhances mitochondria and synaptic function. In conclusion, in high-dose animal studies and in vitro, curcumin exerts a potential beneficial effect on cardiometabolic disease. However, human studies are relatively unconvincing. More intervention studies should be conducted with the new curcumin formulation with improved oral bioavailability.

Keywords: Curcumin; glucose; inflammation; insulin resistance; type 2 diabetes.

Figure 1

Chemical structure of curcuminoids.

Figure 2

The summary of potential mechanisms linking curcumin metabolites to improved glucose, lipid metabolism, antioxidative action, anti-inflammatory action and endothelial function. Refer to the text for more details. ↑—increase; ↓—decrease; ABCA1—ATP-binding cassette A1; ACAT—acyl-CoA cholesterol acyltransferase; Akt—serine/threonine kinase; AMPK—5′ adenosine monophosphate–activated protein kinase; ARE—antioxidant-responsive element; β3AR—β3-adrenergic receptor; CAT—catalase; ChREBP—carbohydrate response element-binding protein; CML—Nε-(carboxymethyl) lysine; COX-2—cyclo-oxygenase 2; CRP—C–reactive protein; CYP7A—cholesterol 7 α-hydroxylase; Egr-1—early growth response-1 gene product; eNOS—endothelial nitric oxide synthase; ER—endoplasmic reticulum; ERK1/2—extracellular signal-regulated protein kinases 1 and 2; FAS—fatty acid synthase; FOXO1—forkhead box protein O1; GCLM—γ-glutamyl-cysteine ligase; G6Pase—glucose–6–phosphatase; GK—glucokinase; GLUT4—glucose transporter 4; GPx—glutathione peroxidase; GSK-3β—glycogen synthase kinase-3 beta; GST—glutathione-S-transferase; HATs—histone acetylases; HMG-CoA reductase—3-Hydroxy-3-methylglutaryl-coenzyme A reductase; HO-1—heme oxygenase1; IL—interleukin; iNOS—inducible nitric oxide synthase; IRS1—insulin receptor substrate-1; JNK—Jun NH2-terminal kinase; LKB1—serine–threonine liver kinase B1; LOX-1—lectin-like oxidised LDL receptor; LPL—lipoprotein lipase; LPS—lipopolysaccharides; LXRα—liver X receptor alpha; MAPK—mitogen-activated protein kinase; MCP-1—monocyte chemoattractant protein 1; MDA—malondialdehyde; MGO—methylglyoxal; NF-kB—nuclear factor kappa B; mTOR—mammalian target of rapamycin; Nrf2—nuclear factor erythroid 2–related factor 2; NQO1—NAD(P)H dehydrogenase [quinone] 1; NPC1L1—Niemann-Pick C1 Like 1; PAI-1—plasminogen activator inhibitor type -1; PARP-1—poly ADP-ribose polymerase-1; PDE—phosphodiesterase; PEPCK—phosphoenolpyruvate carboxykinase; PGE2—prostaglandin E2; PI3K—phosphoinositide 3–kinase; PKC-Bii—protein kinase C; PPAR—peroxisome proliferator-activated receptor; ROS—reactive oxygen species; SCD-1—stearoyl-coenzyme A desaturase 1; SOD—superoxide dismutase; SREBP1c—sterol regulatory element-binding protein 1c; TBARS—thiobarbituric acid reactive substances; TGF-β—transforming growth factor beta; TLR4—toll-like receptors 4; TNFα—tumor necrosis factor α; UCP1—uncoupling protein 1; VEGF—vascular endothelial growth factor.