Identification of bioactive compounds from flowers of black elder (Sambucus nigra L.) that activate the human peroxisome proliferator-activated receptor (PPAR) gamma

TY - JOUR

T1 - Identification of bioactive compounds from flowers of black elder (Sambucus nigra L.) that activate the human peroxisome proliferator-activated receptor (PPAR) gamma

AU - Christensen, Kathrine B

AU - Petersen, Rasmus K

AU - Kristiansen, Karsten

AU - Christensen, Lars P

N1 - Keywords:Sambucus nigra;type 2 diabetes;peroxisome proliferator-activated receptor (PPAR) ¿;adipocyte differentiation;naringenin;fatty acids

PY - 2010/6

Y1 - 2010/6

N2 - Obesity is one of the predisposing factors for the development of overt Type 2 diabetes (T2D). T2D is caused by a combination of insulin resistance and β-cell failure and can be treated with insulin sensitizing drugs that target the nuclear receptor peroxisome proliferator-activated receptor (PPAR) γ. Extracts of elderflowers (Sambucus nigra) have been found to activate PPARγ and to stimulate insulin-dependent glucose uptake suggesting that they have a potential use in the prevention and/or treatment of insulin resistance. Bioassay-guided chromatographic fractionation of a methanol extract of elderflowers resulted in the identification of two well-known PPARγ agonists; α-linolenic acid and linoleic acid as well as the flavanone naringenin. Naringenin was found to activate PPARγ without stimulating adipocyte differentiation. However, the bioactivities of these three metabolites were not able to fully account for the observed PPARγ activation of the crude elderflower extracts and further studies are needed to determine whether this is due to synergistic effects and/or other ligand-independent mechanisms. Elderflower metabolites such as quercetin-3-O-rutinoside, quercetin-3-O- glucoside, kaempferol-3-O-rutinoside, isorhamnetin-3-O-rutinoside, isorhamnetin-3-O-glucoside, and 5-O-caffeoylquinic acid were unable to activate PPARγ. These findings suggest that flavonoid glycosides cannot activate PPARγ, whereas some of their aglycones are potential agonists of PPARγ.

AB - Obesity is one of the predisposing factors for the development of overt Type 2 diabetes (T2D). T2D is caused by a combination of insulin resistance and β-cell failure and can be treated with insulin sensitizing drugs that target the nuclear receptor peroxisome proliferator-activated receptor (PPAR) γ. Extracts of elderflowers (Sambucus nigra) have been found to activate PPARγ and to stimulate insulin-dependent glucose uptake suggesting that they have a potential use in the prevention and/or treatment of insulin resistance. Bioassay-guided chromatographic fractionation of a methanol extract of elderflowers resulted in the identification of two well-known PPARγ agonists; α-linolenic acid and linoleic acid as well as the flavanone naringenin. Naringenin was found to activate PPARγ without stimulating adipocyte differentiation. However, the bioactivities of these three metabolites were not able to fully account for the observed PPARγ activation of the crude elderflower extracts and further studies are needed to determine whether this is due to synergistic effects and/or other ligand-independent mechanisms. Elderflower metabolites such as quercetin-3-O-rutinoside, quercetin-3-O- glucoside, kaempferol-3-O-rutinoside, isorhamnetin-3-O-rutinoside, isorhamnetin-3-O-glucoside, and 5-O-caffeoylquinic acid were unable to activate PPARγ. These findings suggest that flavonoid glycosides cannot activate PPARγ, whereas some of their aglycones are potential agonists of PPARγ.

U2 - 10.1002/ptr.3005

DO - 10.1002/ptr.3005

M3 - Journal article

C2 - 20222152

SN - 0951-418X

VL - 24

SP - 129

EP - 132

JO - Phytotherapy Research

JF - Phytotherapy Research

IS - Suppl 2

ER -