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DOI: 10.1055/s-0030-1264931
Elderflowers (Sambucus nigra L.) have a significant impact on cellular mechanisms related to lipid storage and insulin resistance
Preparations of elderflowers (Sambucus nigra L.) have traditionally been used as diuretics however recent studies suggest that they also have a potential use in the treatment/prevention of conditions associated with the metabolic syndrome. Extracts of elderflowers are known to activate the key regulator of adipocyte differentiation, peroxisome proliferator-activated receptor (PPAR)γ, without stimulating adipocyte differentiation, and furthermore to enhance insulin-stimulated glucose uptake (GU) in adipocytes [1]. The flavanone naringenin was identified as one of the bioactive components whereas major elderflower metabolites were not active [2]. In the present study, we have further investigated the effects of elderflower extracts and metabolites on mechanisms associated with lipid storage and insulin resistance in relation to the metabolic syndrome. Both dichloromethane (DCM) and methanol (MeOH) extracts of elderflowers were found to be able to enhance GU in pig myotubes both with and without insulin-stimulation corresponding with previous studies on mouse abdominal muscle [3]. The nematode Caenorhabditis elegans provides an excellent model system for studying lipid metabolism and fat accumulation in vivo. Extracts of elderflowers were able to significantly reduce fat accumulation as measured by the lipophilic dye Nile red, in C. elegans at concentrations of 200µg/mL, and in particular the DCM extract was one of the most potent plant extracts with more than a 50% reduction of Nile red fluorescence [4]. However, on individual basis major elderflower metabolites do not seem to possess the same magnitude of bioactivity in the tests performed as the extracts. Hence, synergistic effects might be at play warranting further investigations.
References: 1. Christensen KB et al. (2009) Phytother. Res. 23: 1316–1325.
2. Christensen KB et al. (2010) Phytother. Res. in press.
3. Gray AM et al. (2000)J. Nutri. 130: 15–20.
4. Boelt SG et al. (2008) Chem. Physics Lipids 154: S32-S32.