Complementary analytical methods for the phytochemical investigation of ‘Jardin de Granville’, a rose dedicated to cosmetics

Abstract‘Jardin de Granville’ is a new hybrid rose variety dedicated to cosmetic applications. To perform an exhaustive molecular investigation of the non-volatile secondary metabolites in this cultivar, a global approach was developed, combining four chromatographic techniques (HPTLC, HPLC-DAD-ELSD, UHPLC-HRMS and GC–MS). This approach afforded an on-line phytochemical fingerprinting of four plant organs of ‘Jardin de Granville’. Despite the wide diversity of molecular families and the pronounced differences in polarity between the molecules, this analytical strategy enabled an overview of the molecular composition of each sample to be rapidly obtained by HPTLC and HPLC and the molecular content to be correctly identified thanks to coupling with mass spectrometry. Polyphenols were identified in the EtOH/H2O extracts; triterpenes, chlorophyll derivatives and lipids were characterized in the EtOAc extracts, and the fatty acids squalene, α-tocopherol and β-sitosterol were highlighted in the heptane extracts

Cartographies de polluants atmosphériques : influence de l’échantillonnage spatial sur la qualité de l’estimation

National audienc

Evaluation of numerical models used to simulate atmospheric pollution near roadways

International audienc

The over-expression of miR-200a in the hypothalamus of ob/ob mice is linked to leptin and insulin signaling impairment.

International audienceEarly in life, leptin plays a crucial role in hypothalamic neural organization. Leptin, most likely, controls neural gene expression conferring then specific phenotype regarding energy homeostasis. MicroRNAs are new regulators for several physiological functions, including the regulation of metabolism. However, the impact of leptin on hypothalamic microRNA patterns remains unknown. Here, we demonstrate that miR-200a, miR-200b and miR-429 are up-regulated in the hypothalamus of genetically obese and leptin deficient ob/ob mice. Leptin treatment down-regulates these miRNAs in ob/ob hypothalamus. The hypothalamic silencing of miR-200a increased the expression level of leptin receptor and insulin receptor substrate 2, reduced body weight gain, and restored liver insulin responsiveness. In addition, the overexpression of pre-miR-200a in a human neuroblastoma cell line impaired insulin and leptin signaling. These findings link the alteration of leptin and insulin signaling to the up-regulation of hypothalamic miR-200a which could be a new target for treatment of obesity

Maternal resistin predisposes offspring to hypothalamic inflammation and body weight gain

International audienceResistin promotes hypothalamic neuroinflammation and insulin resistance through Toll like receptor 4 (TLR4), this hormone is thought to be a link between obesity and insulin-resistance. Indeed, resistin plasma levels are higher in obese and insulin resistant subjects. However, the impact of maternal resistin on the predisposition of offspring to hypothalamic neuroinflammation is unknown. Here, female mice were treated with resistin during gestation/lactation periods, then hypothalamic neuroinflammation was investigated in male offspring at p28 and p90. At p28, resistin increased the expression of inflammation markers (IL6, TNFα and NFκB) and TLR4 in the hypothalamus and decreased both hypothalamic insulin and leptin receptors' expression. The hypothalamic up-regulation IL6, TNFα and TLR4 was sustained until p90 promoting most likely hypothalamic inflammation. Maternal resistin also increased IL6 and TNFα in the adipose tissue of offspring at p90 associated with a higher body weight gain. In contrast, liver and muscle were not affected. These findings reveal that the augmentation of maternal resistin during gestation and lactation promotes hypothalamic and adipose tissue inflammation of offspring as evidenced by sustained increase of inflammation markers from weaning to adulthood. Thus, maternal resistin programs offspring hypothalamic and adipose tissue inflammation predisposing then offspring to body weight gain