Investigating fuel poverty in the transport sector: toward a composite indicator of vulnerability

International audienceThis paper investigates the issue of fuel poverty and of its measurement in the transport sector. We seek to identify households who run the risk of facing difficulties if fuel prices increase. We show that fuel poverty indicators from the domestic sector are not satisfactory in this regard. They fail to take into account three specificities of the transport sector: (1) the diversity of travel needs, (2) restriction behaviours, and (3) variable capacities to adapt. We propose a composite indicator that targets factors of vulnerabilities. In contrast to the previous indicators, it does not solely focus on budgetary aspects but also reflects conditions of mobility. Three levels of exposition to rising fuel prices are considered, depending on the combinations of factors. We test this indicator on French data and find that 7,8% of French households are identified fuel poor, a further 7,4% fuel vulnerable and a further 3,7% fuel dependent

Comment mesurer la précarité énergétique en matière de transport

National audienceSi des indicateurs existent pour quantifier la précarité énergétique dans le logement, leur simple transposition au domaine du transport n’est pas satisfaisante. Afin de mieux identifier les ménages vulnérables à une hausse des prix des carburants, un « indicateur Composite » est proposé. Il permet de mieux refléter les différents facteurs qui contraignent la mobilité des ménages et leurs possibilités d’adaptation

HAND2 is a novel obesity-linked adipogenic transcription factor regulated by glucocorticoid signalling

Aims/hypothesis Adipocytes are critical cornerstones of energy metabolism. While obesity-induced adipocyte dysfunction is associated with insulin resistance and systemic metabolic disturbances, adipogenesis, the formation of new adipocytes and healthy adipose tissue expansion are associated with metabolic benefits. Understanding the molecular mechanisms governing adipogenesis is of great clinical potential to efficiently restore metabolic health in obesity. Here we investigate the role of heart and neural crest derivatives-expressed 2 (HAND2) in adipogenesis.MethodsHuman white adipose tissue (WAT) was collected from two cross-sectional studies of 318 and 96 individuals. In vitro, for mechanistic experiments we used primary adipocytes from humans and mice as well as human multipotent adipose-derived stem (hMADS) cells. Gene silencing was performed using siRNA or genetic inactivation in primary adipocytes from loxP and or tamoxifen-inducible Cre-ERT2 mouse models with Cre-encoding mRNA or tamoxifen, respectively. Adipogenesis and adipocyte metabolism were measured by Oil Red O staining, quantitative PCR (qPCR), microarray, glucose uptake assay, western blot and lipolysis assay. A combinatorial RNA sequencing (RNAseq) and ChIP qPCR approach was used to identify target genes regulated by HAND2. In vivo, we created a conditional adipocyte Hand2 deletion mouse model using Cre under control of the Adipoq promoter (Hand2AdipoqCre) and performed a large panel of metabolic tests.Results We found that HAND2 is an obesity-linked white adipocyte transcription factor regulated by glucocorticoids that was necessary but insufficient for adipocyte differentiation in vitro. In a large cohort of humans, WAT HAND2 expression was correlated to BMI. The HAND2 gene was enriched in white adipocytes compared with brown, induced early in differentiation and responded to dexamethasone (DEX), a typical glucocorticoid receptor (GR, encoded by NR3C1) agonist. Silencing of NR3C1 in hMADS cells or deletion of GR in a transgenic conditional mouse model results in diminished HAND2 expression, establishing that adipocyte HAND2 is regulated by glucocorticoids via GR in vitro and in vivo. Furthermore, we identified gene clusters indirectly regulated by the GR-HAND2 pathway. Interestingly, silencing of HAND2 impaired adipocyte differentiation in hMADS and primary mouse adipocytes. However, a conditional adipocyte Hand2 deletion mouse model using Cre under control of the Adipoq promoter did not mirror these effects on adipose tissue differentiation, indicating that HAND2 was required at stages prior to Adipoq expression.Conclusions/interpretation In summary, our study identifies HAND2 as a novel obesity-linked adipocyte transcription factor, highlighting new mechanisms of GR-dependent adipogenesis in humans and mice.Data availability Array data have been submitted to the GEO database at NCBI (GSE148699).</p

La précarité énergétique dans le transport

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Temporal activation of signaling pathways controlling translation initiation.

<p>(A) Temporal expression and phosphorylation of representative proteins of key signaling pathways regulating translation initiation in mouse liver during two consecutive days. Western blots were performed on total liver extracts. Naphtol blue black staining of the membranes was used as a loading control. (B) Temporal binding of EIF4E and 4E-BP1 to 7-methyl-GTP-sepharose during two consecutive days. Total liver extracts were incubated with 7-methyl-GTP beads mimicking the mRNA cap structure. After washing of the beads, bound proteins were analyzed by Western blotting. The zeitgeber times (ZT), with ZT0, lights on; ZT12, lights off, at which the animals were sacrificed, are indicated on each panel. The lines through gels indicate where the images have been cropped.</p

Rhythmic translation of ribosomal proteins in mouse liver.

<p>(A) Temporal expression profiles of microarray probes showing a rhythmic ratio of polysomal to total RNAs, ordered by phase. For visualization, data were mean centered and standardized. Log-ratios are color-coded so that red indicates high and green low relative levels of polysomal mRNAs compared to the total fraction. (B) Examples of temporal expression profiles of a subset of rhythmically translated 5′-TOP genes identified in our microarray experiment. Traces represent the levels of mRNA expression measured by microarray in the total RNA (blue line) and polysomal fraction (red line). Data are represented in log scale following standard normalization. (C) Temporal location of <i>Gapdh</i> and selected genes showing translational regulation mRNA on the different gradients obtained after polysomes purification. Pools of RNA obtained from four animals were used for each fraction at each time point. The color intensity represents for each time point the relative abundance of the mRNA in each fraction. Fractions 1–2 represent heavy polysomes, 2–3, light polysomes, and 9–10, free mRNAs. Note that even for <i>Gapdh</i> mRNA, translation slightly decreases at the end of the light period. (D) Temporal expression of selected rhythmically translated ribosomal proteins in liver cytoplasmic extracts during two consecutive days. Naphtol blue black staining of the membranes was used as a loading control. The lines through gels indicate where the images have been cropped. The zeitgeber times (ZT) at which the animals were sacrificed are indicated on each panel.</p

Temporal expression and phosphorylation of translation initiation factors.

<p>(A) Temporal mRNA expression profile of translation initiation factors in mouse liver. For each time point, data are mean ± standard error of the mean (SEM) obtained from four independent animals. (B) Temporal protein expression and phosphorylation of translation initiation factors in mouse liver during two consecutive days. Western blots were realized on total or nuclear (PER2 and BMAL1) liver extracts. PER2 and BMAL1 accumulations are shown as controls for diurnal synchronization of the animals. Naphtol blue black staining of the membranes was used as a loading control. The lines through gels indicate where the images have been cropped. The zeitgeber times (ZT), with ZT0, lights on; ZT12, lights off, at which the animals were sacrificed, are indicated on each panel.</p

Rhythmic transcription of RP mRNA and rRNA through circadian clock regulated expression of UBF1.

<p>(A) Temporal real-time RT-PCR profile of RP pre-mRNA and 45S rRNA precursor expression in mouse liver. For each time point, data are mean ± standard error of the mean (SEM) obtained from four independent animals. (B) Temporal <i>Ubf1</i> mRNA (upper panel) and protein (lower panel) expression in mouse liver. mRNA were measured by real-time RT-PCR and, for each time point, data are mean ± SEM obtained from four independent animals. UBF1 protein expression was measured by Western blot on nuclear extracts during two consecutive days. The lines through gels indicate where the images have been cropped. (C–D) Temporal <i>Ubf1</i> expression in mice devoid of a functional circadian clock. <i>Ubf1</i> expression was measured by real-time RT-PCR with liver RNAs obtained from arrhythmic <i>Cry1</i>/<i>Cry2</i> (C) and <i>Bmal1</i> (D) KO mice and their control littermates (upper panel). Data are mean ± SEM obtained from three and two animals, respectively. Black line corresponds to the WT animals and red line to the KO. Protein levels (lower panel) were measured by Western blot on nuclear extracts. The zeitgeber times (ZT) at which the animals were sacrificed are indicated on each panel. Naphtol blue black staining of the membranes was used as a loading control.</p