Obesogen effects after perinatal exposure of 4,4'-sulfonyldiphenol (Bisphenol S) in C57BL/6 mice.

Bisphenol A were removed from consumer products and replaced by chemical substitutes such as Bisphenol S (BPS). Based on their structural similarity, BPS may be obesogen like Bisphenol A in mice. Our objective was to determine the impact of BPS on lipid homeostasis in C57Bl/6 mice after perinatal and chronic exposure. Pregnant mice were exposed to BPS via the drinking water (0.2; 1.5; 50µg/kg bw/d). Treatment began at gestational day 0 and continued in offspring up to 23-weeks old. Then, offspring mice were fed with a standard or high fat diet. The body weight, food consumption, fat mass and energy expenditure were measured. A lipid load test was performed to check the postprandial triglyceridemia. Plasma parameters and mRNA gene expression in adipose tissues were also analysed. BPS induced overweight in male mice offspring fed with a HFD at the two highest doses. There was no change in food intake and energy expenditure. The overweight was correlated to the fat mass, hyperinsulinemia and hyperleptinemia. The plasma triglyceride clearance was significantly increased with BPS and tyloxapol(®) (triglyceride clearance inhibitor) reversed this phenomenon. BPS induced alteration in mRNA expression of marker genes involved in adipose tissue homeostasis: hormone sensitive lipase, PPARγ, insulin receptor, SOCS3 and adiponectin. This is the first time that BPS is described as obesogenic at low doses and after perinatal and chronic exposure in male mice. BPS potentiated the obesity induced by a HFD by inducing the lipid storage linked to faster lipid plasma clearance.

BPA, an energy balance disruptor.

Bisphenol A (BPA) is used extensively in the world and is present in a diverse range of manufactured articles including dental resins, polycarbonate plastics, and the inner coating of food cans. It is a high volume chemical, with global production at 3.6 × 10(9) kg per year. BPA was identified as a high priority for assessment of human health risk because it was considered to present greatest potential for human exposure. Most studies of the health effects of BPA have focused on endocrine disruption leading to reproductive toxicity, but it displays additional side effects, including liver damage, disrupted pancreatic ß-cell function, thyroid hormone disruption, and obesity-promoting effects. In this article, we reviewed specifically on the effects of BPA in energy balance.

Role of CD36 in oral and postoral sensing of lipids.

Obesity and associated plethora of diseases constitute a major public health challenge worldwide. The conjunction of profound changes in our lifestyle and a thrifty genetic that evolved in an environment of food scarcity largely explains this epidemic situation. Food abundance promotes our specific appetite for the more palatable food generally rich in lipids. It is noteworthy that this attraction for fatty food is not specific to humans. Rats and mice also spontaneously prefer lipid-rich food in a free-choice situation. Detection of lipids in food requires the presence of specific sensors located in strategic places (e.g., oral cavity, small intestine, brain) whose activation results in a modulation of the eating behavior. Recent data strongly suggest that the glycoprotein CD36 plays a significant role in this sensing system.

Cell signaling mechanisms of gustatory perception of lipids: can the taste cells be the target of anti-obesity agents?

It has been well propounded that there exists five basic taste modalities, e.g., sweet, sour, bitter, salty and umami. Recent compelling evidence from rodents and human beings raises the possibility for an additional sixth taste modality devoted to the perception of lipids. A number of studies have suggested that lingual CD36, a glycoprotein, mainly expressed by circumvallate papillae of the tongue, might be implicated in the perception of dietary fat taste. G protein-coupled receptors (GPCRs) are important signaling molecules for many aspects of cellular function. It has been recently shown that these receptors particularly GPR40 and GPR120 might also be involved in lipid taste perception. In this article, we highlight the cell activation mechanisms, responsible for the downstream cell signaling which might help understand the lipid-mediated regulation of feeding behavior, critically involved in the development of several diseases like obesity and other metabolic disorders. We also raise the question whether lipid gustatory cells can be the target of anti-obesity strategies.

[Preliminary evaluation of the insecticide susceptibility in Anopheles gambiae and Culex quinquefasciatus from Lobito (Angola), using WHO standard assay]. / Premiers tests OMS d'évaluation de la sensibilité aux insecticides chez Anopheles gambiae et Culex quinquefasciatus à Lobito, Angola.

Field collections of the most common urban mosquito vectors Anopheles gambiae and Culex quinquefasciatus were carried out in June 2003, March 2004 and November 2005 to gather preliminary data on the insecticide susceptibility in mosquitoes from Lobito (Angola) using the WHO standard bioassays. Bioassays were performed on F0 adults emerging from the field larval collections and on unfed adults from landing catches on volunteers. Batches of mosquitoes from three selected locations (Alto Liro, San Jao and Bela Vista) were exposed for 1 hour to several insecticides such as DDT 4%, carbosulfan 0.4%, permethrin 1%, deltamethrin 0.05% and cyfluthrin 0.15%, in order to estimate the immediate knockdown times (kdT50 and kdT95) and the mortality rate after exposure. The results revealed that mosquito susceptibility to insecticides varied depending on the insecticide, the site and the period of collection. The main local malaria vector A. gambiae (both M and S forms) was basically resistant to DDT and susceptible to all pyrethoids, regardless of the period and the site of collections. The overall mortality rate due to DDT was 73% in Alto Liro, 89% in San Jao and varied depending on the period in Bela Vista between 95% in March 2004 and 100% in November 2005. The mortality due to pyrethoids was 100% at all locations, with the kdT50 and KdT95 times ranging between 9 and 16 minutes and between 18 and 29 minutes, respectively. Concerning the C. quinquefasciatus, populations from Yard and Caponte were resistant to all insecticides tested; the mortality rate was 40% with deltamethrin and 70% with permethrin, while no lethal effect was observed with DDT or carbosulfan. In conclusion, despite its probable high resistance to DDT, the main local malaria vector A. gambiae remained fully susceptible to pyrethroids. This could forecast a good biological efficacy of the scheduled vector control interventions in Angola, based on a large-scale distribution of long-lasting, insecticide-treated nets and on the implementation of indoor residual spraying. The local vector control programme must include well-adapted IEC campaigns and full participation of the community for better management of the insecticide resistance in targeted mosquitoes and for better control of malaria vector populations.

Orosensory perception of dietary lipids in mammals.

Obesity constitutes a major public health problem for the twenty-first century, with its epidemic spread worldwide, particularly in children. The overconsumption of fatty foods greatly contributes to this phenomenon. Rodents and humans display a spontaneous preference for lipid-rich foods. However, the molecular mechanisms underlying this pattern of eating behaviour in mammals remain unclear. The orosensory perception of dietary lipids was long thought to involve only textural and olfactory cues. Recent findings challenge this limited viewpoint, strongly suggesting that the sense of taste also plays a significant role in dietary lipid perception and might therefore be involved in the preference for fatty foods and obesity. This minireview analyses recent data relating to the molecular mechanisms and physiological consequences of this means of orosensory lipid perception.

Surnotification du paludisme : l'exemple des consultations dans les centres de sante de Lobito; Angola

Dans la region holo et hyperendemiques du paludisme; une definition simple de l'acces palustre ne peut pas se fonder sur les donnees cliniques ni sur la densite parasitaire sanguine; quand on la connait ; D'autres variables doivent etre prises en compte; en fonction de l'epidemiologie de chaque region. Dans une region de transmission moyenne; hypo ou mesoendemique; la parasitologie reste importante pour confirmer un diagnostic. Les auteurs ont fait l'experience pendant cinq ans dans une surnotification du paludisme du fait d'un taux excessif d'examens paracliniques rendus positifs. Ils concluent que cet etat de fait n'est pas bon; ni pour la prise en charge de l'acces palustre simple ou d'autres pathologies infectieuses; ni pour les releves epidemiologiques. Le rapport 2008 sur le paludisme de l'OMS avait deja note ce fait en soulignant que de nombreuses statistiques du centre de sante en zone endemique se fondaient sur des donnees cliniques; ce qui entrainait une surestimation de la situation endemique. Beaucoup d'elements sont a prendre en consideration dans cette situation; qui pourrait etre corrigee par une revalorisation du diagnostic parasitologique surtout dans les zones isolees et la creation d'un reseau de diagnostic; capable de renforcer la prise en charge des cas au niveau individuel et le recueil epidemiologique au niveau global

Enquetes paludometriques en 2006 et 2007 dans la province de Benguela; Angola

Une bonne connaissance du facies epidemiologique est la prealable a toute activite de lutte antipaludique. La definition de ce facies epidemiologique doit reposer sur des donnees fiables; or les informations provenant des formations sanitaires sont parfois incorrectes et toujours parcellaires. Ainsi; les diagnostics parasitologiques errones entrainent souvent une mauvaise appreciation du degre d'epidemie palustre. La mise en place des sites sentinelles beneficiant d'un bon monitorage permet des evaluations epidemiologiques correctes. Dans ces travaux; les indices paludometriques obtenus a partir d'une serie enquetes trasversales a passage unique sont ressortis dans trois zones aux situations geographiques et ecologiques differentes et a differentes periodes de l'annee. Cette information est capitale avant la mise en place des methodes de lutte en perspective

Do we taste fat?

Sense of taste informs the body about the quality of ingested foods. Five sub-modalities allowing the perception of sweet, salty, sour, bitter, and umami stimuli are classically depicted. However, the inborn attraction of mammals for fatty foods raises the possibility of an additional orosensory modality devoted to fat perception. For a long time, dietary lipids were thought to be detected only by trigeminal (texture perception), retronasal olfactory, and post-ingestive cues. This minireview analyses recent findings showing that gustation also plays a significant role in dietary lipid perception.

Simple method to obtain symmetry harmonics of point groups.

We propose a simple, self-consistent method to obtain basis functions of irreducible representations of a finite point group. Our method is based on eigenproblem formulation of a projection operator represented as a nonhomogeneous polynomial of angular momentum L. The method is shown to be more efficient than the usual numerical methods when applied to the analysis of high-order symmetry harmonics in cubic and icosahedral groups. For low-order symmetry harmonics the method provides rational coefficients of expansion in the Y(L,M) basis.

[Impact of a new parasitologic laboratory for malaria diagnosis on diagnosis and cost of malaria in a company setting: experience from Angola]. / Impact de la création d'un laboratoire de diagnostic parasitologique du paludisme sur le diagnostic et le cout du paludisme dans une entreprise: une expérience Angolaise.

In malaria endemic areas treating every fever episode as a malaria onset would result in overdiagnosis with a margin of the error varying in function of epidemiological factors. When further compounded by overestimation related to errors in parasitologic diagnosis, clinical misdiagnosis leads to unwarranted hospitalization and inappropriate treatment. In a company setting this would mean unnecessary loss of employee work time. False positive diagnosis causes overestimation of chemoresistance, overconsumption of antimalarial drugs and underestimation of other infectious diseases. Judging from these high costs, it can be assumed that improving the reliability of parasitologic diagnosis would have a positive impact on the quality of clinical management, efficiency of antimalarial use and accuracy of epidemiological surveys. This assumption was confirmed by analysis of data following start-up of a parasitologic laboratory for malaria diagnosis in the health care clinic at Sonamet's fabrication yard in Lobito, Angola. Laboratory personnel receives expert training and audit findings demonstrate consistently reliable diagnosis. This experience underscores the need for reliable parasitologic diagnosis as a prerequisite for any large-scale malaria control program.

Cholesterol dependent downregulation of mouse and human apical sodium dependent bile acid transporter (ASBT) gene expression: molecular mechanism and physiological consequences.

BACKGROUND AND AIMS: Faecal bile acid elimination greatly contributes to cholesterol homeostasis. Synthesised from cholesterol in the liver, bile acids are actively reclaimed in the ileum by the apical sodium dependent bile acid transporter (ASBT). Although the expression level of ASBT affects body cholesterol balance, the impact of cholesterol on ASBT gene expression remains unclear. In this study, the effect of cholesterol on ASBT expression and ileal bile acid uptake was explored in vivo and in vitro. METHODS: ASBT gene expression was assessed by real time quantitative polymerase chain reaction and northern or western blotting, or both, in mice subjected to a 2% cholesterol diet for two weeks, in mouse ileal explants, or in human enterocyte-like Caco-2 cells cultured in sterol enriched or depleted media. Bile acid uptake was determined by measuring [3H]-taurocholic acid influx into in situ isolated ileal loops from mice or into differentiated Caco-2 cells. Molecular analysis of mouse and human ASBT promoters was undertaken with reporter assays, site directed mutagenesis, and electrophoretic mobility shift assays. RESULTS: In mice, cholesterol enriched diet triggered a downregulation of ASBT expression (mRNA and protein), a fall in ileal bile acid uptake, and a rise in the faecal excretion of bile acids. This effect was direct as it was reproduced ex vivo using mouse ileal explants and in vitro in differentiated Caco-2 cells. CONCLUSIONS: This regulation, which involves an original partnership between SREBP-2 and HNF-1alpha transcription factors, affects ileal bile acid recycling and thus might participate in the maintenance of body cholesterol homeostasis.

Impact de la creation d'un laboratoire de diagnostic parasitologique du paludisme sur le diagnostic et le cout du paludisme dans une entreprise : experience angolaise

En zone d'endemie palustre; il est abusif de considerer comme paludisme tout acces febrile; la marge d'erreur variant avec le facies geoclimatique. Quant a cette sur- estimation clinique s'ajoute une sureva l u ation par le diagnostic parasitologique; la gestion du paludisme peut s'alourdir d'inutiles hospitalisations et de traitements repetes; et; dans le cadre d'une entreprise industrielle;d'un nombre considerable de journees inutilement perdues. Les diagnostics positifs errones amenent l'evocation injustifiee de cas de chimioresistance en entrainant une surconsommation d'antipaludiques de derniere generation; tout en occultant les pathologies non palustres. L'absence de fiabilite de l'examen parasitologique se paye donc au prix fort; et seul son retablissement permet une prise en charge clinique de qualite; l'emploi au plus juste des antipaludiques; et des eva l u ations epidemiologiques correctes. C'est la lecon tiree de l'evolution des donnees observees apres implantation; dans le service medical d'une entreprise; d'un laboratoire de diagnostic parasitologique supervise et regulierement audite par des experts. Le constat amene a rappeler que la disponibilite d'un diagnostic parasitologique de qualite est un prealable a toute ambition de controle antipaludique probablement aussi a grande echelle

The gene encoding the human ileal bile acid-binding protein (I-BABP) is regulated by peroxisome proliferator-activated receptors.

Peroxisome proliferator-activator receptors (PPAR) are involved in cholesterol homeostasis through the regulation of bile acids synthesis, composition, and reclamation. As ileal bile acid-binding protein (I-BABP) is thought to play a crucial role in the enterohepatic circulation of bile acids, we investigated whether I-BABP gene expression could also be affected by PPAR. Indeed, treatment with the PPARalpha-PPARbeta/delta agonist bezafibrate led to the up-regulation of I-BABP mRNA levels in the human intestine-derived Caco-2 cells. Cotransfections of the reporter-linked human I-BABP promoter (hI-BABP-2769/+44) together with PPAR and RXR expression vectors demonstrated that the fibrate-mediated induction of the I-BABP gene is dependent on PPARalpha or PPARbeta/delta. Using progressive 5' deletions of the hI-BABP promoter and sequence analysis, we identified a putative PPAR-binding site located at the position -198 and -186 upstream of the transcription initiation site. Electrophoretic mobility shift assays showed that the PPAR/RXR heterodimer can specifically bind to this PPRE-like motif. The deletion of the PPRE within the hI-BABP promoter abolished the PPAR-mediated transactivation in transient transfection assays. The regulation of the I-BABP promoter by PPAR appears species-specific, as the mouse I-BABP promoter, which lacks a conserved PPRE, was not responsive to exogenous PPAR expression in the presence of bezafibrate. Our findings show that the I-BABP gene may be a novel target for PPAR in humans and further emphasize the role for PPAR in the control of bile acid homeostasis.

Hyperinsulinaemia triggered by dietary conjugated linoleic acid is associated with a decrease in leptin and adiponectin plasma levels and pancreatic beta cell hyperplasia in the mouse.

AIMS/HYPOTHESIS: Dietary supplementation with conjugated linoleic acids (CLA) has a fat-reducing effect in various species, but induces severe hyperinsulinaemia and hepatic steatosis in the mouse. This study aimed to determine the causes of the deleterious effects of CLA on insulin homeostasis. METHODS: The chronology of adipose and liver weight, hepatic triglyceride accumulation and selected blood parameters, including lipids, insulin, leptin and adiponectin, was determined in C57BL/6J female mice fed a 1% isomeric mixture of CLA for various periods of time ranging from 2 to 28 days. Insulin secretion was measured in 1-h static incubations of pancreatic islets, and pancreas morphometric parameters were determined in mice fed CLA for 28 days. RESULTS: Plasma levels of leptin and adiponectin sharply decreased after 2 days of CLA feeding, although adipose tissue mass only decreased after day 6. Hyperinsulinaemia developed at day 6 and consistently worsened up to day 28, in parallel with increases in hepatic lipid content. Islets from CLA-fed mice displayed three- to four-fold increased rates of glucose-stimulated insulin secretion, both in the absence and presence of isobutyl methylxanthine or carbachol. The increased insulin-releasing capacity of islets from CLA-fed mice was explained by an increase in beta cell mass and number. CONCLUSIONS/INTERPRETATION: The data suggest that CLA supplementation induces a profound reduction of leptinaemia and adiponectinaemia, followed by hyperinsulinaemia due to the increased secretory capacity of pancreatic islets, leading, in turn, to liver steatosis. These observations cast doubt on the safety of dietary supplements containing CLA.

Development of conjugated linoleic acid (CLA)-mediated lipoatrophic syndrome in the mouse.

Conjugated linoleic acids (CLA) are positional and geometric dienoic isomers of linoleic acid. Dietary CLA supplementation leads to a drop in fat mass in various species, including in humans. The t10,c12-CLA isomer is responsible for this anti-obesity effect. The reduction of fat mass is especially dramatic in the mouse, in which it is associated with severe hyperinsulinemia, insulin resistance and massive liver steatosis. The origin of these adverse side effects and putative chronology of events leading to CLA-mediated lipoatrophic syndrome are presented and discussed in this review.

Dietary lipids modify intestinal lipid-binding protein RNA abundance in diabetic and control rats.

BACKGROUND: Lipid-binding proteins have been identified in the enterocyte, including the cytosolic intestinal and liver fatty acid binding proteins (I-FABP and L-FABP, respectively) as well as the brush border membrane fatty acid transporter (FAT). It is unclear whether variations in the type of dietary lipids or diabetes modify the RNA abundance of these proteins. Diabetes is associated with an increased intestinal lipid uptake, and the lipid uptake is greater in rats fed a semisynthetic saturated fatty acid (SFA) as compared with a polyunsaturated fatty acid (PUFA) diet. METHODS: Male Sprague-Dawley rats were injected with streptozotocin or control vehicle and fed chow or either SFA or PUFA for 2 weeks. Northern blotting was performed on RNA isolated from jejunal and ileal tissues. RESULTS: In controls, feeding SFA as compared with PUFA reduced the jejunal abundance of I-FABP and L-FABP RNA. In diabetic rats, feeding SFA increased the ileal FAT RNA. Feeding PUFA reduced jejunal L-FABP and ileal FAT RNA in diabetic rats as compared with controls. CONCLUSIONS: The enhanced lipid uptakes reported with feeding an SFA diet or with diabetes were not associated with parallel alterations in lipid-binding proteins. We speculate that these lipid-binding proteins act as a storage mechanism for lipids in enterocytes and are not directly involved in lipid uptake.

Erbium-doped fiber laser simultaneously mode locked on more than 24 wavelengths at room temperature.

We demonstrate simultaneous mode locking of more than 24 wavelengths at 3 GHz in an actively mode-locked erbium-doped fiber laser operating at room temperature. The multiwavelength operation is achieved when a frequency shifter and an all-fiber 50-GHz periodic filter are inserted into a ring cavity. Active mode locking is performed with an amplitude modulator, and pulses with a FWHM of 30 ps are obtained.

Oscillating bubbles at the tips of optical fibers in liquid nitrogen.

We report that a bubble with a radius of a few micrometers may be created at a precise location on a metal-coated optical fiber tip immersed in liquid nitrogen by microsecond optical pulses with peak powers of less than 20 mW. Dynamic optical measurements reveal that after termination of the optical pulse the bubble exhibits stable oscillations for several tens of microseconds, at frequencies up to several megahertz, as it slowly collapses.

Differential involvement of peroxisome-proliferator-activated receptors alpha and delta in fibrate and fatty-acid-mediated inductions of the gene encoding liver fatty-acid-binding protein in the liver and the small intestine.

Liver fatty-acid-binding protein (L-FABP) is a cytoplasmic polypeptide that binds with strong affinity especially to long-chain fatty acids (LCFAs). It is highly expressed in both the liver and small intestine, where it is thought to have an essential role in the control of the cellular fatty acid (FA) flux. Because expression of the gene encoding L-FABP is increased by both fibrate hypolipidaemic drugs and LCFAs, it seems to be under the control of transcription factors, termed peroxisome-proliferator-activated receptors (PPARs), activated by fibrate or FAs. However, the precise molecular mechanism by which these regulations take place remain to be fully substantiated. Using transfection assays, we found that the different PPAR subtypes (alpha, gamma and delta) are able to mediate the up-regulation by FAs of the gene encoding L-FABP in vitro. Through analysis of LCFA- and fibrate-mediated effects on L-FABP mRNA levels in wild-type and PPARalpha-null mice, we have found that PPARalpha in the intestine does not constitute a dominant regulator of L-FABP gene expression, in contrast with what is known in the liver. Only the PPARdelta/alpha agonist GW2433 is able to up-regulate the gene encoding L-FABP in the intestine of PPARalpha-null mice. These findings demonstrate that PPARdelta can act as a fibrate/FA-activated receptor in tissues in which it is highly expressed and that L-FABP is a PPARdelta target gene in the small intestine. We propose that PPARdelta contributes to metabolic adaptation of the small intestine to changes in the lipid content of the diet.