Attentional bias and response inhibition in severe obesity with food disinhibition: a study of P300 and N200 event-related potential

International audienceBACKGROUND/OBJECTIVE: In obesity there is growing evidence for common mechanism between food intake regulation and substance use disorders, especially more attentional bias and less cognitive control. In the present study we investigated whether severely obese subjects with or without disordered eating exhibit electroencephalographic (EEG) event-related potential (ERP) modifications as observed in substance abusers. SUBJECTS/METHODS: A total of 90 women were included; 30 in the normal-weight (NW) group (18.5 \textless BMI \textless 24.5 kg/m(2); no food disinhibition or restriction on the Three-Factor Eating Questionnaire) and 60 participants with BMI \textgreater/= 35 kg/m(2) were separated into two groups (n = 30): without food disinhibition (disinhibition score \textless/=8; ObFD- group) and with food disinhibition (score \textgreater8; ObFD+). Clinical and metabolic parameters as well as compartmental aspects (Eating Disorders Inventory-2, EDI-2) were assessed. Participants underwent an ERP recording with an auditory oddball paradigm. RESULTS: The mean +/- SD P300 amplitudes in Pz were significantly (p \textless 0.05) lower in ObFD- (12.4 +/- 4.6) and ObFD+ (12.5 +/- 4.4) groups than in the NW group (15.8 +/- 5.9). The mean +/- SD N200 amplitude in Cz was significantly lower in the ObFD- group (-2.0 +/- 5.4) than in the NW group (-5.2 +/- 4.2 vs; p = 0.035). N200 Cz amplitude was correlated with EDI-2 Binge eating risk score (rho = 0.331; p = 0.01), EDI-2 Body Dissatisfaction score (rho = 0.351; p = 0.007), and Drive for Thinness score (rho = 0.26; p = 0.05). CONCLUSIONS: The present study provides evidence for reduction of P300 and N200 amplitude in obese women and that N200 amplitude may be related to more disordered eating and eating disorder risk. This leads to consider attentional bias and response inhibition as core mechanisms in obesity and as possible targets for new therapeutic strategy

Cinétiques postprandiales d’absorption et d’oxydation des lipides selon l’état émulsionné de la matière grasse ingérée chez le volontaire de poids normal ou obèse

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Ghrelin concentration as an indicator of eating-disorder risk in obese women

International audienceAim. - Eating disorders (EDs), disordered eating (DE) and obesity are thought to have overlapping aetiological processes. DE in obesity can jeopardize weight-loss results, and acyl ghrelin (AG) is a hormone that stimulates food intake and reward processes. The main study objective was to determine whether higher-than-expected concentrations of AG in common obesity are associated with DE symptoms. Methods. - The study population included 84 women, aged 20-55 years, free of established EDs: 55 were severely obese (OB) and 29 were of normal weight (NW). OB participants were stratified into two groups according to their median concentration of fasting AG distribution. The OB women with a high fasting plasma ghrelin concentration (HGC) were compared with both OB women with a low fasting plasma ghrelin concentration (LGC) and NW women. Participants were assessed by the Eating Disorder Inventory (EDI-2), Three-Factor Eating Questionnaire (TFEQ) and Hospital Anxiety and Depression Scale (HADS). Fasting glucose, insulin, leptin and ghrelin plasma concentrations were also quantified. Results. - Between the two AG groups of OB women, there was no statistical difference in either anthropometric or metabolic parameters, HADS, TFEQ or fasting hunger scores. However, the HGC group scored significantly higher than the LGC group on the drive-for-thinness subscale of EDI-2 (9.30 +/- 0.99 vs. 6.46 +/- 0.83, respectively; P = 0.033). Conclusion. - Results support the hypothesis of a potential relationship between fasting plasma AG concentrations and ED risk, regardless of mood and anxiety. AG may be considered a potential biomarker of vulnerability for developing EDs. (C) 2018 Elsevier Masson SAS. All rights reserved

Starch digestibility modulation significantly improves glycemic variability in type 2 diabetic subjects: A pilot study

International audienceBACKGROUND AND AIMS: In type 2 diabetes (T2D) patients, the reduction of glycemic variability and postprandial glucose excursions is essential to limit diabetes complications, beyond HbA1c level. This study aimed at determining whether increasing the content of Slowly Digestible Starch (SDS) in T2D patients' diet could reduce postprandial hyperglycemia and glycemic variability compared with a conventional low-SDS diet. METHODS AND RESULTS: For this randomized cross-over pilot study, 8 subjects with T2D consumed a controlled diet for one week, containing starchy products high or low in SDS. Glycemic variability parameters were evaluated using a Continuous Glucose Monitoring System. Glycemic variability was significantly lower during High-SDS diet compared to Low-SDS diet for MAGE (Mean Amplitude of Glycemic Excursions, p \textless 0.01), SD (Standard Deviation, p \textless 0.05), and CV (Coefficient of Variation, p \textless 0.01). The TIR (Time In Range) [140-180 mg/dL[ was significantly higher during High-SDS diet (p \textless 0.0001) whereas TIRs ≥180 mg/dL were significantly lower during High-SDS diet. Post-meals tAUC (total Area Under the Curve) were significantly lower during High-SDS diet. CONCLUSION: One week of High-SDS Diet in T2D patients significantly improves glycemic variability and reduces postprandial glycemic excursions. Modulation of starch digestibility in the diet could be used as a simple nutritional tool in T2D patients to improve daily glycemic control. REGISTRATION NUMBER: in clinicaltrials.gov: NCT03289494

Overfeeding increases postprandial endotoxemia in men: Inflammatory outcome may depend on LPS transporters LBP and sCD14

International audienceSCOPE: Low-grade inflammation is a recognized hallmark of obesity. Endotoxins absorbed after high-fat meals have recently been implicated. Plasma lipopolysaccharides binding protein (LBP) and soluble cluster of differentiation 14 (sCD14) have also been suggested as clinical markers of endotoxemia. In mice, the ratio LBP/sCD14 has been associated with high fat diet induced inflammation. We tested the hypothesis that healthy subjects develop inflammation differently during weight gain according to changes of LBP/sCD14 ratio. METHODS AND RESULTS: Eighteen healthy men were overfed during 8 wk (+760 kcal/day). Endotoxemia, sCD14, LBP, and IL-6 were measured before and after overfeeding (OF) at fasting (n = 18) and postprandially (subcohort, n = 8). OF did not modify fasting IL-6 but increased the LBP/sCD14 ratio (P = 0.017). Subjects were categorized into tertiles for LBP/sCD14 ratio variation. Subjects in the highest tertile (+90% LBP/sCD14) increased plasma IL-6 (+26%) versus the lowest tertile due to a decrease of sCD14 associated with high LBP. The postprandial accumulation of endotoxins increased after OF (+160%). However, only four responding subjects presented increased postprandial IL-6 accumulation. CONCLUSION: OF increases postprandial endotoxemia but the inflammatory outcome may be modulated by endotoxin handling in plasma. This study supports a new concept whereby inflammation setup during the initial phase of weight gain is linked to the relative variations of LBP and sCD14

Postprandial Endotoxin Transporters LBP and sCD14 Differ in Obese vs. Overweight and Normal Weight Men during Fat-Rich Meal Digestion

International audienceCirculating levels of lipopolysaccharide-binding protein (LBP) and soluble cluster of differentiation 14 (sCD14) are recognized as clinical markers of endotoxemia. In obese men, postprandial endotoxemia is modulated by the amount of fat ingested, being higher compared to normal-weight (NW) subjects. Relative variations of LBP/sCD14 ratio in response to overfeeding are also considered important in the inflammation set-up, as measured through IL-6 concentration. We tested the hypothesis that postprandial LBP and sCD14 circulating concentrations differed in obese vs. overweight and NW men after a fat-rich meal. We thus analyzed the postprandial kinetics of LBP and sCD14 in the context of two clinical trials involving postprandial tests in normal-, over-weight and obese men. In the first clinical trial eight NW and 8 obese men ingested breakfasts containing 10 vs. 40 g of fat. In the second clinical trial, 18 healthy men were overfed during 8 weeks. sCD14, LBP and Il-6 were measured in all subjects during 5 h after test meal. Obese men presented a higher fasting and postprandial LBP concentration in plasma than NW men regardless of fat load, while postprandial sCD14 was similar in both groups. Irrespective of the overfeeding treatment, we observed postprandial increase of sCD14 and decrease of LBP before and after OF. In obese individuals receiving a 10 g fat load, whereas IL-6 increased 5h after meal, LBP and sCD14 did not increase. No direct association between the postprandial kinetics of endotoxemia markers sCD14 and LBP and of inflammation in obese men was observed in this study

Design and Validation of a Diet Rich in Slowly Digestible Starch for Type 2 Diabetic Patients for Significant Improvement in Glycemic Profile

International audienceThis study aimed at designing a-diet high in slowly digestible starch (SDS) by carefully selecting high-SDS starchy products and to validate its implementation, acceptance, and impact on the postprandial glycemic response in patients with type 2 diabetes (T2D). Starchy products were screened and classified as being either high (high-SDS) or low (low-SDS) in SDS (in vitro SDS method). A randomized controlled cross-over pilot study was performed: Eight patients with T2D consumed randomly a high-SDS or a low-SDS diet for one week each, while their glycemic profile was monitored for 6 days. Based on 250 food product SDS analyses and dietary recommendations for patients with T2D, the high-SDS and low-SDS diets were designed. The high-SDS diet significantly increased SDS intake and the SDS/carbohydrates proportion compared to the low-SDS diet (61.6 vs. 11.6 g/day and 30% vs. 6%; p \textless 0.0001, respectively). Increasing the SDS/carbohydrate proportion to 50% of the meal was significantly correlated with a 12% decrease in tAUC0-120 min and a 14% decrease in the glycemic peak value (p \textless 0.001 for both). A high-SDS diet can be easily designed by carefully selecting commercial starchy products and providing relevant recommendations for T2D to improve their glycemic profile

Subcutaneous Adipose Tissue Remodeling during the Initial Phase of Weight Gain Induced by Overfeeding in Humans

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Regulation of energy metabolism and mitochondrial function in skeletal muscle during lipid overfeeding in healthy men

International audienceCONTEXT/OBJECTIVE: The aim of this study was to evaluate the regulation of the fuel partitioning and energy metabolism in skeletal muscle during lipid overfeeding in healthy men. Design/Participants/Intervention: Thirty-nine healthy volunteers were overfed for 56 days with a high-fat diet (3180 kJ/d). Energy metabolism (indirect calorimetry) was characterized in the fasting state and during a test meal before and at the end of the diet. Skeletal muscle biopsies were taken at day 0 and day 56. MAIN OUTCOME MEASURES: Change in gene expression, mitochondrial respiration, nicotinamide adenine dinucleotide (NAD(+)) content, and acetylation of peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha) in skeletal muscle was measured. RESULTS: Overfeeding increased body weight (+2.6 kg) and fat mass concomitantly with a shift in the use of substrates as energy fuel toward preferential oxidation of carbohydrates instead of lipids. Changes in lipid metabolic gene expression supported this observation, with a reduction in pyruvate dehydrogenase kinase 4 expression that could be the consequences of decreased NAD(+) concentration and reduced deacetylase activity of the sirtuins, as supported by hyperacetylation of PGC-1alpha after overfeeding. Interestingly, this reduction of the sirtuin PGC-1alpha pathway was associated with increased mitochondrial gene expression and higher respiration rate under these conditions. CONCLUSION: Adaptation to lipid overfeeding and regulation of fuel partitioning in human muscle appear to rely on a dissociation between the regulatory functions of the sirtuin-PGC-1alpha pathway on fatty acid oxidation and on mitochondrial regulation. This may facilitate lipid storage during a period of positive energy balance while maintaining mitochondrial functions and oxidative capacities

Dairy and industrial sources of trans fat do not impair peripheral insulin sensitivity in overweight women

International audienceBackground: The 2 major dietary sources of trans fatty acids (TFAs) are partially hydrogenated oils and ruminant-derived products. Epidemiologic data suggest that chronic consumption of industrial sources of TFAs could be damaging to insulin sensitivity, but intervention studies on this issue have remained inconclusive. Objective: The trial was designed to compare the effects of dairy compared with industrial sources of TFAs on insulin sensitivity in overweight women. Design: Sixty-three healthy women with abdominal obesity [waist circumference > 88 cm and a body mass index (in kg/m(2)) > 28] were recruited. After a run-in period, the volunteers were randomly assigned to consume 1 of 3 four-week diets: 60 g low-TFA lipids/d (0.54 g/d; n = 21), ruminant TFA-rich lipids (4.86 g/d; n = 21), or industrial TFA-rich lipids (5.58 g/d; n = 21). Changes in peripheral insulin sensitivity were assessed by using hyperinsulinemiceuglycemic clamps. Results: After the intervention period, fasting glycemia and insulinemia and insulin sensitivity were not significantly modified in either group (P > 0.05). Conclusions: These data indicate that consumption of dairy- and industrial-source TFAs for 4 wk at nutritional levels do not impair peripheral insulin sensitivity in insulin-resistant women. Our study may not preassess the effects of TFAs in normal insulin-sensitive individuals. This trial was registered at clinicaltrials.gov as NCT00617435. Am J Clin Nutr 2009;90:88-94