Hemodialysis Affects Wanting and Spontaneous Intake of Protein-Rich Foods in Chronic Kidney Disease Patients.

OBJECTIVES: Protein-energy wasting is a risk factor for mortality and morbidity in hemodialysis patients (HD patients). Food intake could be modified by HD-related changes in the food reward system (i.e., liking and wanting of specific macronutrients). In HD patients on days with and without dialysis, we evaluated (1) the reward system for protein-, fat-, and carbohydrate-rich foods, plasma hormones, and metabolite changes; and (2) the spontaneous ad libitum intake of macronutrients. (DESIGN AND) METHODS: Twenty-four HD patients evaluated their liking and wanting of macronutrients at 7:30 AM and 11:30 AM on a day with and a day without dialysis. Concentrations of hormones and plasma amino acids were determined. An additional 18 HD patients ate what they wanted from a buffet lunch comprising 8 dishes on a day with and a day without dialysis. Healthy subjects, age-, sex-, and body mass index-matched, served as controls. RESULTS: At 11:30 AM, wanting for protein-rich foods was higher on the day with than on the day without dialysis (P < .01), bringing wanting levels close to those of healthy subjects. This increase correlated with changes in the concentrations of plasma amino acids (P < .01). HD patients ate more protein from the buffet on the day with than on the day without dialysis (P < .01) and more than healthy subjects (P < .01). CONCLUSIONS: In HD patients, wanting and spontaneous intake of protein-rich foods increase immediately after dialysis. This increase correlated with decreased concentrations of plasma amino acids. Thus, in clinical practice, protein-rich foods should be recommended during and after dialysis in patients with protein-energy wasting.

Cerebral gustatory activation in response to free fatty acids using gustatory evoked potentials in humans.

There is some evidence of specific oro-detection of FFAs in rodents and humans. The aim of this study was to record gustatory evoked potentials (GEPs) in response to FFA solutions and to compare GEPs in response to linoleic acid solution with GEPs obtained after stimulation with sweet and salty tastants. Eighteen healthy men were randomly stimulated with fatty (linoleic acid), sweet (sucrose), and salty (NaCl) solutions at two concentrations in the first experiment. Control recordings (n = 14) were obtained during stimulation by a paraffin oil mixture without FFA or by water. In the second experiment, 28 men were randomly stimulated with five FFA solutions and a paraffin emulsion. GEPs were recorded with electroencephalographic electrodes at Cz, Fz, and Pz. GEPs were observed in response to FFA in all participants. GEP characteristics did not differ according to the quality and the concentration of the solutions in the first experiment and according to the FFA in the second experiment. This study describes for the first time GEPs in response to FFA and demonstrates that the presence of FFA in the mouth triggers an activation of the gustatory cortex. These data reinforce the concept that fat taste could be the sixth primary taste.

Taste Perception and Cerebral Activity in the Human Gustatory Cortex Induced by Glucose, Fructose, and Sucrose Solutions.

Glucose, fructose, and sucrose are important carbohydrates in Western diets with particular sweetness intensity and metabolisms. No study has compared their cerebral detection and their taste perception. Gustatory evoked potentials (GEPs), taste detection thresholds, intensity perception, and pleasantness were compared in response to glucose, fructose, and sucrose solutions at similar sweetness intensities and at identical molar concentrations. Twenty-three healthy subjects were randomly stimulated with 3 solutions of similar sweetness intensity (0.75 M of glucose, 0.47 M of fructose and 0.29 M of sucrose - sit. A), and with an identical molar concentration (0.29 M - sit. B). GEPs were recorded at gustatory cortex areas. Intensity perception and hedonic values of each solution were evaluated as were gustatory thresholds of the solutions. No significant difference was observed concerning the GEP characteristics of the solutions according to their sweetness intensities (sit. A) or their molar concentration (sit. B). In sit. A, the 3 solutions were perceived to have similar intensities and induced similar hedonic sensations. In sit. B, the glucose solution was perceived to be less intense and pleasant than the fructose and the sucrose solutions (P < 0.001) and the fructose solution was perceived to be less intense and pleasant than the sucrose (P < 0.001). Since GEP recordings were similar for glucose, fructose, and sucrose solutions whatever the concentrations, activation of same taste receptor induces similar cortical activation, even when the solutions were perceived differently. Sweet taste perception seems to be encoded by a complex chemical cerebral neuronal network.

Impairment of the Ability of HDL From Patients With Metabolic Syndrome but Without Diabetes Mellitus to Activate eNOS: Correction by S1P Enrichment.

OBJECTIVE: High-density lipoprotein (HDL) from nondiabetic patients with metabolic syndrome (MetS) displays abnormalities in their lipidome, such as triglyceride enrichment and sphingosine-1-phosphate depletion. We hypothesized that these abnormalities could impair the ability of HDL to stimulate endothelial nitric oxide synthase (eNOS). APPROACH AND RESULTS: Compared with HDL from control subjects, HDL from normoglycemic patients with MetS was 39% richer in triglycerides (P<0.01) and 15% poorer in sphingosine-1-phosphate (P<0.05; n=23 in each group). eNOS activity, assessed by the conversion of L-[3H]arginine to L-[3H]citrulline, was 69% lower in human umbilical vein endothelial cells incubated with HDL from MetS patients than in cells incubated with HDL from controls (P<0.0001). In addition, the activating phosphorylation of eNOS at serine (Ser) 1177 and of Akt (protein kinase B) at Ser473 was 37% (P<0.001) and 39% (P<0.05) lower, respectively, with HDL from MetS patients. Sphingosine-1-phosphate enrichment of HDL from MetS patients restored their ability to stimulate eNOS activity (P<0.05), in relation with a significant increase in eNOS phosphorylation at Ser1177 (P<0.05) and in Akt phosphorylation at Ser473 (P=0.05). By contrast, triglyceride enrichment of HDL from control subjects did not modify eNOS activity (P=0.90) and phosphorylation at Ser1177 (P=0.87). CONCLUSIONS: We provide evidence that the activation of eNOS by HDL is decreased in MetS patients before the appearance of diabetes mellitus and that sphingosine-1-phosphate depletion of HDL is the main factor responsible for this defect. This has important consequences on the impairment of HDL functionality and antiatherogenic properties in these patients.

Insulin response dysregulation explains abnormal fat storage and increased risk of diabetes mellitus type 2 in Cohen Syndrome.

Cohen Syndrome (CS) is a rare autosomal recessive disorder, with defective glycosylation secondary to mutations in the VPS13B gene, which encodes a protein of the Golgi apparatus. Besides congenital neutropenia, retinopathy and intellectual deficiency, CS patients are faced with truncal obesity. Metabolism investigations showed abnormal glucose tolerance tests and low HDL values in some patients, and these could be risk factors for the development of diabetes mellitus and/or cardiovascular complications. To understand the mechanisms involved in CS fat storage, we used two models of adipogenesis differentiation: (i) SGBS pre-adipocytes with VPS13B invalidation thanks to siRNA delivery and (ii) CS primary fibroblasts. In both models, VPS13B invalidation led to accelerated differentiation into fat cells, which was confirmed by the earlier and increased expression of specific adipogenic genes, consequent to the increased response of cells to insulin stimulation. At the end of the differentiation protocol, these fat cells exhibited decreased AKT2 phosphorylation after insulin stimulation, which suggests insulin resistance. This study, in association with the in-depth analysis of the metabolic status of the patients, thus allowed us to recommend appropriate nutritional education to prevent the occurrence of diabetes mellitus and to put forward recommendations for the follow-up of CS patients, in particular with regard to the development of metabolic syndrome. We also suggest replacing the term obesity by abnormal fat distribution in CS, which should reduce the number of inappropriate diagnoses in patients who are referred only on the basis of intellectual deficiency associated with obesity.

Oxidation-induced loss of the ability of HDL to counteract the inhibitory effect of oxidized LDL on vasorelaxation.

Several current diseases are associated with an increase in the oxidation of HDL, which is likely to impair their functionality. Our aim was to identify whether oxidation could change the protective effect of HDL against the deleterious effect on vasoreactivity induced by oxidative stress. HDL from healthy subjects were oxidized in vitro by Cu(2+), and the ability of oxidized HDL to counteract the inhibitory effect of oxidized LDL on acetylcholine-induced vasodilation was tested on isolated rabbit aorta rings. Oxidation of HDL was evidenced by the increase in the 7-oxysterols/cholesterol ratio (3.20 ± 1.12 vs 0.02 ± 0.01 % in native HDL, p < 0.05). Oxidized LDL inhibited endothelium-dependent vasodilation (E max = 50.2 ± 5.0 vs 92.5 ± 1.7 % for incubation in Kreb's buffer, p < 0.05) and native HDL counteracted this inhibition (E max = 72.4 ± 4.8 vs 50.2 ± 5.0 % p < 0.05). At the opposite, oxidized HDL had no effect on oxidized LDL-induced inhibition on endothelium-dependent vasorelaxation (E max = 53.7 ± 4.8 vs 50.2 ± 5.0 %, NS). HDL oxidation is associated with a decreased ability of HDL to remove 7-oxysterols from oxidized LDL. In conclusion, these results show that oxidation of HDL induces the loss of their protective effect against endothelial dysfunction, which could promote atherosclerosis in diseases associated with increased oxidative stress.

Circulating apelin is increased in patients with type 1 or type 2 diabetes and is associated with better glycaemic control.

CONTEXT: Apelin is an adipokine expressed in several tissues and it appears to be involved in energy metabolism. OBJECTIVE: The aim of this study was to determine serum apelin levels in a large cohort of patients with type 1 and type 2 diabetes and control subjects and to correlate the results with glycaemic control. DESIGN AND PARTICIPANTS: One hundred and thirty patients with type 1 diabetes, 98 patients with type 2 diabetes and 162 controls were enrolled in the study. Apelin levels were measured by enzyme-linked immunosorbent assay. RESULTS: Serum apelin levels were significantly higher in type 1 and type 2 diabetic patients than in controls (P < 0·0001). Serum apelin levels were higher in type 1 than in type 2 diabetic patients (P = 0·02). In multivariate analysis, serum apelin levels were higher in patients with type 1 diabetes and in patients with type 2 diabetes versus controls. We found a negative correlation between glycosylated haemoglobin and serum apelin levels in all diabetic patients (r = -0·17, P = 0·008) and in patients with type 2 diabetes (r = -0·24 P = 0·01). No correlation was found in type 1 diabetic patients. CONCLUSION: Our study showed that apelin concentrations were increased in diabetic patients. This rise, which was greater in type 1 than in type 2 diabetic patients, suggests that obesity is not the main determinant of plasma apelin levels. The negative correlation with glycosylated haemoglobin in patients with type 2 diabetes could indicate that apelin plays a role in glycaemic balance and even insulin sensitivity.

Chronic insomnia, high trait anxiety and their comorbidity as risk factors for incident type 2 diabetes mellitus.

The main objective of this study was to evaluate the association of the insomnia-anxiety comorbidity with incident type 2 diabetes (T2D) in a large prospective cohort. We selected adults without diabetes at baseline from the French NutriNet-Santé cohort who had completed the trait anxiety subscale of the Spielberger State-Trait Anxiety Inventory (STAI-T, 2013-2016) and a sleep questionnaire (2014); insomnia was defined according to established criteria. Using multivariable Cox models, we compared T2D risk across 4 groups: no insomnia or anxiety (reference), insomnia alone, anxiety alone (STAI-T ≥ 40), and comorbid anxiety and insomnia. Among 35,014 participants (mean baseline age: 52.4 ± 14.0 years; 76% women), 378 (1.1%) developed T2D over a mean follow-up of 5.9 ± 2.1 years. Overall, 28.5% of the sample had anxiety alone, 7.5%-insomnia alone, and 12.5%-both disorders. In the fully-adjusted model, a higher T2D risk was associated with anxiety-insomnia comorbidity (HR = 1.40; 95% CI 1.01, 1.94), but not with each disorder separately, compared to the group without insomnia or anxiety. The findings supported a positive association between anxiety-insomnia comorbidity and incident T2D among general-population adults. Future research using clinical diagnoses of mental disorders could confirm the findings and guide diabetes prevention programs.

Pravastatin reverses the membrane cholesterol reorganization induced by myocardial infarction within lipid rafts in CD14(+)/CD16(-) circulating monocytes.

Large numbers of monocytes are recruited in the infarcted myocardium. Their cell membranes contain cholesterol-rich microdomains called lipids rafts, which participate in numerous signaling cascades. In addition to its cholesterol-lowering effect, pravastatin has several pleiotropic effects and is widely used as secondary prevention treatment after myocardial infarction (MI). The aim of this study was to investigate the effects of pravastatin on the organization of cholesterol within monocyte membrane rafts from patients who had suffered myocardial infarction. Monocytes from healthy donors and acute MI patients were cultured with or without 4µM pravastatin. Lipid rafts were extracted by Lubrol WX, caveolae and flat rafts were separated using a modified sucrose gradient. Cholesterol level and caveolin-1 expression in lipid rafts were determined. In healthy donors, cholesterol was concentrated in flat rafts (63±3 vs 13±1%, p<0.001). While monocytes from MI patients presented similar cholesterol distribution in both caveolae and flat rafts. Cholesterol distribution was higher in flat rafts in healthy donors, compared to MI patients (63±3 vs 41±2%, p<0.001), with less distribution in caveolae (13±1 vs 34±2%, p<0.001). Pravastatin reversed the cholesterol distribution in MI patients cells between flat rafts (41±2 vs 66±3%, p<0.001) and caveolae (34±2 vs 18±1%, p<0.001). In conclusion, MI redistributes cholesterol from flat rafts to caveolae indicating monocyte membrane reorganization. In vitro pravastatin treatment restored basal conditions in MI monocytes, suggesting another effect of statins.

Retinol-binding protein 4 is an independent factor associated with triglycerides and a determinant of very low-density lipoprotein-apolipoprotein B100 catabolism in type 2 diabetes mellitus.

OBJECTIVE: Retinol-binding protein 4 (rbp4) is an adipokine secreted by adipocytes and liver, whose levels are elevated in type 2 diabetes mellitus (T2DM). Plasma levels of rbp4 and triglycerides are strongly correlated in T2DM. However, we do not know whether this association is direct or indirect via liver fat content, and the link between rbp4 and triglyceride metabolism remains unknown. METHODS AND RESULTS: Liver fat measurement by proton spectroscopy was performed in 221 patients with T2DM, and an in vivo kinetic study with stable isotopes was carried out in 14 patients with T2DM. In multivariate analysis, triglycerides were associated positively with rbp4 (ß=0.273, P<0.0001), apolipoprotein (apo) B (ß=0.258, P<0.0001), and liver fat (ß=0.191, P=0.002) and negatively with high-density lipoprotein cholesterol (ß=-0.442, P<0.0001). rbp4 was correlated positively with apoB100 very-low-density lipoprotein (VLDL) pool (r=0.62, P=0.017) and negatively with VLDL-apoB100 total fractional catabolic rate (r=-0.66, P=0.001). In multivariate analysis, rbp4 (P=0.015), plasma triglycerides (P=0.024), and sex (P=0.026) were independently associated with VLDL-apoB100 total fractional catabolic rate. CONCLUSIONS: In T2DM, plasma rbp4 level is associated with plasma triglycerides, independently of liver fat content. There is a strong independent negative correlation between plasma rbp4 and VLDL-apoB100 total fractional catabolic rate. These data suggest that rbp4 may be involved in the pathophysiology of hypertriglyceridemia in T2DM by reducing VLDL catabolism.

A scoping review of emotion regulation and inhibition in emotional eating and binge-eating disorder: what about a continuum?

BACKGROUND: Emotional eating is defined as a nonpathological eating behavior, whereas binge-eating disorder (BED) is defined as a pathological eating behavior. While different, both share some striking similarities, such as deficits in emotion regulation and inhibition. Previous research has suggested the existence of an "eating continuum" that might reflect the increased severity of overeating behaviors, that is, from nonpathological overeating to BED. The main aims of this scoping review were to explore in the literature the idea of a continuum between emotional eating and BED and to observe whether deficits in emotion regulation and inhibition follow this continuum in terms of severity. The other aims were to hopefully clarify the ill-defined concept of overeating, to question the potential role of positive emotions and to identify potential knowledge gaps. METHOD: A systematic scoping review was conducted following the Preferred Reporting Items for Systematic reviews and Meta-Analyses extension for Scoping Reviews (PRISMA-ScR) guidelines. Two databases (PubMed/Medline and PsycINFO) were examined in complete accordance with the beforehand sharply defined eligibility and exclusion criteria. The main criteria included adults (≥ 18) with emotional eating, BED or overeating and emotion regulation and inhibition as exposure criteria. RESULTS: Thirty-two studies were included in this scoping review. If the results showed a link between emotional eating and BED, with the presence of inhibition and emotion regulation deficits in both eating behaviors, no mention of a continuum between emotional eating and BED was found. CONCLUSION: In the absence of research directly comparing emotional eating and BED in the same studies and testing the potential increase in severity of emotion regulation and inhibition deficits along this continuum, there is currently no certainty that a continuum exists between emotional eating and BED. In the end, the idea of a continuum in terms of increased severity of overeating and in terms of emotion regulation and inhibition deficits between emotional eating and BED appears to be a gap in knowledge in the literature. This scoping review highlights the need for further research to identify knowledge gaps.

Emotional eating (EE) is defined as a nonpathological eating behavior, whereas binge-eating disorder (BED) is defined as a pathological eating behavior. While different, both share some striking similarities, such as deficits in emotion regulation (ER) and inhibition. Previous research has suggested the existence of an "eating continuum" that might reflect the increased severity of overeating behaviors, that is, from nonpathological overeating to BED. The main aims of this scoping review were to explore in the literature the idea of a continuum between EE and BED and to observe whether deficits in ER and inhibition follow this continuum in terms of severity. A systematic scoping review was conducted, and thirty-two studies were included in this review. If the results showed a link between EE and BED, with the presence of inhibition and ER deficits in both eating behaviors, no mention of a continuum between EE and BED, or in relation to a continuum, was found. Thus, in the absence of research directly comparing EE and BED in the same studies and testing the potential increase in severity of ER and inhibition deficits along this continuum, there is currently no certainty about the existence or absence of such a continuum.

Hypothalamic Glucose Hypersensitivity-Induced Insulin Secretion in the Obese Zücker Rat Is Reversed by Central Ghrelin Treatment.

Aims: Part of hypothalamic (mediobasal hypothalamus [MBH]) neurons detect changes in blood glucose levels that in turn coordinate the vagal control of insulin secretion. This control cascade requires the production of mitochondrial reactive oxygen species (mROS), which is altered in models of obesity and insulin resistance. Obese, insulin-resistant Zücker rats are characterized by hypothalamic hypersensitivity to glucose. This initiates an abnormal vagus-induced insulin secretion, associated with an overproduction of mROS in response to a low glucose dose. Here, we hypothesized that ghrelin, known to buffer reactive oxygen species (ROS) via mitochondrial function, may be a major component of the hypothalamic glucose hypersensitivity in the hypoghrelinemic obese Zücker rat. Results: Hypothalamic glucose hypersensitivity-induced insulin secretion of Zücker obese rats was reversed by ghrelin pretreatment. The overproduction of MBH mROS in response to a low glucose load no longer occurred in obese rats that had previously received the cerebral ghrelin infusion. This decrease in mROS production was accompanied by a normalization of oxidative phosphorylation (OXPHOS). Conversely, blocking the action of ghrelin with a growth hormone secretagogue receptor antagonist in a model of hyperghrelinemia (fasted rats) completely restored hypothalamic glucose sensing-induced insulin secretion that was almost absent in this physiological situation. Accordingly, ROS signaling and mitochondrial activity were increased by the ghrelin receptor antagonist. Innovation: These results demonstrate for the first time that ghrelin addressed only to the brain could have a protective effect on the defective control of insulin secretion in the insulin-resistant, hypoghrelinemic obese subject. Conclusions: Ghrelin, through its action on OXPHOS, modulates mROS signaling in response to cerebral hyperglycemia and the consequent vagal control of insulin secretion. In insulin-resistant obese states, brain hypoghrelinemia could be responsible for the nervous defect in insulin secretion.

Changes in Taste Perception in Patients with Minor and Major Cognitive Impairment Linked to Alzheimer's Disease Recorded by Gustatory Evoked Potentials.

BACKGROUND: The need for early diagnosis biomarkers in Alzheimer's disease (AD) is growing. Only few studies have reported gustatory dysfunctions in AD using subjective taste tests. OBJECTIVE: The main purpose of the study was to explore gustatory functions using subjective taste tests and recordings of gustatory evoked potentials (GEPs) for sucrose solution in patients with minor or major cognitive impairment (CI) linked to AD, and to compare them with healthy controls. The secondary objective was to evaluate the relationships between GEPs and the results of cognitive assessments and fasting blood samples. METHODS: A total of 45 subjects (15 healthy subjects, 15 minor CI patients, 15 major CI patients) were included to compare their gustatory functions and brain activity by recording GEPs in response to a sucrose stimulation. CI groups were combined in second analyses in order to keep a high power in the study. Correlations were made with cognitive scores and hormone levels (ghrelin, leptin, insulin, serotonin). RESULTS: Increased P1 latencies and reduced N1 amplitudes were observed in minor or major patients compared to controls. GEPs were undetectable in 6 major and 4 minor CI patients. Thresholds for sucrose detection were significantly higher in the major CI group than in controls or the minor CI group. No correlation was found with hormone levels. CONCLUSIONS: The cortical processing of sensory taste information seems to be altered in patients with minor or major CI linked to AD. This disturbance was identifiable with subjective taste tests only later, at the major CI stage.

Inhibition and shifting across the weight status spectrum.

Executive functioning (EF) is of major interest in the study of cognitive factors involved in obesity. Among EF, shifting is related to behavioral flexibility, and inhibition to the ability to refrain from impulsive behavior. A deficit in those two EF could predict individual difficulties to maintain a healthy lifestyle. Weak evidence of deficits in shifting and inhibition in individuals of higher Body Mass Index (BMI) have been observed. The objective was to clarify the relationship between inhibition and shifting regarding weight status group differences in healthy adults. Two neuropsychological tests from the Test of Attentional Performance (TAP) battery were used to measure EF performance of three groups of men and women: normal-weight (NW, n = 38), overweight (OW, n = 40) and obesity (OB, n = 37). The results show that individuals with higher BMI have lower inhibition capacities and that classically used weight status categories might not capture cognitive variability. No differences in shifting were observed concerning weight status nor BMI. This paper provides new insights on cognitive factors in obesity by presenting data from healthy individuals with overweight and obesity. The results support that assessing inhibition capacities might be of interest in a clinical setting for patients with difficulties to lose weight.

PNPLA3 polymorphism influences liver fibrosis in unselected patients with type 2 diabetes.

CONTEXT: Recently, it has been shown that an allele in the adiponutrin (PNPLA3) gene was strongly associated with increased liver fat content (LFC) and liver fibrosis independent of visceral adiposity and insulin resistance. OBJECTIVE: In this study, we set out to determine whether the PNPLA3 rs738409 polymorphism was associated with liver fibrosis in unselected patients with type 2 diabetes. DESIGN, SETTING AND PARTICIPANTS: Two hundred and thirty-four patients with type 2 diabetes were included in this study. MAIN OUTCOME MEASURES: LFC was evaluated using (1) H-MR spectroscopy; fibrosis was measured using the non-invasive FibroTest(®). RESULTS: Advanced liver fibrosis (stage F2 or above) was observed in 10.2% of the patients while 149 (63.6%) patients had steatosis. The prevalence of steatosis and fibrosis was higher in minor G allele carriers than that in C allele homozygote carriers (70.3 vs 57.1%; P=0.04 and 14.7 vs 7.5%; P=0.07 respectively). In multivariate analysis, the predictive variables for advanced liver fibrosis were age (≥60) (P=0.005), sex (female) (P=0.004) and rs 738409 PNPLA3 polymorphism (P=0.01); body mass index (BMI) and LFC were not associated with liver fibrosis. CONCLUSIONS: This study confirms that in patients with type 2 diabetes who were not selected for liver abnormalities, liver fibrosis was related to the rs738409 polymorphism independent of BMI or LFC.

Increased body fat mass reduces the association between fructosamine and glycated hemoglobin in obese type 2 diabetes patients.

Obesity is increasing in patients with type 2 diabetes. A possible reduced association between fructosamine and glycated hemoglobin (HbA1c) in obese individuals has been previously discussed, but this has never been specifically evaluated in type 2 diabetes, and the potential influence of body fat mass and fat distribution has never been studied. We studied 112 type 2 diabetes patients with assessment of fat mass, liver fat and fat distribution. Patients with body mass index (BMI) above the median (34.9 kg/m2 ), versus BMI below the median, had a correlation coefficient between fructosamine and HbA1c significantly reduced (r = 0.358 vs r = 0.765). In the whole population, fructosamine was correlated negatively with BMI and fat mass. In multivariate analysis, fructosamine was associated with HbA1c (positively) and fat mass (negatively), but not with BMI, liver fat or fat distribution. The association between fructosamine and HbA1c is significantly reduced in the most obese type 2 diabetes patients, and this is mostly driven by increased fat mass.

Implicit food odour priming effects on reactivity and inhibitory control towards foods.

The food environment can interact with cognitive processing and influence eating behaviour. Our objective was to characterize the impact of implicit olfactory priming on inhibitory control towards food, in groups with different weight status. Ninety-one adults completed a modified Affective Shifting Task: they had to detect target stimuli and ignore distractor stimuli while being primed with non-attentively perceived odours. We measured reactivity and inhibitory control towards food pictures. Priming effects were observed on reactivity: participants with overweight and obesity were slower when primed with pear and pound cake odour respectively. Common inhibitory control patterns toward foods were observed between groups. We suggest that non-attentively perceived food cues influence bottom-up processing by activating distinguished mental representations according to weight status. Also, our data show that cognitive load influences inhibitory control toward foods. Those results contribute to understanding how the environment can influence eating behaviour in individuals with obesity.

Delivery of oral nutrition supplement in hospital: Evaluation of professional practices in evaluation of nutritional status and representations of ONS by the caregivers and patients.

BACKGROUND: Nutritional evaluation and detection of malnutrition are based on criteria recommended by French health authorities. In practice, doctors do not always ensure strict implementation of the recommendations. The aim of this study is to evaluate professional practices in France regarding nutritional follow-up on arrival, during and after the hospitalization of inpatients who have oral nutritional supplements (ONS) prescribed and to discuss how ONS are seen by medical staff and patients. METHODS: A prospective study including patients consecutively admitted to digestive surgery and endocrinology units of the Dijon university hospital was conducted. Malnutrition risk at hospital admission was identified using anthropometric and biological criteria: Body Mass Index, percentage of weight loss, albumin, prealbumin, C-reactive protein and Mini Nutritional Assessment. Nutritional evaluation and monitoring of inpatients on arrival, during and after hospitalization was analyzed. Interviews were held with caregivers and patients to raise the question of their attitudes toward ONS. RESULTS: The sample was composed of 61 patients. At the beginning of hospitalization, nutritional evaluation of patients was satisfactory. Follow-up during hospitalization was not optimal and depends on the degree of malnutrition. Post-hospitalization testing for albumin was rare, whereas ONS were regularly prescribed. ONS was viewed differently by caregivers and inpatients, which makes the status of ONS ambiguous. CONCLUSION: Our results show good evaluation of nutritional status of inpatients at the beginning of hospitalization but low follow-up during and after hospitalization. Representation of ONS differed between caregivers and patients leading to a confusion around them. Therefore, interdisciplinary work is necessary to encourage systematic assessment of nutritional status in patients and standardize the message regarding ONS.

Differential Cerebral Gustatory Responses to Sucrose, Aspartame, and Stevia Using Gustatory Evoked Potentials in Humans.

Aspartame and Stevia are widely substituted for sugar. Little is known about cerebral activation in response to low-caloric sweeteners in comparison with high-caloric sugar, whereas these molecules lead to different metabolic effects. We aimed to compare gustatory evoked potentials (GEPs) obtained in response to sucrose solution in young, healthy subjects, with GEPs obtained in response to aspartame and Stevia. Twenty healthy volunteers were randomly stimulated with three solutions of similar intensities of sweetness: Sucrose 10 g/100 mL of water, aspartame 0.05 g/100 mL, and Stevia 0.03 g/100 mL. GEPs were recorded with EEG (Electroencephalogram) electrodes. Hedonic values of each solution were evaluated using the visual analog scale (VAS). The main result was that P1 latencies of GEPs were significantly shorter when subjects were stimulated by the sucrose solution than when they were stimulated by either the aspartame or the Stevia one. P1 latencies were also significantly shorter when subjects were stimulated by the aspartame solution than the Stevia one. No significant correlation was noted between GEP parameters and hedonic values marked by VAS. Although sucrose, aspartame, and Stevia lead to the same taste perception, cerebral activation by these three sweet solutions are different according to GEPs recording. Besides differences of taste receptors and cerebral areas activated by these substances, neural plasticity, and change in synaptic connections related to sweet innate preference and sweet conditioning, could be the best hypothesis to explain the differences in cerebral gustatory processing after sucrose and sweeteners activation.

Study of Small Intestinal Bacterial Overgrowth in a Cohort of Patients with Abdominal Symptoms Who Underwent Bariatric Surgery.

INTRODUCTION: Small intestinal bacterial overgrowth (SIBO) is a common complication of bariatric surgery. Digestive decontamination treatments with oral antibiotic therapy vary and are not codified. This retrospective study was conducted to analyse the characteristics of bariatric surgery patients who underwent a glucose breath test (GBT) and to analyse the effectiveness of the antibiotic decontamination therapy. MATERIALS AND METHODS: A total of 101 operated patients (Roux-en-Y bypass (RYB), omega bypass (ΩB) and sleeve gastrectomy (SG)) who underwent a GBT (75 g/250 mL) were included. Anthropometric data, symptoms of SIBO, type of surgery, use of proton pump inhibitors (PPIs) and antibiotic therapy were analysed. The effectiveness of the antibiotic treatment, defined by improvement of the symptoms, was evaluated during the follow-up. RESULTS: Of the 85 women and 16 men included (48.5 ± 3.6 years old), 63 underwent RYB, 31 underwent ΩB and 7 underwent SG. The GBT was positive in 83% of the patients. A positive test was associated with age (p < 0.001), female sex (p < 0.01) and PPI use (p < 0.01), but there was no significant difference according to the type of surgery. Sixty-one percent of patients treated with gentamicin/metronidazole sequential antibiotic therapy and 58% of patients treated with metronidazole alone achieved treatment efficacy (with no significant difference in efficacy between these treatments). CONCLUSION: SIBO should be systematically considered in the context of abdominal symptoms in bariatric surgery patients, regardless the type of surgery, particularly in patients who are older or female and after PPI treatment. Digestive decontamination appears to be similar between gentamycin/metronidazole and metronidazole treatments.