Lean Ones Research Articles

Road Traffic Noise, Obesity, and the Risk of Incident Type 2 Diabetes: A Cohort Study in UK Biobank.

Objectives: To assess the association of road traffic noise exposure with Type 2 Diabetes (T2D) risk, and to explore the potential moderation effect of obesity. Methods: A total of 305,969 participants from the UK Biobank Cohort - an open access cohort of 500,000 participants recruited in the United Kingdom (UK) between 2006 and 2010 - were included in the study. A Cox proportional hazard model was fitted to assess the association between road traffic noise exposure and T2D. Results: A total of 19,303 participants were diagnosed with T2D during the 11.9-year median follow-up period. For every 10 dB increase in road traffic noise, there was a 4% increase in T2D risk (HR = 1.04, 95%CI: 1.01, 1.07). Besides, a significant positive interaction was observed between obesity and road traffic noise (P interaction <0.001) for the risk of T2D. The association of road traffic noise with T2D was stronger in overweight and obese participants (HR = 1.04, 95% CI: 1.01–1.08), but not significant among lean ones (HR = 0.96, 95% CI: 0.86–1.07). Conclusion: Our study observed a longitudinal association of road traffic noise exposure with T2D risk, which was stronger among overweight and obese individuals than the lean ones.

Profinite ∞-operads

We show that a profinite completion functor for (simplicial or topological) operads with good homotopical properties can be constructed as a left Quillen functor from an appropriate model category of ∞-operads to a certain model category of profinite ∞-operads. The construction is based on a notion of lean ∞-operad, and we characterize those ∞-operads weakly equivalent to lean ones in terms of homotopical finiteness properties. Several variants of the construction are also discussed, such as the cases of unital (or closed) ∞-operads and of ∞-categories.

The compound annual growth rate of the fibrosis-4 index in chronic hepatitis B patients.

Chronic hepatitis B (CHB) patients with low disease activity are at risk of liver fibrosis. The age-adjusted fibrosis-4 index (FIB4-AA), developed in our previous publication, and was implemented to evaluate the tendency of liver fibrosis in these patients. We aimed to investigate the rate of liver fibrosis in CHB patients with low disease activity. Resuming our previous study, the FIB-4 changes of 244 antiviral treatment-naïve CHB patients, with a total of 1243.48 person-years, were reviewed. Among the cohort, patients were categorized as FIB4-AA positive or negative according to the results of their last FIB4-AA minus their initial FIB-4 during at least 18 months of observation time. The compound annual growth rate (CAGR) of FIB-4 was calculated for the FIB4-AA positive and negative groups. The assumed healthy controls had an FIB-4 CAGR calculated to be 2.34% for both men and women, while the FIB-4 CAGR of the whole study cohort was 2.84% ± 6.01%. FIB4-AA positive effectively identifies CHB patients with higher mean FIB-4 CAGR (7.11% ± 3.88% vs. -2.36% ± 3.52%, p < 0.0001). Overweight CHB patients had 10 times smaller mean FIB-4 CAGR than lean ones (0.38% ± 10.35% vs. 3.83% ± 8.88%, p=0.009). An increase in FIB4-AA over at least 18 months in CHB patients with relatively low disease activity meant they were at greater risk of liver fibrosis, and these patients had a mean FIB-4 CAGR of 7.11%. The FIB-4 CAGR was compatible with the findings of previous studies on the collagen proportionate area in viral hepatitis patients.

New Insights on the PBMCs Phospholipidome in Obesity Demonstrate Modulations Associated with Insulin Resistance and Glycemic Status.

(1) Background: Obesity and type 2 diabetes have been suspected to impact both intrinsic metabolism and function of circulating immune cells. (2) Methods: To further investigate this immunometabolic modulation, we profiled the phospholipidome of the peripheral blood mononuclear cells (PBMCs) in lean, normoglycemic obese (OBNG) and obese with dysglycemia (OBDysG) individuals. (3) Results: The global PBMCs phospholipidome is significantly downmodulated in OBDysG unlike OBNG patients when compared to lean ones. Multiple linear regression analyses show a strong negative relationship between the global PBMCs phospholipidome and parameters assessing insulin resistance. Even though all classes of phospholipid are affected, the relative abundance of each class is maintained with the exception of Lyso-PC/PC and Lyso-PE/PE ratios that are downmodulated in PBMCs of OBDysG compared to OBNG individuals. Interestingly, the percentage of saturated PC is positively associated with glycated hemoglobin (HbA1c). Moreover, a few lipid species are significantly downmodulated in PBMCs of OBDysG compared to OBNG individuals, making possible to distinguish the two phenotypes. (4) Conclusions: This lipidomic study highlights for the first-time modulations of the PBMCs phospholipidome in obese patients with prediabetes and type 2 diabetes. Such phospholipidome remodeling could disrupt the cell membranes and the lipid mediator’s levels, driving an immune cell dysfunction.

Adenovirus transduction to express human ACE2 causes obesity-specific morbidity in mice, impeding studies on the effect of host nutritional status on SARS-CoV-2 pathogenesis

The COVID-19 pandemic has paralyzed the global economy and resulted in millions of deaths globally. People with co-morbidities like obesity, diabetes and hypertension are at an increased risk for severe COVID-19 illness. This is of overwhelming concern because 42% of Americans are obese, 30% are pre-diabetic and 9.4% have clinical diabetes. Here, we investigated the effect of obesity on disease severity following SARS-CoV-2 infection using a well-established mouse model of diet-induced obesity. Diet-induced obese and lean control C57BL/6 N mice, transduced for ACE2 expression using replication-defective adenovirus, were infected with SARS-CoV-2, and monitored for lung pathology, viral titers, and cytokine expression. No significant differences in tissue pathology or viral replication was observed between AdV transduced lean and obese groups, infected with SARS-CoV-2, but certain cytokines were expressed more significantly in infected obese mice compared to the lean ones. Notably, significant weight loss was observed in obese mice treated with the adenovirus vector, independent of SARS-CoV-2 infection, suggesting an obesity-dependent morbidity induced by the vector. These data indicate that the adenovirus-transduced mouse model of SARS-CoV-2 infection, as described here and elsewhere, may be inappropriate for nutrition studies.

A conceptual hybrid project management model for construction projects

Abstract The commonly adopted project management approach is the traditional plan-driven model, which sometimes is not the most appropriate approach to complex construction projects subject to successive changes, where more agile approaches might be more adequate. The objective of this paper is to provide a hybrid project management approach that not only draws on traditional project management approaches, but also on agile and lean ones, and that seeks to promote change, boost interaction with the client and increase project value, by using the agile approach component to increase the probability of success of construction projects; and to eliminate waste by embodying the lean approach component. The paper thoroughly reviews the available literature on different project management approaches and proposes a hybrid project management model for construction projects, presenting and discussing key traditional, agile and lean practices.

Dietary Lactate Supplementation Protects against Obesity by Promoting Adipose Browning in Mice.

Yogurt has been widely used in weight-loss foods to prevent obesity, but its molecular nature remains unclear. Lactate is a major ingredient of yogurt, while its cognate cell surface receptor GPR81 is highly expressed in adipose tissues in mammals. Here we hypothesized that dietary lactate supplementation might activate GPR81 to promote adipose browning. Studying mouse models, we observed that GPR81 was substantially lowered in adipose tissue of obese mice compared with that for lean ones, whereas its expression was markedly up-regulated by a β3-adrenergic receptor (β3-AR) agonist. The deficiency of GPR81 greatly attenuated experimental adipose browning and thermogenesis. Importantly, oral administration of lactate effectively induced adipose browning, enhanced thermogenesis, improved dyslipidemia, and protected mice against high-fat-diet-induced obesity. Mechanistically, p38 mitogen-activated protein kinase might serve as a key downstream effect or of GPR81. Collectively, our findings revealed a critical role of GPR81 in adipose browning and provided a new insight into obesity management by modulating lactate-GPR81 signaling axis.

Fecal microbiota transplantation alters the susceptibility of obese rats to type 2 diabetes mellitus.

Obesity is one of the susceptibility factors for type 2 diabetes (T2DM), both of which could accelerate the aging of the body and bring many hazards. A causal relationship is present between intestinal microbiota and body metabolism, but how the microbiota play a role in the progression of obesity to T2DM has not been elucidated. In this study, we transplanted healthy or obese-T2DM intestinal microbiota to ZDF and LZ rats, and used 16S rRNA and targeted metabonomics to evaluate the directional effect of the microbiota on the susceptibility of obese rats to T2DM. The glycolipid metabolism phenotype could be changed bidirectionally in obese rats instead of in lean ones. One possible mechanism is that the microbiota and metabolites alter the structure of the intestinal tract, and improve insulin and leptin resistance through JAK2 / IRS / Akt pathway. It is worth noting that 7 genera, such as Lactobacillus, Clostridium and Roche, can regulate 15 metabolites, such as 3-indolpropionic acid, acetic acid and docosahexaenoic acid, and have a significant improvement on glycolipid metabolism phenotype. Attention to intestinal homeostasis may be the key to controlling obesity and preventing T2DM.

Numerical investigation of self-sustaining modes of 2D planar detonations under concentration gradients in hydrogen–oxygen mixtures

Self-sustaining modes of detonations in non-uniform mixtures for hydrogen and oxygen are numerically studied. Concentration gradients are set vertical to the direction of detonation propagation, with equivalence ratios decreasing from rich values to lean ones. High-resolution codes based on the fifth-order weighted essentially non-oscillatory (WENO) scheme in spatial discretization and the 3rd-order Additive Runge-Kutta (ARK) schemes in time discretization, with detailed chemical kinetics model, are developed. Two-dimensional (2D) numerical simulations are conducted in a 2D planar geometry, non-uniform distributions are then precisely controlled as a function of width. The cellular structures and transmissions, failure and re-initiation mechanisms of detonation fronts are characterized. Results show that the low concentration gradient produces the multi-head mode of detonation with continuous adaptation of velocities and multicellular structures to local concentration. The high concentration gradient generates single-head mode with detonation re-initiation at channel walls produced by reflected transverse Mach waves. Specially, the intermediate distribution between the low and high concentration gradients induces an alternation mode between singe-head and multi-head detonations.

2001-P: Glycemic and Energy Homeostasis Profiles in Women with Different Metabolic Phenotypes of Obesity in Nutritionist Health Study

Objective: To compare components of glycemic and energy homeostasis in women with metabolically healthy normal weight (MHNW) and metabolically unhealthy (MUNW), metabolically unhealthy overweight/obese (MUO) and metabolically healthy (MHO) phenotypes. Methodology: Cross-sectional study with 104 women (18-45 years): 30 MHNW, 17 MUNW, 27 MHO, 30 MUO. Overweight was considered BMI ≥ 25 kg/m² and metabolic health without of changes in blood pressure, glycemic, lipemic levels and cardiovascular disease. The standard mixed meal tolerance test and indirect calorimetry were performed (assessments at -15, 0, 30, 60, 120 and 180 min). The quantifications were: areas under the curve (AUC) for glucose, insulin, C peptide, glucagon and GLP-1; insulin sensitivity (IS) by oral glucose insulin sensitivity index; energy expenditure, respiratory quotient, and carbohydrate and lipid oxidation rate were measured at rest and after oral stimulation. Results: The groups did not differ regarding age and HbA1c levels. IS was decreased in MUO compared to MHNW and MHO (p&amp;lt;0.001). Insulin AUC was lower in MUO compared to MHNW (p=0.02), and C-peptide AUC was increased in MHO and MUO compared to MHNW (p&amp;lt;0.001). Resting energy expenditure was increased in overweight individuals compared to lean individuals (p &amp;lt;0.01). The lipid oxidation rate at time 30 min. was lower in MHNW and MUNW compared to MUO (p &amp;lt;0.01). Conclusion: In young and normoglycemic women, there was lower IS and insulin secretion for the MUO phenotype. The greater rate of lipid oxidation in this group compared to the lean ones may be a reflection of the lower IS, and the inability to switch the use of energy substrate to the higher carbohydrate availability after oral stimulation. BMI is not an ideal indicator of the presence or absence of metabolic health. However, even in MHO individuals’, physiological adaptations may happen to maintain the metabolic parameters within normal range. Disclosure F.B. Ribeiro: None. I. Solar: None. R.G. Freitas: None. A.S. Hanada: None. M.G. Barbosa: None. C.M. Xavier: None. N.S.K. Crouchan: None. V.F.D. Santos: None. B.G. Neto: None. I.T. Silva: None. L.G.D. Folchetti: None. B. Almeida Pititto: None. S.G. Ferreira-Vivolo: None. A.J. Vasques: None. Funding Fundação de Apoio a Pesquisa do Estado de São Paulo (2017/10185-9)

Depletion of Blautia Species in the Microbiota of Obese Children Relates to Intestinal Inflammation and Metabolic Phenotype Worsening.

Cross-sectional studies conducted with obese and control subjects have suggested associations between gut microbiota alterations and obesity, but the links with specific disease phenotypes and proofs of causality are still scarce. The present study aimed to profile the gut microbiota of lean and obese children with and without insulin resistance to characterize associations with specific obesity-related complications and understand the role played in metabolic inflammation. Through massive sequencing of 16S rRNA gene amplicons and data analysis using a novel permutation approach, we have detected decreased incidence of Blautia species, especially Blautia luti and B. wexlerae, in the gut microbiota of obese children, which was even more pronounced in cases with both obesity and insulin resistance. There was also a parallel increase in proinflammatory cytokines and chemokines (gamma interferon [IFN-γ], tumor necrosis factor alpha [TNF-α], and monocyte chemoattractant protein 1 [MCP-1]) in feces of obese children compared to those of lean ones. B. luti and B. wexlerae were also shown to exert an anti-inflammatory effect in peripheral blood mononuclear cell cultures in vitro, compared to non-obesity-associated species. We suggest that the depletion of B. luti and B. wexlerae species in the gut ecosystem may occur in cases of obesity and contribute to metabolic inflammation leading to insulin resistance.IMPORTANCE Child obesity constitutes a risk factor for developing insulin resistance which, if sustained, could lead to more severe conditions like type 2 diabetes (T2D) in adulthood. Our study identified previously unknown species whose depletion (Blautia luti and Blautia wexlerae) is associated with insulin resistance in obese individuals. Our results also indicate that these bacterial species might help to reduce inflammation causally linked to obesity-related complications. Childhood is considered a window of opportunity to tackle obesity. These new findings provide, therefore, valuable information for the future design of microbiota-based strategies for the early prevention of obesity-related complications.

Insulin-like growth factor 1 and insulin-like growth factor binding protein-3 as predictive biomarkers of depression and migraine in obese women

IntroductionObesity and its comorbidity, depression and migraine, are highly prevalent conditions and public health problems of enormous scope that are responsible for the significant quality of life impairment and financial cost. Insulin-like growth factor-1 (IGF-1) and its main binding protein, insulin-like growth factor binding protein-3 (IGFBP-3) are related to metabolic diseases such as growth deficiency, obesity, cancer, neurological, and cardiovascular diseases. The objective of this study was to explore IGF-1 and IGFBP-3 in obesity-associated depression and migraine. Also, we aimed to evaluate the association of IGF-1 and IGFBP-3 with clinical features of depression and migraine.Patients and methodsA cross-sectional controlled study included 50 healthy lean control group and 100 obese women who were subdivided into three subgroups: obese without depression and migraine (n=27), patients with depression (n=24), and patients with migraine (n=49). Clinical, neurological, and psychiatric evaluation of all patients was done. We measured IGF-1 and IGFBP-3 by commercial enzyme-linked immunosorbent assay.ResultsOur study showed a significantly lower level of IGF-1 and IGFBP-3 in obese women compared with lean ones. Even more importantly, obese women with depression as well as migraine had significantly lower IGF-1 and IGFBP-3 than those without depression and migraine. Interestingly, the lower levels of IGF-1 and IGFBP-3 in obese women with depression and migraine were significantly negatively correlated with depression score, BMI, and homeostasis model assessments of insulin resistance. Linear regression analysis test in obese patients showed that BMI and depression scores were independently correlated with serum IGF-1. However, BMI, fasting serum insulin, and depression scores were independently correlated with serum IGFBP-3.ConclusionsObese women with depression and migraine had significantly lower IGF-1 and IGFBP-3 than those without depression and migraine.

Hepatic Gluconeogenic Response to Single and Long-Term SGLT2 Inhibition in Lean/Obese Male Hepatic G6pc-Reporter Mice.

Sodium-glucose cotransporter 2 inhibitor (SGLT2i) consistently reduces blood glucose levels in type 2 diabetes mellitus but increases hepatic gluconeogenic gene expression and glucose production, offsetting its glucose-lowering effect. This study aimed to elucidate the effect of SGLT2i on hepatic gluconeogenic response and its mechanism in both insulin-sensitive and insulin-resistant states. A hepatic mouse model was generated to show liver-specific expression of Gaussia luciferase (GLuc) driven by the gluconeogenic enzyme gene G6pc promoter. Hepatic gluconeogenic response was evaluated by measuring plasma GLuc activity. SGLT2i was given to lean and obese mice in single gavage administration or 4-week dietary administration with controlled feeding every 3 hours. In lean mice, single-dose SGLT2i increased plasma GLuc activity from 2 hours after administration, decreasing blood glucose and plasma insulin from 1 to 2 hours after administration. In obese mice, which had higher plasma GLuc activity than lean ones, SGLT2i did not further increase GLuc activity despite decreased blood glucose and plasma insulin. Hepatic Akt and GSK3β phosphorylation was attenuated by single-dose SGLT2i in lean mice in accordance with the plasma insulin decrease, but not in obese mice. Long-term SGLT2i administration, which increased plasma GLuc activity in lean mice, decreased it in obese mice from 3 weeks after initiation, with increased hepatic Akt and GSK3β phosphorylation. In conclusion, single SGLT2i administration increases hepatic gluconeogenic response in lean insulin-sensitive mice, but not in obese insulin-resistant mice. Long-term SGLT2i administration relieves obesity-induced upregulation of the hepatic gluconeogenic response by restoring impeded hepatic insulin signaling in obese insulin-resistant mice.

Effect of a 24-week weight management program on serum leptin level in correlation to anthropometric measures in obese female: A randomized controlled clinical trial

BackgroundObesity is a major contributor to preventable disease and death across the globe. Obesity is complex. Although its risk factors are myriad and compounding, there is an urgent need for a deeper understanding of the way risk factors interact with each other. Leptin is a peptide regulates food intake and body weight. However, the notion of leptin as an anti-obesity hormone was called into question because obesity is typically associated with high leptin levels and not leptin deficiency thus, we aimed to measure leptin levels in obese female in correlation to anthropometric measures and to evaluate the impact of weight loss on its level and metabolic parameters. Subject and methodscase-control study enrolled 40 control groups, 50 obese women. We measured anthropometric measures BMI, Waist/hip ratio (WHR). Fat mass index (FMI%) and free fat mass index (FFMI%) were assessed by dual energy X-Ray absorptiometry (DEXA) The serum levels of leptin were measured by ELISA. ResultsOur results revealed that serum leptin levels were higher in obese women compared to controls. Moreover, it was positively correlated to anthropometric measures, glycemic and lipid profile. Linear regression analysis revealed that BMI was the main independent studied parameters associated with serum leptin level among other clinical and laboratory biomarkers. Interestingly, after 12 weeks of following the Mediterranean diet (MD)–based weight loss program, serum leptin levels were decreased. Logistic regression analysis was performed to detect the main predictors' biomarkers associated with weight loss among obese women. We found that serum leptin and FMI% were an independent predictor of response with odds ratios of 1.69 and 1.64 respectively (P < 0.001), Receiver operating characteristic analyses revealed that the AUC of serum leptin in discriminating obese women from lean ones was 0.893 (95% CI = 0.815–0.917) with sensitivity = 90%, specificity = 96%, and the cutoff values was 36.32 ng/ml. ConclusionSerum leptin could be a valuable diagnostic marker of obesity and its comorbidities. Moreover, significant weight loss leads to decrease serum leptin levels and improvement of glycemic and lipid profiles.

Obesity paradox in cancer: Is bigger really better?

While obesity is widely recognized as a risk factor for cancer, survival among patients with cancer is often higher for obese than for lean individuals. Several hypotheses have been proposed to explain this “obesity paradox,” but no consensus has yet emerged. Here, we propose a novel hypothesis to add to this emerging debate which suggests that lean healthy persons present conditions unfavorable to malignant transformation, due to powerful natural defenses, whereby only rare but aggressive neoplasms can emerge and develop. In contrast, obese persons present more favorable conditions for malignant transformation, because of several weight‐associated factors and less efficient natural defenses, leading to a larger quantity of neoplasms comprising both nonaggressive and aggressive ones to regularly emerge and progress. If our hypothesis is correct, testing would require the consideration of the raw quantity, not the relative frequency, of aggressive cancers in obese patients compared with lean ones. We also discuss the possibility that in obese persons, nonaggressive malignancies may prevent the subsequent progression of aggressive cancers through negative competitive interactions between tumors.

The Association Between ENT Diseases and Obesity in Pediatric Population: A Systemic Review of Current Knowledge.

Obesity in pediatric population is an important global problem. The prevalence of obesity in children is dramatically rising. According to World Health Organization, about 41 million children under the age of 5 years are obese or overweight worldwide. Overweight and obesity are well-known risk factors for a number of health disorders. Diseases commonly observed in this group of patients are metabolic disorders, type 2 diabetes mellitus, cardiovascular diseases, fatty liver disease, musculoskeletal problems, and many others. The main aim of this study was to present the current knowledge of the association between childhood obesity and common otorhinolaryngological disorders. It is suggested that obese children are more prone to suffer from otorhinolaryngological illnesses than the lean ones. Obesity may predispose to otorhinolaryngological diseases in various ways. It strongly interferes with the immune system (increases serum levels of interleukin 6, tumor necrosis factor, C-reactive protein, and leptin and reduces adiponectin concentration) affecting organs of the upper respiratory tract. Additionally, obesity induces mechanical disorders in the upper airways. According to our review, obesity predisposes to otitis media with effusion, acute otitis media, recurrent otitis media, obstructive sleep apnea, sensorineural hearing loss, adenotonsillar hypertrophy, and post-/perioperative complications after adenotonsillectomy. Obesity in children significantly correlates with both obstructive sleep apnea (OSA) and asthma and constitutes a significant component of "OSA, obesity, asthma" triad.

Estradiol protects against ovariectomy-induced susceptibility to the anabolic effects of glucocorticoids in rats

Glucocorticoids increase appetite and body weight gain in rats and ovariectomy (OVX) induces obesity, while estrogen (E) replacement attenuates OVX-induced changes. It is known that animals with obesity are more responsive to glucocorticoids anabolic effects than lean ones. This study aimed to evaluate the effects of ovariectomy and the protective role of estradiol on the responses induced by prolonged treatment with corticosterone or dexamethasone on energy homeostasis. For this, female Wistar rats subjected to SHAM or OVX surgery, composing the SHAM, OVX, and OVX + E groups, received water/ETOH or corticosterone (15 mg/l) and water or dexamethasone (0.5 μg/l) as drinking fluid for 28 days. The OVX + E group, since the first day, was daily treated with estradiol (10 μg/0.2 ml/rat SC). OVX induced enhancement of body weight gain, food intake, area of the adipocytes and weight of retroperitoneal adipose tissue, plasma cholesterol and glucose intolerance, with reduction on uterus weight. In OVX animals, treatment with glucocorticoids induced increases on body weight gain, food intake, weight of retroperitoneal adipose tissue, area of adipocytes of retroperitoneal and perigonadal + perirenal fat depots, plasma triglycerides (corticosterone), and glycemic response after GTT (dexamethasone), with minor effects on SHAM group. Estradiol treatment to OVX rats prevented these effects induced by glucocorticoids, in addition to decrease body weight gain, fat accumulation and glucose intolerance, and to increase weight of uterus, triglycerides and free fatty acids plasma levels. These data demonstrate that protection against glucocorticoids-induced anabolic responses in females is eliminated by ovariectomy and estradiol can prevent these responses.

Metabolic Changes Induced by High-Fat Meal Evoke Different Microvascular Responses in Accordance with Adiposity Status.

Background Frequently, ingestion of lipids exceeds our daily requirements and constantly exposes humans to circulating lipid overload which may lead to endothelial dysfunction (ED), the earliest marker of atherosclerosis. Nailfold videocapillaroscopy (NVC) technique can detect ED on microcirculation. Using NVC, we aimed to demonstrate if metabolic alterations evoked by high-fat meals can act differently on microvascular endothelial reactivity in lean and women with obesity. Methods Women, aged between 19 and 40 years, were allocated to control group (CG) and with obesity group (OBG) and were subjected to blood analysis for determination of glucose, total cholesterol (TC), triglycerides (TG), and low-density lipoprotein cholesterol (LDL-c) and high-density lipoprotein cholesterol (HDL-c) and NVC evaluation at fasting and 30, 60, 120, and 180-min after high-fat meal ingestion. NVC technique evaluated microvascular reactivity through the following variables: red blood cell velocity (RBCV) at rest and after 1-min ischemia (maximal red blood cell velocity, RBCVmax) and time taken to reach it (TRBCVmax). A P value ≤0.05 was considered significant. Results High-fat meal promoted a two-phase response in both groups: one until 60-min, associated with glucose and insulin levels, and the other after 120-min, associated with TG levels. Significant differences between groups were observed concerning insulin and HDL-c concentrations only at fasting and TC, TG, and LDL-c levels in all-time points. Regarding microvascular reactivity, RBCV, RBCVmax, and TRBCVmax were significantly different in OBG at 30-min compared to baseline. RBCVmax and TRBCVmax were significantly different in CG at 30-min and 60-min comparing to fasting. In all-time points, OBG presented RBCV, RBCVmax , and TRBCVmax significantly different in comparison to CG. ConclusionHigh-fat meal worsened ED on microcirculation in women with obesity and induced impairment of endothelial function in lean ones, reinforcing the association between high-fat meal and atherosclerosis.

PO-209 Effects of aerobic exercise on oxidant/anti-oxidant indexes and gut microbiota in young obese volunteers

&#x0D; Objective The mean body mass index (BMI) and the prevalence of obese and overweight individuals increasing substantially worldwide during the previous three decades. Variation in gut microorganisms might play an important role in the pathogenesis of obesity, but the mechanisms by which gut microbiota promote metabolic disturbances are not well understood. Exercise is associated with altered gut microbial composition, but few studies have investigated whether the gut microbiota and associated metabolites are modulated by exercise training in humans. We explored the impact of 8 weeks aerobic exercise on serum oxidant and anti-oxidant indexes and gut microbiota.&#x0D; Methods All 40 young male volunteers are enrolled in the study, the lean ones (n=11), which BMI≤22 are as control group. And the obese ones (n=29), which BMI &gt; 28 participated in the 8 weeks aerobic exercise. The body weight and BMI of each volunteers were recorded. The serum malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPx) and total antioxidant capacity (TAOC) were measured by ELISA. The composition and diversity of gut microbiota were analyzed with 16S rDNA sequencing.&#x0D; Results ① Compared with the control, the level of serum GPx, SOD and TAOC decreased significantly (P &lt; 0.001), and the MDA increased significantly (P &lt; 0.001) in the obese group. After the 8 weeks aerobic exercise intervention, the MDA level decreased significantly (P＜0.01), the TAOC level increased significantly (P &lt; 0.01), and there were no significant changes in the level of GPX and SOD.&#x0D; ② Compared with the control, the ratio of Bifidobacteriaceae, Alcaligenaceae, Erysipelotrichaceae, and Verrucomicrobiaceae decreased significantly(p＜0.05) in the obese group, and the ratio of Ruminococcaceae, Helicobacteraceae increased significantly (P＜0.05). After the 8 weeks aerobic exercise intervention, the ratio of Bifidobacteriaceae, Alcaligenaceae increased significantly (P＜0.05)，and the ratio of Ruminococcaceae reduced remarkably (p＜0.05). The ACE index was significantly increased after the intervention (P &lt; 0.05).&#x0D; ③ Through the correlation analysis of the data above, there was a certain correlation between the serum oxidant/anti-oxidant indexes and gut microbiota composition. After the aerobic exercise, there was a positive correlation between MDA and Ruminococcaceae、TAOC and Bifdobacteriace (P＜0.05)；a negative correlation between MDA and Bifdobacteriace、TAOC and Ruminococcaceae (P＜0.05). After 8 weeks of aerobic exercise, MDA level was negatively correlated with ACE index (r=-0.466，P＜0.05).&#x0D; Conclusions ① Compared with the control, there was a significant increase of serum oxidation index and the serum anti-oxidation index dropped significantly among the obese subjects, which indicated that the accumulation of serum free radicals might be one of the causes of obesity. The 8 weeks aerobic exercise intervention can enhance the antioxidant capacity effectively.&#x0D; ② Compared with the control, the proportion of Bifidobacteriaceae in the obese group was significantly decreased, and the proportion of the bacteria with direct correlation to obesity, such as Ruminococcaceae increased significantly. 8 weeks aerobic exercise could inverse these changes among the obese subjects, suggested that the improvement of body phenotype of obese subjects was closely related to the effective regulation of their gut microbiota structure.The change of ACE index indicated that aerobic exercise could increase the diversity of gut microbiota.&#x0D; ③ Combined the correlation analysis of gut microbiota diversity index showed that there were tight correlation between the serum oxidant/anti-oxidant indexes and the gut microbiota composition and structure. It might caused metabolic disorders and eventually increased fat accumulation and changed the host body phenotype.&#x0D; &#x0D; &#x0D;

Adipokines and C-peptide in overweight and obese pregnant women.

The aim of the study was to evaluate the levels of adipokines such as adiponectin, resistin, leptin as well as C-peptide in overweight and obese pregnant women. The adipokines and C-peptide concentrations were measured in the group of 38 overweight/obese pregnant women (BMI > 25 kg/m2) and in 42 pregnant women of normal weight (BMI < 25 kg/m2) with ELISA tests between 24th and 34th weeks of gestation. The overweight/obese women compared to lean ones were characterized by significantly higher concentrations of leptin (43.44 ± 31.41 vs. 21.29 ± 12.67 ng/mL, p = 0.0001) and C-peptide (2.77 ± 1.88 vs. 2.25 ± 1.42 ng/mL, p = 0.034). There were no significant differences between groups in resistin (17.39 ± 7.59 vs. 15.76 ± 6.64 ng/mL, NS) and adiponectin (6.93 ± 3.52 vs. 8.07 ± 6.53 μg/mL, NS) levels. In the overweight/obese patients, no relationships between the adipokines, C-peptide and CRP concentrations were found. BMI was negatively correlated with the resistin levels (R = -0.406, p = 0.011). The significant correlation between leptin and C-peptide concentrations was observed in the study group (R = 0.517, p = 0.012). In the control group, the negative correlation between adiponectin concentrations and BMI was shown (R = -0.446, p = 0.003). The higher levels of leptin in the overweight and obese pregnant women seem to reflect the leptin resistance condition and the higher levels of C-peptide in this group is suggestive for hyperinsulinemia. The positive correlation between C-peptide and leptin levels but not with resistin and adiponectin might confirm the role of leptin in the hyperinsulinemia development in overweight and obesity during pregnancy.