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Early-life events are associated with the risk of obesity and comorbidities later in life. The gut microbiota-whose composition is influenced by genetics and environmental factors-could be involved. Since the microbiota affects metabolism and fat storage, early-life insults could contribute to the occurrence of obesity driven, in part, by microbiota composition. We examined associations of gut bacteria with early-life events, nutritional status, and body composition in the Nutritionist's Health Study (NutriHS). A cross-sectional study of 114 female participants examining early-life data, body composition, and biological samples was conducted. Fecal microbiota structure was determined targeting the V4 region of the 16S rRNA gene. Principal coordinates analysis (PCoA) and permutational multivariate analysis of variance (PERMANOVA) were used to test the impact of variables on microbial diversity. Profiles were identified using the Jensen-Shannon divergence matrix and Calinski-Harabasz index. Differential abundance between the categories of exclusive breastfeeding duration and nutritional status was tested using DESeq2. In the sample [median age 28 years and body mass index (BMI) 24.5 kg/m ], 2 microbiota profiles driven by the or genus were identified. An estimated 9.1% of the variation was explained by the profiles (p < 0.001), 2.1% by nutritional status (p = 0.004), and 1.8% by exclusive breastfeeding (p = 0.012). The proportion of participants with BMI <25 kg/m and who were breastfed for at least 6 months was higher in the profile (p < 0.05). Findings in a -driven profile of healthy women reinforce that early-life events play a role in defining gut microbiota composition, confirming the importance of exclusive breastfeeding for infant gut colonization in establishing a protective profile against adiposity-related outcomes in adulthood.

•The energy-adjusted dietary inflammatory index was associated with markers of insulin resistance, inflammation, and body adiposity.•The energy-adjusted dietary inflammatory index was inversely correlated with the abundance of the Eubacterium.xylanophilum.group.•The energy-adjusted dietary inflammatory index was directly correlated with the abundance of Actinomyces.•Actinomyces were significantly more abundant in the highest (most proinflammatory) energy-adjusted dietary inflammatory index quartile.•Actinomyces could be involved in the association between the dietary inflammatory index with visceral adiposity. To deepen the understanding of the influence of diet on weight gain and metabolic disturbances, we examined associations between diet-related inflammation and body composition and fecal bacteria abundances in participants of the Nutritionists’ Health Study. Early-life, dietary and clinical data were obtained from 114 women aged ≤45 years. A validated food frequency questionnaire was used to calculate the energy-adjusted dietary inflammatory index (E-DII). Participants’ data were compared by E-DII quartiles using ANOVA or Kruskal-Wallis. Associations of DXA-determined body composition with the E-DII were tested by multiple linear regression using DAG-oriented adjustments. Fecal microbiota was analyzed targeting the V4 region of the 16S rRNA gene. Spearman correlation coefficients were used to test linear associations; differential abundance of genera across the E-DII quartiles was assessed by pair-wise comparisons. E-DII score was associated with total fat (b=1.80, p<0.001), FMI (b=0.08, p<0.001) and visceral fat (b=1.19, p=0.02), independently of maternal BMI, birth type and breastfeeding. E-DII score was directly correlated to HOMA-IR (r=0.30; p=0.004), C-reactive protein (r=0.29; p=0.003) and to the abundance of Actinomyces, and inversely correlated to the abundance of Eubacterium.xylanophilum.group. Actinomyces were significantly more abundant in the highest (most proinflammatory) E-DII quartile. Association of E-DII with markers of insulin resistance, inflammation, body adiposity and certain gut bacteria are consistent with beneficial effects of anti-inflammatory diet on body composition and metabolic profile. Bacterial markers, such as Actinomyces, could be involved in the association between the dietary inflammation with visceral adiposity. Studies designed to explore how a pro-inflammatory diet affects both central fat deposition and gut microbiota are needed.

Background and aims The gut microbiome is associated with obesity, mainly mediated by bacteria-produced short-chain fatty acids (SCFAs). It is unknown how SCFA concentrations are associated with the phenotypes metabolically healthy normal weight (MHNW), metabolically unhealthy normal weight (MUNW), metabolically healthy obese/overweight (MHO), and metabolically unhealthy obese/overweight (MUO). We compared plasma and fecal SCFA concentrations among adult women categorized according to the metabolic phenotypes mentioned above and examined associations between SCFA and adiposity and components of energy and glucose homeostasis. Methods This was a cross-sectional study involving 111 participants. Body composition was assessed by DEXA. Energy and glycemic homeostasis were assessed by the standard mixed-meal tolerance test coupled with indirect calorimetry. SCFAs were quantified by gas chromatography and mass spectrometry. Results Only plasma propionate was increased in the MHNW phenotype compared to the MHO and MUO phenotypes [ p  < 0.05]. Fecal propionate and butyrate concentrations and plasma propionate concentrations were inversely associated with total and visceral adiposity [ p  < 0.05]. Fecal and plasma SCFA concentrations were associated with reduced glucose, insulin and HbA1c levels, increased fasting and postprandial GLP-1 levels; and more preserved beta-cell function [ p  < 0.05]. Fecal and plasma SCFA concentrations were positively correlated with resting energy expenditure and lipid oxidation rate and inversely correlated with the oxidation rate of carbohydrates [ p  < 0.05]. Conclusion These findings reinforce the concept that fecal and plasma SCFA concentrations are linked to specific components of energy and glucose homeostasis; and body adiposity. However, it was not possible to discriminate the different metabolic phenotypes of adiposity based on the determination of fecal SCFA concentrations.

The aim of this study was to examine whether paternal and maternal body mass indexes (BMIs) were independently associated with obestatin and visfatin levels in adult offspring. This cross-sectional analysis included 124 women who participated in the Nutritionists’ Health Study (NutriHS) at baseline. Early life events, anthropometry, dual-energy x-ray absorptiometry–determined body composition and blood sample were obtained. Associations of parental BMI with outcomes (obestatin and visfatin) were tested by multiple linear regression, using minimal sufficient adjustments recommended by Directed Acyclic Graph. Participants’ mean BMI was 25 ± 5 kg/m2 and 74% were metabolically healthy. Median obestatin and visfatin levels were 56.4 pg/mL (42–72) and 17.7 ng/mL (14–21.8), respectively. Eleven percent of mothers and 39% of fathers were overweight/obese. Daughters born from overweight/obese mothers had higher BMI than those born from normal weight women (P = 0.003). In adjusted regression model, offspring obestatin levels were associated with maternal BMI (β = –0.03; P = 0.045) and paternal BMI (β = –0.02; P = 0.048) independently of maternal and paternal education, maternal age, and maternal use of tobacco, alcohol, and/or drugs. No association was detected with visfatin levels. Inverse associations of maternal and paternal BMIs with offspring obestatin concentrations in women could suggest a utility of this biomarker of energy regulation determined in early adulthood. Whether obestatin could be an indicator of protection against obesity-related disorders in the life course requires investigation in studies designed to test such hypothesis. •Maternal and paternal body mass indexes are inversely associated with offspring obestatin levels in women.•Parental adiposity could be a factor that influences weight control of offspring.•Possible utility of obestatin as biomarker of energy regulation in early adulthood.•Could obestatin be a protective marker against obesity-related disorders?

This study investigated the association between fermentable oligo-di-mono-saccharides and polyols (FODMAPs) intake, problematic foods, body adiposity, and gastrointestinal symptoms in 44 women with irritable bowel syndrome (IBS). Around 84% reported to have excluded some food from their diet. Adiposity was not associated with the frequency of gastrointestinal symptoms and IBS severity. Controlling for BMI, there were significant correlations between number of problematic foods versus waist circumference ( r  = 0.306; p  = 0.049) and protein intake ( r  = −0.378; p  = 0.014). The IBS severity correlated to the carbohydrate intake ( r  = −0.320; p  = 0.039). Patients with diarrhea demonstrated statistical tendency to restrict the intake of fat ( p  = 0.058), free fructose ( p  = 0.07), and oligosaccharides ( p  = 0.051). Patients with mucus in the stool had higher lactose intake ( p  = 0.025). The number of food considered problematic was higher for patients who reported stomach burning ( p  = 0.0001). Associations among adiposity, gastrointestinal symptoms, problematic food, and FODMAPs were identified and reaffirm the role of individualized nutritional treatment in the management of IBS.