@article{pmid30991877,

title = {High intake of dietary fructose in overweight/obese teenagers associated with depletion of Eubacterium and Streptococcus in gut microbiome},

author = {R B Jones and T L Alderete and J S Kim and J Millstein and F D Gilliland and M I Goran},

year  = {2019},

date = {2019-01-01},

journal = {Gut Microbes},

volume = {10},

number = {6},

pages = {712--719},

abstract = {Background: A western high fat, high carbohydrate diet has been shown to be associated with decreased gut bacterial diversity and reductions in beneficial bacteria. This gut bacteria dysbiosis could develop in early life and contribute to chronic disease risk such as obesity, type 2 diabetes and non-alcoholic fatty liver disease.Objective: To determine how dietary macronutrients are associated with the relative abundance of gut bacteria in healthy adolescents.Methods: Fifty-two obese participants (12-19 years) from two studies, many who were primarily of Hispanic background, provided fecal samples for 16S rRNA gene sequencing. Dietary macronutrients were assessed using 24-hour diet recalls and body composition was assessed using DEXA. General regression models assuming a negative binomial distribution were used to examine the associations between gut bacteria and dietary fiber, saturated fat, unsaturated fats, protein, added sugar, total sugar and free fructose after adjusting for age, gender, race/ethnicity, body fat percentage, study and caloric intake.Results: The genera Eubacterium (Benjamini-Hochberg (BH) corrected p-value = 0.10) and Streptococcus (BH corrected p-value = 0.04) were inversely associated with dietary fructose intake. There were no other significant associations between abundances of gut microbes and other dietary macronutrients, including fiber, fat, protein, total sugar or added sugar.Conclusions: High dietary fructose was associated with lower abundance of the beneficial microbes Eubacterium and Streptococcus, which are involved with carbohydrate metabolism.},

keywords = {microbiome, sugar},

pubstate = {published},

tppubtype = {article}

}

@article{pmid31297972,

title = {Maternal blood pressure mediates the association between maternal obesity and infant weight gain in early postpartum},

author = {P K Berger and J F Plows and R B Jones and N K Pollock and T L Alderete and J H Ryoo and M I Goran},

year  = {2019},

date = {2019-01-01},

journal = {Pediatr Obes},

volume = {14},

number = {11},

pages = {e12560},

abstract = {It is unknown to what extent higher maternal blood pressure (BP) in early postpartum impacts the relationship between higher maternal weight status and greater infant weight gain in early postpartum. To evaluate the mediating role of higher maternal BP at 1 month postpartum on the association between higher maternal weight status at 1 month postpartum and greater infant weight gain over 6 months postpartum. Participants were 169 Hispanic mother-infant pairs. Maternal body mass index (BMI) and BP were assessed at 1 month postpartum. Infant weight was measured at 1 and 6 months postpartum to calculate weight-for-age z scores (WAZ). Multiple linear regression models were used for prediction, and Sobel test was used to determine mediation. Controlling for maternal pre-pregnancy BMI, age, delivery mode, infant sex, and infant birth weight revealed that both maternal BMI (β = .29) and BP (β = .32) predicted infant WAZ gain (both P ≤ .03). However, the relationship between infant WAZ gain and maternal BMI was no longer significant after further adjustment for maternal BP, which remained significant (P < .05). Maternal BP explained 23.6% (Sobel T = 2.01) of the association between maternal BMI at 1 month and infant WAZ gain over 6 months. Our data suggest that higher maternal weight status at 1 month postpartum is related to greater infant weight gain over 6 months postpartum, and this relationship is mediated by higher maternal BP at 1 month postpartum.},

keywords = {microbiome, sugar},

pubstate = {published},

tppubtype = {article}

}

@article{pmid29493105,

title = {Probiotic supplementation increases obesity with no detectable effects on liver fat or gut microbiota in obese Hispanic adolescents: a 16-week, randomized, placebo-controlled trial},

author = {R B Jones and T L Alderete and A A Martin and B A Geary and D H Hwang and S L Palmer and M I Goran},

year  = {2018},

date = {2018-01-01},

journal = {Pediatr Obes},

volume = {13},

number = {11},

pages = {705--714},

abstract = {Numerous studies have shown that there are links between obesity, liver fat and the gut microbiome. However, there are mixed results on whether probiotics could impact the gut microbiome and/or help to decrease liver fat and obesity outcomes. This study aimed to determine whether a probiotic supplement (VSL#3® ) intervention altered gut microbiota and/or gut hormones associated with appetite regulation. The secondary aim of this study was to determine whether VSL#3® altered body composition and liver fat and fibrosis. We conducted a double-blind, randomized placebo-controlled trial in 19 obese Latino adolescents. The intervention consisted of three packets per day of VSL#3® or a matched placebo for 16 weeks. Pre-intervention and post-intervention measures included gut microbial abundance, gut appetite regulating hormones, anthropometrics, body composition, liver fat and liver fibrosis. We conducted linear models to determine whether there were any significant differences in the changes in these outcomes following VSL#3® intervention. Compared with placebo, adolescents that received VSL#3 had significant increases in total adiposity (%) (+1.7 ± 0.6 vs. -1.3 ± 0.5, p < 0.01) and trunk adiposity (%) (+3.3 ± 0.8 vs. -1.8 ± 0.8, p < 0.01) with no significant effects on liver fat/fibrosis, insulin/glucose, gut microbial abundances or gut hormones. VSL#3 supplementation may lead to increased adiposity in obese Latino adolescents with no significant detectable changes in gut microbiota, gut appetite-regulating hormones, liver fat and fibrosis and dietary intake. However, it is important to note that recruitment efforts were terminated early and the sample size fell short of what was planned for this trial.},

keywords = {liver fat, microbiome},

pubstate = {published},

tppubtype = {article}

}

@article{pmid27903830,

title = {Early-Life Sugar Consumption Affects the Rat Microbiome Independently of Obesity},

author = {E E Noble and T M Hsu and R B Jones and A A Fodor and M I Goran and S E Kanoski},

year  = {2017},

date = {2017-01-01},

journal = {J. Nutr.},

volume = {147},

number = {1},

pages = {20--28},

abstract = {The gut microbiome has been implicated in various metabolic and neurocognitive disorders and is heavily influenced by dietary factors, but there is a paucity of research on the effects of added sugars on the gut microbiome. With the use of a rodent model, our goal was to determine how added-sugar consumption during the juvenile and adolescent phase of development affects the gut microbiome. Forty-two juvenile male Sprague-Dawley rats [postnatal day (PND) 26; 50-70 g] were given access to 1 of 3 different 11%-carbohydrate solutions designed to model a range of monosaccharide ratios commonly consumed in sugar-sweetened beverages: 1) 35% fructose:65% glucose, 2) 50% fructose:50% glucose, 3) 65% fructose:35% glucose, and 4) control (no sugar). After ad libitum access to the respective solutions for the juvenile and adolescent period (PND 26-80), fecal samples were collected for next-generation 16S ribosomal RNA sequencing and multivariate microbial composition analyses. Energy intake, weight change, and adiposity index were analyzed in relation to sugar consumption and the microbiota. Body weight, adiposity index, and total caloric intake did not differ as a result of sugar consumption. However, sugar consumption altered the gut microbiome independently of anthropometric measures and caloric intake. At the genus level, Prevotella [linear discriminant analysis (LDA) score = -4.62; P < 0.001] and Lachnospiraceae incertae sedis (LDA score = -3.01; P = 0.03) were reduced, whereas Bacteroides (LDA score = 4.19; P < 0.001), Alistipes (LDA score = 3.88; P < 0.001), Lactobacillus (LDA score = 3.78; P < 0.001), Clostridium sensu stricto (LDA score = 3.77; P < 0.001), Bifidobacteriaceae (LDA score = 3.59; P = 0.001), and Parasutterella (LDA score = 3.79; P = 0.004) were elevated by sugar consumption. No overall pattern could be attributable to monosaccharide ratio. Early-life sugar consumption affects the gut microbiome in rats independently of caloric intake, body weight, or adiposity index; these effects are robust across a range of fructose-to-glucose ratios.},

keywords = {microbiome, sugar},

pubstate = {published},

tppubtype = {article}

}