Body weight development and body composition of the VEH and MET exposed OE-NPY^DβH offspring.

<p>Body weight development of the female (a) and male (b) offspring. GTT and EchoMRI marked on the figures. The gray shaded area = western diet (WD). Fat mass (FM; g) of the VEH and MET exposed OE-NPY^DβH female (c) and male (d) offspring at 4 (during RD) and 7 months (during WD). The weight of inguinal^# (iWAT), gonadal/epididymal (gWAT/eWAT), retroperitoneal (rWAT), mesenteric (mWAT) white adipose tissue and brown adipose tissue (BAT) of the female (e) and male (f) offspring at 7 months. n(females) = 11 in VEH and 8 in MET exposed offspring and n(males) = 20 in VEH and 14 in MET exposed offspring. ^#n = 13 in iWAT of the MET exposed male offspring. Significances by 2-RM-ANOVA and Sidak’s multiple comparisons test (a, b) and Student’s t-test (c-f). The data expressed as mean ± SEM, *P < 0.05, **P < 0.01 and ***P < 0.001.</p

Glucose homeostasis.

<p>Glucose tolerance test of the VEH and MET exposed OE-NPY^DβH female and male offspring at 3 months during RD (a, d) and at 6 months during WD (b, e), respectively. Corresponding AUC values of the GTTs (c, f). n(females) = 11 in VEH and 8 in MET exposed offspring and n(males) = 20 in VEH and 13 in MET exposed offspring. Significances by 2-RM-ANOVA (a, b, d, e) and Student’s t-test (c, f). The data expressed as mean ± SEM, *P < 0.05, **P < 0.0.1.</p

Composition of the gut microbiota.

<p>Occupation of microbiota by 8 most prominent phyla in the VEH and MET exposed OE-NPY^DβH and VEH exposed WT female and male offspring at 10–11 weeks (a,b). Weighted PCoA of the VEH OE-NPY^DβH vs. MET OE-NPY^DβH vs. VEH WT female offspring microbiota where principal coordinates PC1 explains 40.61% and PC2 18.93% of the total variance (c). Unweighted PCoA of the VEH OE-NPY^DβH vs. MET OE-NPY^DβH vs. VEH WT female offspring microbiota where PC1 explains 18.76% and PC2 16.23% of the total variance (d). Weighted PCoA of the VEH OE-NPY^DβH vs. MET OE-NPY^DβH vs. VEH WT male offspring microbiota where PC1 explains 45.69% and PC2 13.27% of the total variance (e). Unweighted PCoA of the VEH OE-NPY^DβH vs. MET OE-NPY^DβH vs. VEH WT male offspring microbiota where PC1 explains 20.26% and PC2 14.51% of the total variance (f). Red squares and triangles = VEH OE-NPY^DβH female (<i>n</i> = 6) and male (<i>n</i> = 5) offspring, respectively; blue triangles and squares = MET OE-NPY^DβH female (<i>n</i> = 6) and male (<i>n</i> = 6), offspring, respectively; orange circles = VEH WT female (<i>n</i> = 6) and male (<i>n</i> = 6) offspring. Plots produced by Qiime.</p

Relative abundancies of gut bacteria at different taxonomical levels at 10–11 weeks.

<p>Relative abundance of <i>Bacteroidetes</i> (a), <i>Firmicutes</i> (b), <i>Proteobacteria</i> (c), <i>Erysipelotrichaceae</i> (d), <i>Odoribacter</i> (e), <i>Parabacteroides</i> (f) and <i>Sutterella</i> (g) in the VEH OE-NPY^DβH (gray boxes) and MET OE-NPY^DβH (white boxes) female and male offspring. Relative abundance expressed as decimal number where 1 corresponds to 100%. Box plots showing the 25^th, 75^th percentile and median and the whiskers extending from minimum to maximum together with all data points, <i>n</i> = 5–6. Significances by 2-way ANOVA, *P < 0.05.</p

Comparison of the serum profile, HOMA-IR, HOMA-β and QUICKI of the VEH and MET exposed OE-NPY^DβH offspring at 7 months.

<p>Comparison of the serum profile, HOMA-IR, HOMA-β and QUICKI of the VEH and MET exposed OE-NPY^DβH offspring at 7 months.</p

The gut microbiota comparison between VEH exposed OE-NPY^DβH and WT offspring at 10–11 weeks.

<p>The gut microbiota comparison between VEH exposed OE-NPY^DβH and WT offspring at 10–11 weeks.</p

Metabolic parameters of the VEH exposed OE-NPY^DβH and WT female and male offspring at 3, 4, 6 and 7 months.

<p>Metabolic parameters of the VEH exposed OE-NPY^DβH and WT female and male offspring at 3, 4, 6 and 7 months.</p

Correlation of gut microbiota composition to metabolic parameters.

<p>Correlation of the abundance of <i>Firmicutes</i> with GTT at 3 months (a), fat mass at 4 months (b), liver weight at 7 months (c), <i>Bacteroidetes</i> with GTT at 3 months (d), <i>Proteobacteria</i> with cholesterol at 7 months (e), <i>Clostridia</i> with fat mass at 4 months (f) and liver weight at 7 months (g) and α-diversity with liver weight at 7 months (h) in the VEH OE-NPY^DβH (<i>n</i> = 5), MET OE-NPY^DβH (<i>n</i> = 6) and VEH WT male (<i>n</i> = 6) offspring. Correlation of the abundance of <i>Bacilli</i> with serum cholesterol at 7 months (i) in the VEH OE-NPY^DβH (<i>n</i> = 6), MET OE-NPY^DβH (<i>n</i> = 6), and VEH WT (<i>n</i> = 6) female offspring. Black circles = VEH OE-NPY^DβH, open circles = MET OE-NPY^DβH, red and blue triangles = WT female and male offspring, respectively. P-values and r by Spearman correlation.</p

Early fecal microbiota composition in children who later develop celiac disease and associated autoimmunity

<p><b>Objectives:</b> Several studies have reported that the intestinal microbiota composition of celiac disease (CD) patients differs from healthy individuals. The possible role of gut microbiota in the pathogenesis of the disease is, however, not known. Here, we aimed to assess the possible differences in early fecal microbiota composition between children that later developed CD and healthy controls matched for age, sex and HLA risk genotype.</p> <p><b>Materials and methods:</b> We used 16S rRNA gene sequencing to examine the fecal microbiota of 27 children with high genetic risk of developing CD. Nine of these children developed the disease by the age of 4 years. Stool samples were collected at the age of 9 and 12 months, before any of the children had developed CD. The fecal microbiota composition of children who later developed the disease was compared with the microbiota of the children who did not have CD or associated autoantibodies at the age of 4 years. Delivery mode, early nutrition, and use of antibiotics were taken into account in the analyses.</p> <p><b>Results:</b> No statistically significant differences in the fecal microbiota composition were found between children who later developed CD (<i>n</i> = 9) and the control children without disease or associated autoantibodies (<i>n</i> = 18).</p> <p><b>Conclusions:</b> Based on our results, the fecal microbiota composition at the age of 9 and 12 months is not associated with the development of CD. Our results, however, do not exclude the possibility of duodenal microbiota changes or a later microbiota-related trigger for the disease.</p