14 research outputs found
Maternal emulsifier consumption induces anxiety–related states in male offspring.
No full text(A–D) Open field performance in 9–week–old male (A and B) (n = 9 CTRL–CTRL; n = 9 CTRL–Emul; n = 6 Emul–CTRL; n = 6 Emul–Emul) and female (C and D) (n = 9 CTRL–CTRL; n = 8 CTRL–Emul; n = 5 Emul–CTRL; n = 5 Emul–Emul) offspring born of control and emulsifier–exposed mothers, including time spent per zone (A and C) and total distance traveled (B and D). (E, F) Time spent in the light compartment during the dark–light box test in 9–week–old male (E) (n = 9 CTRL–CTRL; n = 9 CTRL–Emul; n = 6 Emul–CTRL; n = 6 Emul–Emul) and female (F) (n = 9 CTRL–CTRL; n = 8 CTRL–Emul; n = 5 Emul–CTRL; n = 5 Emul–Emul) offspring born of control and emulsifier–exposed mothers. (G–J) Short–term memory parameters in 10–week–old male (G and H) (n = 9 CTRL–CTRL; n = 9 CTRL–Emul; n = 4 Emul–CTRL; n = 6 Emul–Emul) and female (I and J) (n = 7 CTRL–CTRL; n = 7 CTRL–Emul; n = 3 Emul–CTRL; n = 4 Emul–Emul) offspring born of control and emulsifier–exposed mothers, including discrimination index (G and I) and exploratory time (H and J). Data are derived from 1 single experiment. Data are expressed as mean ± SEM. Statistical analysis was performed by two–way ANOVA followed by Sidak’s post hoc analysis. *p 10.6084/m9.figshare.22742759. (TIF)</p
S2 Fig -
No full text(A) PCA plot showing the distribution of sequenced samples (n = 4 CTRL and n = 5 Emul). (B) Representative 20× images of POMC neurons in the ARC of control and emulsifiers–treated male offspring at P21. (C) Number of POMC neurons per section of control and emulsifier offspring at P21 (n = 3 mice/group). (D) POMC neuronal area of control and emulsifier offspring at P21 (n = 20 neurons per animal; 3 mice/group). Data are expressed as mean ± SEM. Statistical analysis was performed by t test. POMC: pro–opiomelanocortin; 3V: third ventricle; ns: non–significant. The data underlying this figure can be found at DOI:10.6084/m9.figshare.22742759. (TIF)</p
Maternal emulsifier consumption programs offspring metabolic and neuropsychological health in mice.
No full textModern lifestyle is associated with a major consumption of ultra-processed foods (UPF) due to their practicality and palatability. The ingestion of emulsifiers, a main additive in UPFs, has been related to gut inflammation, microbiota dysbiosis, adiposity, and obesity. Maternal unbalanced nutritional habits during embryonic and perinatal stages perturb offspring's long-term metabolic health, thus increasing obesity and associated comorbidity risk. However, whether maternal emulsifier consumption influences developmental programming in the offspring remains unknown. Here, we show that, in mice, maternal consumption of dietary emulsifiers (1% carboxymethyl cellulose (CMC) and 1% P80 in drinking water), during gestation and lactation, perturbs the development of hypothalamic energy balance regulation centers of the progeny, leads to metabolic impairments, cognition deficits, and induces anxiety-like traits in a sex-specific manner. Our findings support the notion that maternal consumption of emulsifiers, common additives of UPFs, causes mild metabolic and neuropsychological malprogramming in the progeny. Our data call for nutritional advice during gestation
Metabolic outcomes derived from western diet consumption on female offspring from emulsifier–treated dams.
No full text(A) Schematic illustration of offspring treatment until adulthood. (B) Six–hour fasting blood glucose levels at 22 weeks of age, after 11 weeks of WD exposure (n = 8 CTRL–CTRL; n = 10 CTRL–Emul; n = 8 Emul–CTRL; n = 8 Emul–Emul). (C) Plasma insulin levels after 6 h of fasting at 22 weeks of age, after 11 weeks of WD exposure (n = 8 CTRL–CTRL; n = 10 CTRL–Emul; n = 8 Emul–CTRL; n = 8 Emul–Emul). (D) Plasma leptin levels after 6 h of fasting at 22 weeks of age, after 11 weeks of WD exposure (n = 8 CTRL–CTRL; n = 10 CTRL–Emul; n = 8 Emul–CTRL; n = 8 Emul–Emul). (E) Body weight at 22 weeks of age, after 11 weeks of WD exposure (n = 8 CTRL–CTRL; n = 10 CTRL–Emul; n = 8 Emul–CTRL; n = 8 Emul–Emul). (F) gWAT weight normalized by total body weight and represented as % of control animals at 22 weeks of age, after 11 weeks of WD exposure (n = 8 CTRL–CTRL; n = 10 CTRL–Emul; n = 8 Emul–CTRL; n = 8 Emul–Emul). (G) GTT and (H) AUC (n = 8 CTRL–CTRL; n = 10 CTRL–Emul; n = 8 Emul–CTRL; n = 8 Emul–Emul) at 19 weeks of age, after 8 weeks of WD exposure. (I) ITT and (J) AUC (n = 8 CTRL–CTRL; n = 10 CTRL–Emul; n = 8 Emul–CTRL; n = 8 Emul–Emul) at 19 weeks of age, after 8 weeks of WD exposure. Data are derived from 1 single experiment. Data are expressed as mean ± SEM. Statistical analysis was performed by two–way ANOVA followed by Sidak’s post hoc analysis. *p p p 10.6084/m9.figshare.22742759. AUC, area under the curve; GTT, glucose tolerance test; gWAT, gonadal white adipose tissue; ITT, insulin tolerance test; WD, western–style diet.</p
Emulsifiers induce mild glucose intolerance in female mice before the onset of pregnancy.
No full text(A) Experimental design of maternal emulsifier consumption highlighting the period of maternal characterization. (B) Daily water consumption of control and emulsifier–treated females before mating (n = 5/group). (C) Daily food intake of control and emulsifier–treated females before mating (n = 5/group). (D) Body weight of control and emulsifier–treated females before mating (n = 10 CTRL and n = 10 Emul). (E) GTT and (F) AUC of control and emulsifier females before mating (n = 10 CTRL and n = 10 Emul). (G) Fasting blood glucose levels of control and emulsifier–supplemented females before mating (n = 10 CTRL and n = 10 Emul). (H) Plasma leptin levels after 6 h in fasting of control and emulsifier–treated females before mating (n = 8 CTRL and n = 8 Emul). Data are derived from 1 single experiment. Data are expressed as mean ± SEM. Statistical analysis was performed with an unpaired t test in B, C, D, F, G, H, and by two–way ANOVA followed by Sidak’s post hoc analysis in E. *p 10.6084/m9.figshare.22742759. AUC, area under the curve; GTT, glucose tolerance test.</p
Metabolic impairments derived from western diet consumption are not exacerbated in male offspring from emulsifier–treated dams.
No full text(A) Schematic illustration of offspring treatment until adulthood. (B) Body weight at 22 weeks of age, after 11 weeks of WD exposure (n = 8 CTRL–CTRL; n = 7 CTRL–Emul; n = 7 Emul–CTRL; n = 5 Emul–Emul). (C) eWAT weight normalized by total body weight and represented as % of control animals at 22 weeks of age, after 11 weeks of WD exposure (n = 8 CTRL–CTRL; n = 7 CTRL–Emul; n = 7 Emul–CTRL; n = 5 Emul–Emul). (D) GTT and (E) AUC (n = 8 CTRL–CTRL; n = 7 CTRL–Emul; n = 7 Emul–CTRL; n = 5 Emul–Emul) at 19 weeks of age, after 8 weeks of WD exposure. (F) ITT and (G) AUC (n = 8 CTRL–CTRL; n = 7 CTRL–Emul; n = 7 Emul–CTRL; n = 5 Emul–Emul) at 19 weeks of age, after 8 weeks of WD exposure. (H) Six–hour fasting blood glucose levels at 22 weeks of age, after 11 weeks of WD exposure (n = 8 CTRL–CTRL; n = 7 CTRL–Emul; n = 7 Emul–CTRL; n = 5 Emul–Emul). (I) Plasma insulin levels after 6 h of fasting at 22 weeks of age, after 11 weeks of WD exposure (n = 8 CTRL–CTRL; n = 7 CTRL–Emul; n = 7 Emul–CTRL; n = 5 Emul–Emul). (J) Plasma leptin levels after 6 h of fasting at 22 weeks of age, after 11 weeks of WD exposure (n = 8 CTRL–CTRL; n = 7 CTRL–Emul; n = 7 Emul–CTRL; n = 5 Emul–Emul). Data are derived from 1 single experiment. Data are expressed as mean ± SEM. Statistical analysis was performed by two–way ANOVA followed by Sidak’s post hoc analysis. The data underlying this figure can be found at DOI:10.6084/m9.figshare.22742759. AUC, area under the curve; eWAT, epididymal white adipose tissue; GTT, glucose tolerance test; ITT, insulin tolerance test; WD, western–style diet.</p
Emulsifiers induce mild maternal glucose intolerance.
No full text(A) Experimental design of maternal emulsifier consumption highlighting the period of maternal characterization. (B) Daily food intake of control and emulsifier–treated dams post–weaning (n = 6/group). (C) Body weight of control and emulsifier–treated dams post–weaning (n = 15 CTRL and n = 15 Emul). (D) gWAT weight normalized by total body weight and represented as % of control animals of control and emulsifier dams post–weaning (n = 15 CTRL and n = 15 Emul). (E) GTT and (F) AUC of control and emulsifier–treated dams post–weaning (n = 15 CTRL and n = 15 Emul). (G) Fasting blood glucose levels of control and emulsifier–treated dams post–weaning (n = 15 CTRL and n = 15 Emul). (H) Plasma leptin levels after 6 h of fasting of control and emulsifier–treated dams post–weaning (n = 6 CTRL and n = 7 Emul). (I) Plasma insulin levels after 6 h of fasting of control and emulsifier–treated dams post–weaning (n = 7 CTRL and n = 7 Emul). Data in B, H, and I are derived from 1 single experiment. Data in C, D, E, F, and G are pools from 2 different experiments. Data are expressed as mean ± SEM. Statistical analysis was performed with an unpaired t test in B, C, D, F, G, H, and I and by two–way ANOVA followed by Sidak’s post hoc analysis in E. *p p p 10.6084/m9.figshare.22742759. (TIF)</p
Hypothalamic feeding–related neuropeptides are altered upon maternal emulsifier consumption.
No full text(A) Volcano plot of transcript expression in the MBH between control and emulsifier offspring at weaning. Threshold for FC (±1.5) and FDR (p n = 4 CTRL and n = 5 Emul). (B) Cytoscape plot of the down–regulated enriched pathways (p n = 4 CTRL and n = 5 Emul). (D) Transcript expression of orexigenic and anorexigenic peptides in the MBH in female offspring from control and emulsifier–exposed dams at weaning (n = 7 CTRL and n = 7 Emul). (E) Representative immunofluorescence images showing AgRP staining density in the PVH of control and emulsifier male offspring at weaning and integrated density quantification (n = 6 mice/group). (F) Representative immunofluorescence images showing α–MSH staining density in the PVH of control and emulsifier male offspring at weaning and integrated density quantification (n = 5 mice/group). Data in C and D are derived from 1 single experiment. Data in E and F are pools from 2 different experiments. Data are expressed as mean ± SEM. Statistical analysis was performed by unpaired t test in C, D, E, and F. *p p 10.6084/m9.figshare.22742759. Pomc, pro–opiomelanocortin; Cart, cocaine–and amphetamine–regulated transcript; Agrp, agouti–related peptide; Npy, neuropeptide Y; Pcsk1, proprotein convertase 1; Mcr3, melanocortin 3 receptor; Mcr4, melanocortin 4 receptor; α–MSH, alpha–melanocyte–stimulating hormone; PVH, paraventricular hypothalamic nucleus; 3V, third ventricle; DEG, differentially expressed gene; FC, fold change; FDR, false discovery rate; MBH, mediobasal hypothalamus.</p
Male offspring from emulsifier–treated dams respond normally to leptin.
No full text(A) Food intake of males at 20 weeks of age (n = 9 CTRL–CTRL; n = 9 CTRL–Emul; n = 6 Emul–CTRL; n = 5 Emul–Emul). (B) Food intake of females at 20 weeks of age (n = 9 CTRL–CTRL; n = 12 CTRL–Emul; n = 6 Emul–CTRL; n = 8 Emul–Emul). (C) Average overnight food intake of males after vehicle (Vh) (n = 8 CTRL–CTRL; n = 8 CTRL–Emul; n = 5 Emul–CTRL; n = 5 Emul–Emul) or leptin (Lep) (n = 8 CTRL–CTRL; n = 8 CTRL–Emul; n = 5 Emul–CTRL; n = 5 Emul–Emul) injection at 20 weeks of age. (D) Overnight body weight after vehicle (n = 8 CTRL–CTRL; n = 8 CTRL–Emul; n = 5 Emul–CTRL; n = 5 Emul–Emul) or leptin (n = 8 CTRL–CTRL; n = 8 CTRL–Emul; n = 5 Emul–CTRL; n = 5 Emul–Emul) injection in males at 20 weeks of age. Data in A, B, C, and D are pools from 2 different experiments. Data are expressed as mean ± SEM. Statistical analysis was performed by two–way ANOVA followed by Sidak’s post hoc analysis in A, B, and by t test in C and D. ns: not significant; *p p 10.6084/m9.figshare.22742759. (TIF)</p
List of differentially expressed genes (DEGs) and gene ontology (GO) enriched pathway analysis of the down–regulated genes obtained from RNA sequencing of P21 male offspring from control and emulsifiers–treated dams.
No full textList of differentially expressed genes (DEGs) and gene ontology (GO) enriched pathway analysis of the down–regulated genes obtained from RNA sequencing of P21 male offspring from control and emulsifiers–treated dams.</p
