bioRxiv Science⌕ Search

bioRxiv · 10.1101/2022.10.11.511721

Maternal age, obesity and hyperglycaemia are associated with a delay in preimplantation development in a mouse model of type 2 diabetes

Abstract

Aims/hypothesisDelayed maternal age, obesity and diabetes are associated with reduced fertility. We investigated how age and obesity/metabolic syndrome impact fertility and hypothesized that its decrease is due to defects in preimplantation embryo development. MethodsThree groups of female C57Bl6 mice (12 weeks, 9 months and 1 year old) were fed either a high fat diet for 8 weeks, to induce obesity and the metabolic syndrome, or a control chow diet. Body weight and composition, glucose tolerance and insulin resistance were assessed. Fecundity was evaluated by mating and pregnancy rates, as well as number of embryos. Embryo quality was assessed morphologically, and cell fate composition was analysed in preimplantation embryos by state-of-the-art single cell quantitative confocal image analysis. ResultsThe high fat diet was associated with increased adiposity, glucose intolerance and insulin resistance, especially in the older mice. Fecundity was affected by age, more than by the diet. Both age and high fat diet were associated with reduced cell fate allocation, indicating a delay in preimplantation embryo development, and with increased expression of GATA3, an inhibitor of placentation. Conclusion/InterpretationThese results support that age and the metabolic syndrome reduce fertility through mechanisms which are present at conception very early in pregnancy. What is already known about this subject?O_LILifestyle changes in modern societies have led to an increase in obesity and type 2 diabetes, and women tend to become pregnant later than ever. These factors have a negative influence on female fecundity. C_LIO_LIIn mice, diet induced obesity is associated with poor quality oocytes that affect overall embryonic development. C_LI What is the key question?O_LIDo age and high fat diet influence cell fate differentiation during preimplantation embryo development? C_LI What are the new findings?O_LIBody composition and glucose metabolism are altered due to high fat diet even when weight is not affected in young animals. C_LIO_LIAlthough there are no differences in mating and fertilization rates, embryo quality is lower with high fat diet. C_LIO_LICells not fully committed to a cell fate (epiblast or primitive endoderm) are increased in embryos from mature dams or fed a high fat diet, indicating a delay in preimplantation embryo development. C_LI How might this impact on clinical practice in the foreseeable future?O_LIOur findings show a delay in early embryo development associated to obesity and maternal age. This delay could be responsible for the low fertility observed in women with type 2 diabetes and obesity. C_LI

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Lilao-Garzon, J., Brito-Casillas, Y., Quesada-Canales, O., Wagner, A. M., Munoz-Descalzo, S.. 2022-10-12. Maternal age, obesity and hyperglycaemia are associated with a delay in preimplantation development in a mouse model of type 2 diabetes. https://doi.org/10.1101/2022.10.11.511721

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Alveolar and airway progenitors converge on an epigenetically encoded profibrotic state

During organ regeneration, epithelial transitional states arise from progenitors and instruct the mesenchyme to remodel the extracellular matrix. However, the identity of the progenitors, the mechanisms underlying this transition, and why these states persist in tissue fibrosis often remain elusive. Here, using lineage tracing in mice, we show that the profibrotic KRT5-/KRT17+ state in pulmonary fibrosis arises convergently from alveolar type (AT) 2 and airway secretory cells. AT1 cells generate neither KRT5-/KRT17+ nor AT2 cells. TGF-{beta}/SMAD3 acts through KMT2A and p300 to epigenetically reprogram human AT2 cells into the KRT5-/KRT17+ state. In human pulmonary fibrosis, KRT5-/KRT17+ cells slough off, and transitional cells re-epithelialize the denuded basement membrane. Transcriptionally convergent states arise in injured kidney, skin, and intestine. This work reframes fibrogenesis as the accumulation of a conserved profibrotic transitional state via ongoing turnover, not persistence alone, and nominates the state transition and its epigenetic regulators as therapeutic targets.

developmental biology↗

Dynamic mechanical sorting biases niche occupancy and lineage outcome during development of bilayered glandular epithelia

Tissue compartmentalization into basal and luminal domains is a hallmark of glandular epithelia, yet how fate boundaries are established and stabilized during dynamic morphogenesis remains a major unresolved question. Here, using mouse embryonic explants, organoids, quantitative live imaging and genetic perturbations, we show that basal-luminal compartmentalization is not maintained by fixed boundaries, but through continuous positional corrections. We show that differences in cellular adhesion and actomyosin contractility drive these positional corrections by promoting active cell sorting. We further find that these mechanical differences influence lineage specification by controlling cell positioning rather than directly instructing cell fate. Before commitment, mosaic, but not uniform, perturbation of cell mechanics alters niche occupancy and biases lineage outcome, indicating that relative mechanical properties determine access to fate-instructive niches. Conversely, perturbation of Notch and YAP remodels compartment-specific mechanical properties and cell-positioning dynamics, revealing a reciprocal coupling between lineage state and mechanical sorting. Conservation of this mechanism across four glandular epithelia of distinct origins and functions identifies dynamic mechanical sorting as a general strategy for maintaining robust tissue compartmentalization during the extensive growth and cellular rearrangements of branching morphogenesis.

developmental biology↗

Unbiased lineage tracing across the adipose organ decouples developmental origin from anatomical and transcriptomic identities

The developmental origins of individual adipose depots and whether embryonic lineage dictates adult function remain unresolved. Here, we apply in utero CRISPR-mediated barcoding lineage tracing to construct the first unbiased clonal map of adipose organ development in mice. The developmental hierarchy we uncover challenges several conventions. Remarkably, interscapular brown fat, used as the prototypical brown fat, is the most developmentally isolated brown fat; depots sharing Myf5/Pax3 lineage markers fail to cluster together; mesenteric white fat shares unexpected high clonal ancestry with brown fats despite a radically divergent transcriptome; and subcutaneous white adipose tissues converge transcriptomically despite distant developmental origins. These findings call for a reinterpretation of single-marker lineage tracing data across the adipose organ and propose that adipose depot identity is not solely encoded by embryonic lineage but is substantially shaped by the anatomical niche.

developmental biology↗