Integrating Spatial and Single‐Nucleus Transcriptomic Data to Assess the Effects of Intrauterine Hyperglycemia on Fetal Pancreatic Development

Maternal pregestational diabetes mellitus (PGDM) can lead to adverse fetal outcomes, including lasting impacts on pancreatic development. However, the specific impacts of maternal PGDM on cellular functions and intercellular communication within the fetal pancreas remain poorly understood. Here, sin...

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Published inAdvanced science Vol. 12; no. 22; pp. e2411126 - n/a
Main Authors Deng, Yu, Wan, Shuting, Yuan, Zan, Yang, Huixia
Format Journal Article
LanguageEnglish
Published Germany John Wiley & Sons, Inc 01.06.2025
John Wiley and Sons Inc
Wiley
Subjects
Animals
Cells
Diabetes
Diabetes, Gestational - genetics
Diabetes, Gestational - metabolism
Female
Fetal Development - genetics
fetal pancreas
Fetus - metabolism
Genes
Glucose
Homeostasis
Humans
Hyperglycemia
Hyperglycemia - genetics
Hyperglycemia - metabolism
Insulin
Metabolism
Mice
Pancreas
Pancreas - embryology
Pancreas - metabolism
pregestational diabetes mellitus
Pregnancy
single‐nucleus RNA sequencing
spatial transcriptomics
Transcriptome - genetics
Womens health
pregestational diabetes mellitus
fetal pancreas
single‐nucleus RNA sequencing
spatial transcriptomics
Online AccessGet full text
ISSN2198-3844
2198-3844
DOI10.1002/advs.202411126

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Abstract Maternal pregestational diabetes mellitus (PGDM) can lead to adverse fetal outcomes, including lasting impacts on pancreatic development. However, the specific impacts of maternal PGDM on cellular functions and intercellular communication within the fetal pancreas remain poorly understood. Here, single‐nucleus RNA sequencing and spatial transcriptomics (ST) are employed to investigate cellular responses and spatial changes in the fetal pancreas (E16.5 and E18.5) under maternal PGDM conditions. The findings reveal significant cellular heterogeneity among acinar and beta cells, along with pronounced metabolic stress responses. More importantly, decreased insulin secretion is observed and accompanied by the compensatory increase of Pdx1, Nkx6.2, and Mafa, and substantial alterations in cell‐cell communication across multiple cell types. ST analysis further highlights enhanced spatial enrichment in cellular niches exposed to maternal PGDM. These findings provide valuable insights into the molecular mechanisms underlying fetal pancreatic response to maternal PGDM and offer a detailed spatiotemporal perspective on these processes. Maternal pregestational diabetes mellitus (PGDM) induced metabolic stress in fetal mice pancreas, alongside significantly decreased insulin secretion, altered cell‐cell communication, and distinct changes in cellular niches.
AbstractList Maternal pregestational diabetes mellitus (PGDM) can lead to adverse fetal outcomes, including lasting impacts on pancreatic development. However, the specific impacts of maternal PGDM on cellular functions and intercellular communication within the fetal pancreas remain poorly understood. Here, single-nucleus RNA sequencing and spatial transcriptomics (ST) are employed to investigate cellular responses and spatial changes in the fetal pancreas (E16.5 and E18.5) under maternal PGDM conditions. The findings reveal significant cellular heterogeneity among acinar and beta cells, along with pronounced metabolic stress responses. More importantly, decreased insulin secretion is observed and accompanied by the compensatory increase of Pdx1, Nkx6.2, and Mafa, and substantial alterations in cell-cell communication across multiple cell types. ST analysis further highlights enhanced spatial enrichment in cellular niches exposed to maternal PGDM. These findings provide valuable insights into the molecular mechanisms underlying fetal pancreatic response to maternal PGDM and offer a detailed spatiotemporal perspective on these processes.
Abstract Maternal pregestational diabetes mellitus (PGDM) can lead to adverse fetal outcomes, including lasting impacts on pancreatic development. However, the specific impacts of maternal PGDM on cellular functions and intercellular communication within the fetal pancreas remain poorly understood. Here, single‐nucleus RNA sequencing and spatial transcriptomics (ST) are employed to investigate cellular responses and spatial changes in the fetal pancreas (E16.5 and E18.5) under maternal PGDM conditions. The findings reveal significant cellular heterogeneity among acinar and beta cells, along with pronounced metabolic stress responses. More importantly, decreased insulin secretion is observed and accompanied by the compensatory increase of Pdx1, Nkx6.2, and Mafa, and substantial alterations in cell‐cell communication across multiple cell types. ST analysis further highlights enhanced spatial enrichment in cellular niches exposed to maternal PGDM. These findings provide valuable insights into the molecular mechanisms underlying fetal pancreatic response to maternal PGDM and offer a detailed spatiotemporal perspective on these processes.
Maternal pregestational diabetes mellitus (PGDM) can lead to adverse fetal outcomes, including lasting impacts on pancreatic development. However, the specific impacts of maternal PGDM on cellular functions and intercellular communication within the fetal pancreas remain poorly understood. Here, single‐nucleus RNA sequencing and spatial transcriptomics (ST) are employed to investigate cellular responses and spatial changes in the fetal pancreas (E16.5 and E18.5) under maternal PGDM conditions. The findings reveal significant cellular heterogeneity among acinar and beta cells, along with pronounced metabolic stress responses. More importantly, decreased insulin secretion is observed and accompanied by the compensatory increase of Pdx1, Nkx6.2, and Mafa, and substantial alterations in cell‐cell communication across multiple cell types. ST analysis further highlights enhanced spatial enrichment in cellular niches exposed to maternal PGDM. These findings provide valuable insights into the molecular mechanisms underlying fetal pancreatic response to maternal PGDM and offer a detailed spatiotemporal perspective on these processes. Maternal pregestational diabetes mellitus (PGDM) induced metabolic stress in fetal mice pancreas, alongside significantly decreased insulin secretion, altered cell‐cell communication, and distinct changes in cellular niches.
Maternal pregestational diabetes mellitus (PGDM) can lead to adverse fetal outcomes, including lasting impacts on pancreatic development. However, the specific impacts of maternal PGDM on cellular functions and intercellular communication within the fetal pancreas remain poorly understood. Here, single‐nucleus RNA sequencing and spatial transcriptomics (ST) are employed to investigate cellular responses and spatial changes in the fetal pancreas (E16.5 and E18.5) under maternal PGDM conditions. The findings reveal significant cellular heterogeneity among acinar and beta cells, along with pronounced metabolic stress responses. More importantly, decreased insulin secretion is observed and accompanied by the compensatory increase of Pdx1, Nkx6.2, and Mafa, and substantial alterations in cell‐cell communication across multiple cell types. ST analysis further highlights enhanced spatial enrichment in cellular niches exposed to maternal PGDM. These findings provide valuable insights into the molecular mechanisms underlying fetal pancreatic response to maternal PGDM and offer a detailed spatiotemporal perspective on these processes. Maternal pregestational diabetes mellitus (PGDM) induced metabolic stress in fetal mice pancreas, alongside significantly decreased insulin secretion, altered cell‐cell communication, and distinct changes in cellular niches.
Maternal pregestational diabetes mellitus (PGDM) can lead to adverse fetal outcomes, including lasting impacts on pancreatic development. However, the specific impacts of maternal PGDM on cellular functions and intercellular communication within the fetal pancreas remain poorly understood. Here, single-nucleus RNA sequencing and spatial transcriptomics (ST) are employed to investigate cellular responses and spatial changes in the fetal pancreas (E16.5 and E18.5) under maternal PGDM conditions. The findings reveal significant cellular heterogeneity among acinar and beta cells, along with pronounced metabolic stress responses. More importantly, decreased insulin secretion is observed and accompanied by the compensatory increase of Pdx1, Nkx6.2, and Mafa, and substantial alterations in cell-cell communication across multiple cell types. ST analysis further highlights enhanced spatial enrichment in cellular niches exposed to maternal PGDM. These findings provide valuable insights into the molecular mechanisms underlying fetal pancreatic response to maternal PGDM and offer a detailed spatiotemporal perspective on these processes.Maternal pregestational diabetes mellitus (PGDM) can lead to adverse fetal outcomes, including lasting impacts on pancreatic development. However, the specific impacts of maternal PGDM on cellular functions and intercellular communication within the fetal pancreas remain poorly understood. Here, single-nucleus RNA sequencing and spatial transcriptomics (ST) are employed to investigate cellular responses and spatial changes in the fetal pancreas (E16.5 and E18.5) under maternal PGDM conditions. The findings reveal significant cellular heterogeneity among acinar and beta cells, along with pronounced metabolic stress responses. More importantly, decreased insulin secretion is observed and accompanied by the compensatory increase of Pdx1, Nkx6.2, and Mafa, and substantial alterations in cell-cell communication across multiple cell types. ST analysis further highlights enhanced spatial enrichment in cellular niches exposed to maternal PGDM. These findings provide valuable insights into the molecular mechanisms underlying fetal pancreatic response to maternal PGDM and offer a detailed spatiotemporal perspective on these processes.
Author Deng, Yu
Yang, Huixia
Yuan, Zan
Wan, Shuting
AuthorAffiliation 3 Annoroad Gene Technology (Beijing) Co., Ltd Beijing 100176 China
4 Agricultural Bioinformatics Key Laboratory of Hubei Province Hubei Engineering Technology Research Center of Agricultural Big Data College of Informatics Huazhong Agricultural University Wuhan 430070 China
2 Beijing Key Laboratory of Maternal Fetal Medicine of Gestational Diabetes Mellitus Beijing 100034 China
1 Department of Obstetrics and Gynecology Peking University First Hospital No. 8 Xishiku Street Beijing 100034 China
AuthorAffiliation_xml – name: 3 Annoroad Gene Technology (Beijing) Co., Ltd Beijing 100176 China
– name: 1 Department of Obstetrics and Gynecology Peking University First Hospital No. 8 Xishiku Street Beijing 100034 China
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  fullname: Deng, Yu
  organization: Beijing Key Laboratory of Maternal Fetal Medicine of Gestational Diabetes Mellitus
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  fullname: Wan, Shuting
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  givenname: Zan
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  email: yanghuixia@bjmu.edu.cn
  organization: Beijing Key Laboratory of Maternal Fetal Medicine of Gestational Diabetes Mellitus
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Keywords pregestational diabetes mellitus
fetal pancreas
single‐nucleus RNA sequencing
spatial transcriptomics
Language English
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Snippet Maternal pregestational diabetes mellitus (PGDM) can lead to adverse fetal outcomes, including lasting impacts on pancreatic development. However, the specific...
Abstract Maternal pregestational diabetes mellitus (PGDM) can lead to adverse fetal outcomes, including lasting impacts on pancreatic development. However, the...
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StartPage e2411126
SubjectTerms Animals
Cells
Diabetes
Diabetes, Gestational - genetics
Diabetes, Gestational - metabolism
Female
Fetal Development - genetics
fetal pancreas
Fetus - metabolism
Genes
Glucose
Homeostasis
Humans
Hyperglycemia
Hyperglycemia - genetics
Hyperglycemia - metabolism
Insulin
Metabolism
Mice
Pancreas
Pancreas - embryology
Pancreas - metabolism
pregestational diabetes mellitus
Pregnancy
single‐nucleus RNA sequencing
spatial transcriptomics
Transcriptome - genetics
Womens health
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Title Integrating Spatial and Single‐Nucleus Transcriptomic Data to Assess the Effects of Intrauterine Hyperglycemia on Fetal Pancreatic Development
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