Endocrinology ·
Maternal diabetes alters neonatal piglet islet function and beta-cell structure
A study in genetically diabetic and reporter pig models found that offspring exposed to maternal hyperglycaemia had impaired neonatal islet glucose responsiveness and changes in beta- and delta-cell populations. Molecular findings included altered glucose-sensing and calcium-buffering markers, but the results are from an animal model and do not establish effects in human offspring.
- Neonatal piglets exposed to maternal hyperglycaemia had impaired islet glucose responsiveness.
- Beta- and delta-cell populations increased by 35% and 47%, respectively.
- Molecular findings included altered GLUT2 and calbindin D28K expression.
- The findings are from an animal model, not human offspring.
Researchers compared neonatal piglets born to hyperglycaemic mothers (PHGs) with those born to normoglycaemic mothers (PNGs), using in vivo glucose testing, pancreatic tissue-slice assays, morphological analyses, proteomics and single-cell RNA sequencing. The study aimed to characterise how maternal hyperglycaemia affects neonatal islet function and beta cells. The source does not report the number of piglets studied.
PHGs were hyperglycaemic, hyperinsulinaemic and insulin resistant at birth, and had delayed glucose and insulin responses after oral glucose administration. In pancreatic tissue slices, basal insulin secretion was elevated while glucose responsiveness was nearly blunted. PHG islets had 35% more beta cells and 47% more delta cells, alongside increased insulin and somatostatin content and larger islet clusters. Molecular findings included near-absence of GLUT2 and calbindin D28K, an ATF4-associated stress signature, and changes in signalling components.
The findings provide mechanistic evidence about fetal exposure to maternal diabetes in a pig model, which the authors selected for similarities in endocrine pancreas development. They do not show that the same changes occur in human neonates or establish later clinical outcomes; the results should not be used to guide clinical care.
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Diabetologia: Pregestational maternal diabetes primes neonatal beta cell dysfunction with structural remodelling, impaired calcium buffering and altered mTORC2–Gαq–PKCα signalling in a pig model ↗This is an automated AI-condensed summary that has not yet been reviewed by an editor. Always consult the full item at the original source.