ArticleThe Journal of clinical investigation2014
Maternal diet-induced microRNAs and mTOR underlie β cell dysfunction in offspring.
Article in The Journal of clinical investigation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
64 citing papers in PubMed, 1 synthesis or guideline pooled it, 115 citations in OpenAlex.
- Little appetite for obesity: meta-analysis of the effects of maternal obesogenic diets on offspring food intake and body mass in rodents.International journal of obesity (2005) · 2015Pooled it
- Placental mTOR signalling links mitochondrial dysfunction, nutrient transport and neonatal beta cell perturbations in mice.Diabetologia · 2025Article
- Placental mitochondrial calcium uniporter modulates offspring susceptibility to metabolic dysfunction.Molecular metabolism · 2025Article
- Metformin and insulin exacerbate one-carbon metabolism deficits in pregnant growth restricted rats and impacts the placenta, fetal liver and pancreas.The Journal of physiology · 2025Article
- Lack of maternal exposure to somatostatin leads to diet-induced insulin and leptin resistance in mouse male offspring.Journal of molecular endocrinology · 2025Article
- Improved glucose handling in female rat offspring of a hypertensive pregnancy with intrauterine growth restriction.Physiological reports · 2025Article
- Metabolic syndrome in children and adolescents: definitions, epidemiology, pathophysiology, interventions, and challenges.Frontiers in endocrinology · 2025Review
- Article
- Loss of O-GlcNAcylation modulates mTORC1 and autophagy in β cells, driving diabetes 2 progression.JCI insight · 2024Article
- Overnutrition in the early postnatal period influences lifetime metabolic risk: Evidence for impact on pancreatic β-cell mass and function.Journal of diabetes investigation · 2024Review
- Circadian Disruption across Lifespan Impairs Glucose Homeostasis and Insulin Sensitivity in Adult Mice.Metabolites · 2024Article
- Sweet Spot Regulation of Maternal Metabolic Health and Nutrition on β-Cell Mass in the Offspring.Advances in anatomy, embryology, and cell biology · 2024Review
- RISING STARS: Mechanistic insights into maternal-fetal cross talk and islet beta-cell development.The Journal of endocrinology · 2023Review
- Impact of placental mTOR deficiency on peripheral insulin signaling in adult mice offspring.Journal of molecular endocrinology · 2023Article
- Sex Differences in Pancreatic β-Cell Physiology and Glucose Homeostasis in C57BL/6J Mice.Journal of the Endocrine Society · 2023Article
- Time-dependent effects of endogenous hyperglucagonemia on glucose homeostasis and hepatic glucagon action.JCI insight · 2023Article
- Review
- Article
- Review
- Maternal low protein diet and fetal programming of lean type 2 diabetes.World journal of diabetes · 2022Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
A maternal diet that is low in protein increases the susceptibility of offspring to type 2 diabetes by inducing long-term alterations in β cell mass and function. Nutrients and growth factor signaling converge through mTOR, suggesting that this pathway participates in β cell programming during fetal development. Here, we revealed that newborns of dams exposed to low-protein diet (LP0.5) throughout pregnancy exhibited decreased insulin levels, a lower β cell fraction, and reduced mTOR signaling. Adult offspring of LP0.5-exposed mothers exhibited glucose intolerance as a result of an insulin secretory defect and not β cell mass reduction. The β cell insulin secretory defect was distal to glucose-dependent Ca2+ influx and resulted from reduced proinsulin biosynthesis and insulin content. Islets from offspring of LP0.5-fed dams exhibited reduced mTOR and increased expression of a subset of microRNAs, and blockade of microRNA-199a-3p and -342 in these islets restored mTOR and insulin secretion to normal. Finally, transient β cell activation of mTORC1 signaling in offspring during the last week of pregnancy of mothers fed a LP0.5 rescued the defect in the neonatal β cell fraction and metabolic abnormalities in the adult. Together, these findings indicate that a maternal low-protein diet alters microRNA and mTOR expression in the offspring, influencing insulin secretion and glucose homeostasis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.