ArticleAmerican journal of physiology. Endocrinology and metabolism2012
Developmental programming of neonatal pancreatic β-cells by a maternal low-protein diet in rats involves a switch from proliferation to differentiation.
Article in American journal of physiology. Endocrinology and metabolism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 52 citations in OpenAlex.
- Multifaceted functions of transcription regulatory factor X6 (RFX6): from pancreatic development to cancer progression.Cancer cell international · 2025Review
- Review
- Chronic late gestation fetal hyperglucagonaemia results in lower insulin secretion, pancreatic mass, islet area and beta- and α-cell proliferation.The Journal of physiology · 2024Article
- Impact of Ionizing Radiation Exposure on Placental Function and Implications for Fetal Programming.International journal of molecular sciences · 2024Review
- Sweet Spot Regulation of Maternal Metabolic Health and Nutrition on β-Cell Mass in the Offspring.Advances in anatomy, embryology, and cell biology · 2024Review
- Maternal diet during pregnancy and adaptive changes in the maternal and fetal pancreas have implications for future metabolic health.Frontiers in endocrinology · 2024Review
- Intrauterine and early-life malnutrition in rats disrupts the circadian rhythm programming of energy metabolites through adulthood.PloS one · 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
- A low-protein maternal diet during gestation affects the expression of key pancreatic β-cell genes and the methylation status of the regulatory region of theFrontiers in veterinary science · 2023Article
- Maternal low protein diet and fetal programming of lean type 2 diabetes.World journal of diabetes · 2022Review
- Mechanisms Underlying the Expansion and Functional Maturation of β-Cells in Newborns: Impact of the Nutritional Environment.International journal of molecular sciences · 2022Review
- Protein restriction during lactation causes transgenerational metabolic dysfunction in adult rat offspring.Frontiers in nutrition · 2022Article
- Understanding the Long-Lasting Effects of Fetal Nutrient Restriction versus Exposure to an Obesogenic Diet on Islet-Cell Mass and Function.Metabolites · 2021Review
- Changes Induced by Mind-Body Intervention Including Epigenetic Marks and Its Effects on Diabetes.International journal of molecular sciences · 2021Review
- Bioenergetic Evolution Explains Prevalence of Low Nephron Number at Birth: Risk Factor for CKD.Kidney360 · 2020Review
- Article
- Prenatal Malnutrition-Induced Epigenetic Dysregulation as a Risk Factor for Type 2 Diabetes.International journal of genomics · 2019Review
- Developmental origins of nonalcoholic fatty liver disease as a risk factor for exaggerated metabolic and cardiovascular-renal disease.American journal of physiology. Endocrinology and metabolism · 2018Review
- Effects of Biotin Supplementation During the First Week Postweaning Increases Pancreatic Islet Area, Beta-Cell Proportion, Islets Number, and Beta-Cell Proliferation.Journal of medicinal food · 2018Article
- Susceptibility background for type 2 diabetes in eleven Mexican Indigenous populations: HNF4A gene analysis.Molecular genetics and genomics : MGG · 2017Article
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Maternal low-protein diets (LP) impair pancreatic β-cell development, resulting in later-life failure and susceptibility to type 2 diabetes (T2D). We hypothesized that intrauterine and/or postnatal developmental programming seen in this situation involve altered β-cell structure and relative time course of expression of genes critical to β-cell differentiation and growth. Pregnant Wistar rats were fed either control (C) 20% or restricted (R) 6% protein diets during pregnancy (1st letter) and/or lactation (2nd letter) in four groups: CC, RR, RC, and CR. At postnatal days 7 and 21, we measured male offspring β-cell fraction, mass, proliferation, aggregate number, and size as well as mRNA level for 13 key genes regulating β-cell development and function in isolated islets. Compared with CC, pre- and postnatal LP (RR) decreased β-cell fraction, mass, proliferation, aggregate size, and number and increased Hnf1a, Hnf4a, Pdx1, Isl1, Rfx6, and Slc2a2 mRNA levels. LP only in pregnancy (RC) also decreased β-cell fraction, mass, proliferation, aggregate size, and number and increased Hnf1a, Hnf4a, Pdx1, Rfx6, and Ins mRNA levels. Postnatal LP offspring (CR) showed decreased β-cell mass but increased β-cell fraction, aggregate number, and Hnf1a, Hnf4a, Rfx6, and Slc2a2 mRNA levels. We conclude that LP in pregnancy sets the trajectory of postnatal β-cell growth and differentiation, whereas LP in lactation has smaller effects. We propose that LP promotes differentiation through upregulation of transcription factors that stimulate differentiation at the expense of proliferation. This results in a decreased β-cell reserve, which can contribute to later-life predisposition to T2D.
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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.