ArticlePediatric research2026
Downregulation of insulin receptor isoform A in the forebrain of fetal growth-restricted rats.
Article in Pediatric research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
1 citing paper in PubMed.
- Insulin and IGF signaling in the brain: multilevel regulation of synaptic and network homeostasis.Frontiers in endocrinology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChildren with asymmetrical fetal growth restriction (FGR), whose head size is relatively preserved, often have a poor neurodevelopmental prognosis. Insulin receptor isoform A (IR-A) is predominantly expressed in neurons and is important in neurodevelopment. This study investigated changes in brain IR-A expression in neonatal FGR model rats.
methodsFGR model rats were generated by maternal caloric restriction (CR). Glucose uptake and the expression of glucose transporter (GLUT) genes in the brain and liver, and of the IR-A gene in the brain were compared between CR and control group neonates. Gene expression in the brain was examined by RNA sequencing. Brain IR-A localization was analyzed using immunohistochemistry.
resultsThe brain-to-liver ratios for organ weight and glucose uptake were significantly higher in CR rats. GLUT gene expression was maintained in the CR brain. Whole brain IR-A expression was reduced in CR rats. Furthermore, IR-A expression was decreased in the forebrain of CR rats, but not changed in the hindbrain.
conclusionThe regional differences in IR-A in the FGR rat brain indicate that an endocrinological mechanism regulates brain IR-A to maintain brain function under nutrient deficiency. However, a decrease in IR-A in the fetal period may cause postnatal brain impairment. IMPACT: Insulin receptor isoform A (IR-A) expression is reduced in the neonatal brain of asymmetrical fetal growth restriction (FGR) model rats generated by maternal caloric restriction. IR-A expression is decreased in the forebrain, which is important for cognitive brain functions, whereas IR-A expression is maintained in the hindbrain, which is important for basic vital activities. The expression of genes related to forebrain development is significantly decreased, while the expression of genes related to hindbrain development is increased in neonatal FGR model rats. These results can explain why FGR infants have a poor neurodevelopmental prognosis despite their brain size being relatively protected.
Indexed as
Identifiers
41006887What Socratic holds
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 Socratic graph.