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Updated: Feb 17, 2026
Primary Culture of Rat Adrenocortical Cells and Assays of Steroidogenic Functions
Published on: March 12, 2019
Insulin-like Growth Factor 1 Mediates Adrenal Development Dysfunction in Offspring Rats Induced by Prenatal Food
Zheng He1, Feng Lv2, Yufeng Ding3
1Department of Pharmacology, Wuhan University School of Basic Medical Sciences, Wuhan, China; Department of Pharmacy, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Insights
Prenatal food restriction (PFR) in rats leads to adrenal dysfunction by suppressing insulin-like growth factor 1 (IGF1) signaling. A high-fat diet post-weaning reverses this by enhancing IGF1 signaling and adrenal function.
Area of Science:
- Endocrinology
- Developmental Biology
- Metabolic Syndrome
Background:
- Prenatal food restriction (PFR) disrupts the hypothalamic-pituitary-adrenal axis and alters glucose/lipid metabolism in offspring.
- Understanding the intrauterine mechanisms of adrenal dysfunction induced by PFR is crucial.
Purpose of the Study:
- To investigate the intrauterine programming mechanism of adrenal dysfunction in PFR offspring rats.
- To analyze the impact of PFR on adrenal steroidogenesis and the IGF1 signaling pathway.
Main Methods:
- Pregnant Wistar rats underwent dietary restriction (50% intake) from gestational days 11-20.
- Offspring were exposed to a high-fat diet (HFD) post-weaning.
- Assessed fetal/maternal corticosterone, adrenal steroidogenic enzyme expression, and IGF1 signaling pathway components.
Main Results:
- PFR fetuses exhibited lower body weight and reduced expression of key steroidogenic enzymes (StAR, P450scc, 3β-HSD, P450c11).
- Maternal and fetal corticosterone levels were elevated in PFR groups, with suppressed adrenal IGF1 signaling (IGF1, IGF1R, Akt1).
- Post-weaning HFD increased body weight gain, corticosterone, adrenal steroid 21-hydroxylase, P450c11 expression, and IGF1 signaling in PFR offspring.
Conclusions:
- In utero PFR elevates corticosterone, inhibiting adrenal IGF1 signaling and steroidogenesis.
- Post-weaning HFD enhances adrenal steroidogenesis via improved IGF1 signaling in PFR offspring.
Background:
Our previous study demonstrated that prenatal food restriction (PFR) could induce the dysfunction of the hypothalamic-pituitary-adrenal axis and glucocorticoid-related glucose and lipid metabolic alterations in adult offspring rats.
Aim Of The Study:
To investigate the intrauterine programming mechanism of adrenal dysfunction in the PFR offspring rats.
Methods:
From gestational days (GDs) 11-20, pregnant Wistar rats were fed a restricted diet (50% of the daily food intake of control rats, 60 g/kg·d). Some were executed at GD20, while the others survived to full-term delivery; all pups were fed a high-fat diet (HFD) after weaning. The serum corticosterone concentration, expression level of adrenal steroidal synthetase, and insulin-like growth factor 1 (IGF1) signaling pathway were tested.
Results:
We confirmed that the fetal body weight of the PFR group was lower than that of the control group, and the mRNA expression of adrenal steroidogenic acute regulatory protein, cytochrome P450 cholesterol side chain cleavage, 3β-hydroxysteroid dehydrogenase, and steroid 11β-hydroxylase (P450c11) were decreased in the PFR fetal rats. The maternal and fetal serum corticosterone levels were significantly increased in the PFR groups. Furthermore, the expression of the adrenal IGF1 signaling pathway (including IGF1, IGF1R, and Akt1) was suppressed. However, after a post-weaning HFD, the body weight gain rates and serum corticosterone levels were elevated, and the expression of adrenal steroid 21-hydroxylase and P450c11, as well as the IGF1 signaling pathway, were significantly increased in the PFR group.
Conclusions:
These results showed that a higher level of circulation corticosterone by PFR in utero inhibited adrenal IGF1 signaling and steroidogenesis, whereas post-weaning HFD induced adrenal steroidogenesis by an enhanced IGF1 signaling.
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