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Updated: Jun 6, 2026
Monitoring Dynamic Growth of Retinal Vessels in Oxygen-Induced Retinopathy Mouse Model
Published on: April 2, 2021
Postnatal weight gain modifies severity and functional outcome of oxygen-induced proliferative retinopathy
Andreas Stahl1, Jing Chen, Przemyslaw Sapieha
1Department of Ophthalmology, Harvard Medical School, Children’s Hospital Boston, Boston, Massachusetts 02115, USA.
Insights
Poor postnatal nutrition and weight gain in mice significantly prolong retinopathy and cause lasting visual deficits. This highlights the critical role of early nutrition in preventing vision loss and retinopathy of prematurity.
Area of Science:
- Ophthalmology
- Developmental Biology
- Neonatology
Background:
- Postnatal weight gain is linked to retinopathy of prematurity (ROP) in clinical settings.
- Pathophysiological mechanisms require investigation in animal models.
Purpose of the Study:
- To investigate the impact of postnatal nutritional supply and weight gain on the severity and duration of retinopathy in mice.
- To explore the underlying molecular and metabolic factors contributing to ROP severity.
Main Methods:
- Utilized a mouse model with controlled genetic background and birth weights.
- Manipulated postnatal nutrition to create groups with poor, medium, and extensive weight gain.
- Assessed retinopathy severity, duration, retinal vascular endothelial growth factor (VEGF) expression, serum metabolic markers, and visual function in adult mice.
Main Results:
- Poor weight gain (PWG) mice showed a prolonged phase of retinopathy (20 days vs. 6 days) compared to extensive weight gain mice.
- A strong parabolic association (r(2) = 0.83) was observed between postnatal weight gain and oxygen-induced retinopathy severity.
- PWG mice exhibited prolonged retinal VEGF overexpression and metabolic disturbances (low glucose, insulin, IGF-1; high ghrelin), leading to visual deficits.
Conclusions:
- Poor postnatal nutritional supply and slow weight gain are critical factors in the development and severity of retinopathy.
- Prolonged VEGF overexpression and metabolic dysregulation mediate the link between poor nutrition and protracted retinopathy.
- Early nutritional interventions may be crucial for preventing long-term visual impairment in conditions like retinopathy of prematurity.
Abstract:
In clinical studies, postnatal weight gain is strongly associated with retinopathy of prematurity (ROP). However, animal studies are needed to investigate the pathophysiological mechanisms of how postnatal weight gain affects the severity of ROP. In the present study, we identify nutritional supply as one potent parameter that affects the extent of retinopathy in mice with identical birth weights and the same genetic background. Wild-type pups with poor postnatal nutrition and poor weight gain (PWG) exhibit a remarkably prolonged phase of retinopathy compared to medium weight gain or extensive weight gain pups. A high (r(2) = 0.83) parabolic association between postnatal weight gain and oxygen-induced retinopathy severity is observed, as is a significantly prolonged phase of proliferative retinopathy in PWG pups (20 days) compared with extensive weight gain pups (6 days). The extended retinopathy is concomitant with prolonged overexpression of retinal vascular endothelial growth factor in PWG pups. Importantly, PWG pups show low serum levels of nonfasting glucose, insulin, and insulin-like growth factor-1 as well as high levels of ghrelin in the early postoxygen-induced retinopathy phase, a combination indicative of poor metabolic supply. These differences translate into visual deficits in adult PWG mice, as demonstrated by impaired bipolar and proximal neuronal function. Together, these results provide evidence for a pathophysiological correlation between poor postnatal nutritional supply, slow weight gain, prolonged retinal vascular endothelial growth factor overexpression, protracted retinopathy, and reduced final visual outcome.
