Maternal diabetes affects rat offspring retinal structure and function: Sex-specific vulnerabilities at infancy

• Published in: Life sciences (1973) Vol. 327; p. 121852
• Main Authors: Realinho, Ana M., Boia, Raquel, Paiva, Beatriz, Correia, Raquel G., Gaspar, Rita, Ambrósio, António F., Baptista, Filipa I.
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier Inc 15-08-2023
• Subjects: Insulin therapy; Maternal diabetes; Neurodevelopment; Offspring retina; Photoreceptors; Sex differences; Maternal diabetes; Offspring retina; Neurodevelopment; Photoreceptors; Sex differences; Insulin therapy
• ISSN: 0024-3205; 1879-0631
• DOI: 10.1016/j.lfs.2023.121852

Maternal diabetes negatively impacts the offspring's brain, but little is known about its effects on the retina, which is also part of the central nervous system. We hypothesized that maternal diabetes adversely influences offspring retina development leading to structural and functional deficits.
Retinal structure and function were evaluated at infancy, by optical coherence tomography and electroretinography, in male and female offspring of control, diabetic and diabetic-treated with insulin Wistar rats.
Maternal diabetes induced a delay in male and female offspring eye-opening, while insulin treatment expedited it. Structural analysis showed that maternal diabetes decreased the thickness of the inner and outer segment layer of photoreceptors in male offspring. Electroretinography also revealed that maternal diabetes decreased the amplitude of scotopic b-wave and flicker response in males, suggesting bipolar cells and cone photoreceptor dysfunction, an effect not observed in females. Conversely, maternal diabetes decreased cone arrestin protein levels in female retinas, while not affecting cone photoreceptor number. Dam insulin therapy was efficient in preventing the offspring photoreceptor changes.
Our results suggest that photoreceptors are affected by maternal diabetes, which may account for visual impairments at infancy. Notably, both male and female offspring presented specific vulnerabilities to hyperglycemia in this sensitive period of development.