Mild Hypophagia and Associated Changes in Feeding-Related Gene Expression and c-Fos Immunoreactivity in Adult Male Rats with Sodium Valproate-Induced Autism.

Researchers studied eating problems in rats with autism-like traits. These rats ate less food and gained weight more slowly than typical rats. When hungry, their brains didn't respond normally - the usual signals that tell the body 'I'm hungry, I need food' weren't working properly. This suggests that eating difficulties in autism might not just be about food preferences, but also problems with how the brain processes hunger signals.

This study examined feeding behaviors in adult male rats with sodium valproate-induced autism (VPA model). Researchers compared food intake, body weight, brain activation patterns, and gene expression between VPA rats and controls under various feeding conditions. VPA rats consumed less 'bland' chow both when food was freely available and after periods of deprivation. They also showed slower weight gain compared to controls.

Brain imaging revealed abnormal hunger processing in VPA rats - while control rats showed expected changes in brain activation when hungry, VPA rats did not show these normal responses. Gene expression patterns related to feeding also failed to change appropriately in response to hunger in VPA rats, suggesting fundamental disruptions in appetite regulation mechanisms.

Results suggest eating difficulties in autism may involve disrupted hunger processing rather than just food preferences. This could inform development of interventions targeting appetite regulation mechanisms and support clinical understanding of feeding challenges in autistic individuals.

Animal model findings may not directly translate to humans. Sample size not reported. Study limited to male rats only. Single autism model used. No assessment of food texture, taste, or preference variations that are clinically relevant in autism.

A core yet understudied symptom of autism is aberrant eating behaviour, including extremely narrow food preferences. Autistic individuals often refuse to eat despite hunger unless preferred food is given. We hypothesised that, apart from aberrant preference, underfeeding stems from abnormal hunger processing. Utilising an adult male VPA rat, a model of autism, we examined intake of 'bland' chow in animals maintained on this diet continuously, eating this food after fasting and after both food and water deprivation.

We assessed body weight in adulthood to determine whether lower feeding led to slower growth. Since food intake is highly regulated by brain processes, we looked into the activation (c-Fos immunoreactivity) of central sites controlling appetite in animals subjected to food deprivation vs. fed ad libitum. Expression of genes involved in food intake in the hypothalamus and brain stem, regions responsible for energy balance, was measured in deprived vs. sated animals. We performed our analyses on VPAs and age-matched healthy controls.

We found that VPAs ate less of the 'bland' chow when fed ad libitum and after deprivation than controls did. Their body weight increased more slowly than that of controls when maintained on the 'bland' food. While hungry controls had lower c-Fos IR in key feeding-related areas than their ad libitum-fed counterparts, in hungry VPAs c-Fos was unchanged or elevated compared to the fed ones. The lack of changes in expression of feeding-related genes upon deprivation in VPAs was in contrast to several transcripts affected by fasting in healthy controls.

We conclude that hunger processing is dysregulated in the VPA rat.