Introduction

In the human brain the hypothalamus acts as a signal station for hormonal release throughout the body. This includes the regulation of hunger and satiety hormones. Due to the role the hypothalamus plays in hunger and satiety, it has been the main brain structure studied when considering how obesity affects the brain. In a recent study published in Molecular Neurobiology, Aline Haas de Mello and colleagues decided to take the prior research a step further and look at the effects of obesity on the hypothalamus, hippocampus, prefrontal cortex, and striatum. Knowing that obesity does affect at least one of these brain areas, the hypothalamus, they really wanted to explore whether omega-3 fatty acids attenuated the effects of obesity induced damage or not. 

Methods

To begin the researchers split a group of rats into two groups, one that would eat a standard diet that would cause weight to be maintained, and the other would eat a high fat diet that would induce obesity. The rats ate this diet for a total of ten weeks. After six weeks each diet group was split in half again, with half of each group receiving oral omega-3 fatty acids and the other half receiving oral saline treatment. The amount of fish oil (omega-3 fatty acids) used in this study equates to roughly 32 milligrams per kilogram of body weight per day in humans. After the ten weeks were up the rats were euthanized and the brain areas were inspected for evidence of inflammation, oxidation, and Krebs cycle enzyme disruption.

Results

After examining the brain areas of the rats in all four groups inflammation was observed. There was more inflammation observed in the obese rats compared to the control rats. Then when observing the Krebs cycle, varying enzyme activities were inhibited in multiple brain areas. When looking at the mitochondrial respiratory chain, complexes I and II in the striatum were inhibited by obesity but the effects were reverted in the mice that were orally administered omega-3 fatty acids. 

Discussion

While many areas of the brain were affected by obesity, the specific areas that seemed to provide significant results were in the dopamine pathway. The dopamine pathway plays a major role in how the reward system works (Shultz, 1998). The motivational drive involving food is associated at the cellular level to dopamine that is present in the striatum (Volkow, Wise, & Baler, 2017).

When examining the striatum, one of the major findings was impairment in the mitochondrial respiratory chain in obese rats. The mitochondrial respiratory chain is responsible for a large portion of cellular energy synthesis (DiMauro & Schon, 2003). It was observed that when the mitochondrial respiratory chain was interrupted in the striatum that increased the amount of reactive oxygen species (ROS) formed (de Mello et al., 2018). When the rate of ROS production is chronically increased, the accumulation of ROS associated damage can result in cell dysfunction and eventually cell death (Suski et al., 2011). 

The striatum contains medium spiny neurons that are activated by dopamine. This is either accomplished through the direct or indirect pathway (Bateup et al., 2010). Alterations in these striatal pathways has been shown to have an effect on pathological consumption disorders like obesity and addiction (London et al., 2018). With the alterations in the mitochondrial respiratory chain in complexes I and II in the striatum that led to an increased ROS production rate in the obese rats, it was inferred that there was a potential for striatal cell damage (de Mello et al., 2018).

While the underlying mechanisms regarding omega-3 fatty acids in the brain are still being studied, multiple studies have shown that omega-3 fatty acids are essential for brain development and function (Bailes et al., 2020). Therefore, it was no surprise when the impairment of the mitochondrial respiratory chain was reverted by the presence of omega-3 fatty acids in the diet (de Mello et al., 2018). As the authors of the study alluded, adding omega-3 fatty acids into the diet can help prevent damage to the striatum that would lead to less healthy eating habits due to a disruption in the medium spiny neurons in the dopamine pathway. 

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