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How Do Dietary Fats Lead to Obesity?

Researchers from Brazil investigate how the regular consumption of dietary fats can cause damage to neurons that control food intake and energy expenditure.

A region of the brain known as the mediobasal hypothalamus (MBH) contains groups of neurons that function as a nutrient sensor and aid in the regulation of food intake and energy expenditure. Normally, this region tries to match the calories consumed with our need for energy. In turn, this helps to maintain a healthy weight. However, research has shown that eating a high-fat diet can alter this balance and lead to weight gain.

Hypothalamic inflammation in response to the consumption of dietary fats can be detected as early as one day after the introduction of a high-fat diet. Prolonged exposure to dietary fats leads to irreversible hypothalamic neuronal damage resulting in leptin and insulin resistance.

In a recent study published in the Journal of Neuroinflammation, researchers from Brazil used an animal model to investigate how the ingestion of dietary fats and the activation of the inflammatory response in the hypothalamus lead to weight gain. They observed significant biochemical changes in the brain of the mice fed a high-fat diet. The researchers noticed a cascade of biochemical processes that included the molecules responsible for sensing energy intake. The study results showed that the molecules that normally protect against the effects of a high-fat diet (called neurotrophic factors) are damaged when the diet is sustained.

This was not a human subjects study. However, if it holds true for humans, it suggests that overeating rich and fatty foods may promote functional and structural changes in the brain.

Written by Debra A. Kellen, PhD

Reference:  Ramalho, A. F., Bombassaro, B., Dragano, N. R., Solon, C., Morari, J., Fioravante, M., … & Araujo, E. P. (2018). Dietary fats promote functional and structural changes in the median eminence blood/spinal fluid interface—the protective role for BDNF. Journal of Neuroinflammation15(1), 10. DOI:  10.1186/s12974-017-1046-8



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