Study links inflammation in the hypothalamus to hyperadiposity
By dominguez // 2021-04-01
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In this study, researchers at Ewha Womans University in South Korea investigated the molecular mechanisms that link obesity to inflammation in the hypothalamus. Their findings were published in the journal Nutrition Research.
  • Inflammation is a distinct feature of obesity.
  • Insulin resistance is associated with increased inflammation in the adipose tissue and the liver.
  • Recent studies also suggest a possible link between inflammation in the hypothalamus -- which governs systemic metabolism by linking neuronal and endocrine signals -- and metabolic diseases like obesity.
  • However, the mechanisms underlying this link is poorly understood.
  • The researchers hypothesized that a high-fat diet (HFD) triggers metabolic inflammation via transcriptional changes in the hypothalamus.
  • To test their hypothesis, they characterized obesity-related in vivo transcriptional alterations in the hypothalamus and their effects on functional networks.
  • The researchers fed mice with either a control diet (CD) or HFD for 20 weeks before conducting microarray and gene ontology analyses of the animals' hypothalami.
  • They reported that in the brains of HFD-fed mice, immune-related pathways, including inflammatory and cytokine signaling, were overrepresented. This was not the case with the CD-fed mice.
  • Secondary analysis of leptin-deficient obese mouse hypothalamus also revealed enriched gene sets for tumor necrosis factor-a signaling pathways and cancer pathways similar to those found in the hypothalami of HFD-fed mice.
Based on these findings, the researchers concluded that inflammation in the hypothalamus is linked to hyperadiposity rather than the primary causes of obesity, such as dietary fat and genetic mutation. Journal Reference: Park JH, Yoo Y, Han J, Park YJ. ALTERED EXPRESSION OF INFLAMMATION-ASSOCIATED GENES IN THE HYPOTHALAMUS OF OBESITY MOUSE MODELS. Nutrition Research. October 2019;70:40–49. DOI: 10.1016/j.nutres.2018.06.006
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