Diet-induced obesity leads to devastating and common chronic diseases, fueling ongoing interest in determining new mechanisms underlying both obesity and its consequences. It is now well known that chronic overnutrition produces a unique form of inflammation in peripheral insulin target tissues, and efforts to limit this inflammation have met with some success in preserving insulin sensitivity in obese individuals. Recently, the activation of inflammatory pathways by dietary excess has also been observed among cells located in the mediobasal hypothalamus, a brain area that exerts central control over peripheral glucose, fat, and energy metabolism. Here we review progress in the field of diet-induced hypothalamic inflammation, drawing key distinctions between metabolic inflammation in the hypothalamus and that occurring in peripheral tissues. We focus on specific stimuli of the inflammatory response, the roles of individual hypothalamic cell types, and the links between hypothalamic inflammation and metabolic function under normal and pathophysiological circumstances. Finally, we explore the concept of controlling hypothalamic inflammation to mitigate metabolic disease.


Article metrics loading...

Loading full text...

Full text loading...


Literature Cited

  1. Flegal KM, Carroll MD, Kit BK, Ogden CL. 1.  2012. Prevalence of obesity and trends in the distribution of body mass index among US adults, 1999–2010. JAMA 307:491–97 [Google Scholar]
  2. Ogden CL, Carroll MD, Kit BK, Flegal KM. 2.  2012. Prevalence of obesity and trends in body mass index among US children and adolescents, 1999–2010. JAMA 307:483–90 [Google Scholar]
  3. Hotamisligil GS. 3.  2006. Inflammation and metabolic disorders. Nature 444:860–67 [Google Scholar]
  4. Odegaard JI, Chawla A. 4.  2013. Pleiotropic actions of insulin resistance and inflammation in metabolic homeostasis. Science 339:172–77 [Google Scholar]
  5. Xu H, Barnes GT, Yang Q, Tan G, Yang D. 5.  et al. 2003. Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance. J. Clin. Investig. 112:1821–30 [Google Scholar]

Data & Media loading...

  • Article Type: Review Article
This is a required field
Please enter a valid email address
Approval was a Success
Invalid data
An Error Occurred
Approval was partially successful, following selected items could not be processed due to error