Neuroinflammatory basis of metabolic syndrome

Sudarshana Purkayastha, Dongsheng Cai

Research output: Contribution to journalReview articlepeer-review

111 Scopus citations


Inflammatory reaction is a fundamental defense mechanism against threat towards normal integrity and physiology. On the other hand, chronic diseases such as obesity, type 2 diabetes, hypertension and atherosclerosis, have been causally linked to chronic, low-grade inflammation in various metabolic tissues. Recent cross-disciplinary research has led to identification of hypothalamic inflammatory changes that are triggered by overnutrition, orchestrated by hypothalamic immune system, and sustained through metabolic syndrome-associated pathophysiology. While continuing research is actively trying to underpin the identity and mechanisms of these inflammatory stimuli and actions involved in metabolic syndrome disorders and related diseases, proinflammatory IκB kinase-β (IKKβ), the downstream nuclear transcription factor NF-κB and some related molecules in the hypothalamus were discovered to be pathogenically significant. This article is to summarize recent progresses in the field of neuroendocrine research addressing the central integrative role of neuroinflammation in metabolic syndrome components ranging from obesity, glucose intolerance to cardiovascular dysfunctions.

Original languageEnglish (US)
Pages (from-to)356-363
Number of pages8
JournalMolecular Metabolism
Issue number4
StatePublished - Nov 2013


  • CNS
  • Hypothalamus
  • IKKβ/NF-κB pathway
  • Inflammation
  • Obesity
  • Type 2 diabetes

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology


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