TY - JOUR
T1 - Neuroinflammatory basis of metabolic syndrome
AU - Purkayastha, Sudarshana
AU - Cai, Dongsheng
N1 - Funding Information:
The authors sincerely thank Cai lab members for related research. D.C. is supported by NIH R01 DK078750, R01 AG031774, and American Diabetes Association Grant 1-12-BS-20. D.C. is a recipient of Irma T. Hirschl Scholarship.
PY - 2013/11
Y1 - 2013/11
N2 - 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.
AB - 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.
KW - CNS
KW - Hypothalamus
KW - IKKβ/NF-κB pathway
KW - Inflammation
KW - Obesity
KW - Type 2 diabetes
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U2 - 10.1016/j.molmet.2013.09.005
DO - 10.1016/j.molmet.2013.09.005
M3 - Review article
AN - SCOPUS:84889025109
SN - 2212-8778
VL - 2
SP - 356
EP - 363
JO - Molecular Metabolism
JF - Molecular Metabolism
IS - 4
ER -