TY - JOUR
T1 - Hypothalamic microinflammation
T2 - A common basis of metabolic syndrome and aging
AU - Tang, Yizhe
AU - Purkayastha, Sudarshana
AU - Cai, Dongsheng
N1 - Funding Information:
The authors sincerely thank Cai's laboratory members for conducting research related to this topic, supported by NIH R01 DK078750, R01 AG031774 and R01 HL113180 (all to D. Cai).
Publisher Copyright:
© 2014 Elsevier Ltd.
PY - 2015
Y1 - 2015
N2 - Chronic microinflammation is a hallmark of many aging-related neurodegenerative diseases as well as metabolic syndrome-driven diseases. Recent research indicates that chronic caloric excess can lead to hypothalamic microinflammation, which in turn participates in the development and progression of metabolic syndrome disorders such as obesity, glucose intolerance, and hypertension. Additionally, it was recently shown that increasing age after young adulthood can cause hypothalamic microinflammation independently of nutritional status, mediating a central mechanism of systemic aging. Taken together, these findings suggest that the hypothalamus has a fundamental role, via hypothalamic microinflammation, in translating overnutrition and aging into complex outcomes. Here we summarize recent work and suggest a conceptual model in which hypothalamic microinflammation is a common mediator of metabolic syndrome and aging.
AB - Chronic microinflammation is a hallmark of many aging-related neurodegenerative diseases as well as metabolic syndrome-driven diseases. Recent research indicates that chronic caloric excess can lead to hypothalamic microinflammation, which in turn participates in the development and progression of metabolic syndrome disorders such as obesity, glucose intolerance, and hypertension. Additionally, it was recently shown that increasing age after young adulthood can cause hypothalamic microinflammation independently of nutritional status, mediating a central mechanism of systemic aging. Taken together, these findings suggest that the hypothalamus has a fundamental role, via hypothalamic microinflammation, in translating overnutrition and aging into complex outcomes. Here we summarize recent work and suggest a conceptual model in which hypothalamic microinflammation is a common mediator of metabolic syndrome and aging.
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U2 - 10.1016/j.tins.2014.10.002
DO - 10.1016/j.tins.2014.10.002
M3 - Review article
C2 - 25458920
AN - SCOPUS:84924295797
SN - 0166-2236
VL - 38
SP - 36
EP - 44
JO - Trends in Neurosciences
JF - Trends in Neurosciences
IS - 1
ER -
