Medical Research

Electroacupuncture: A Feasible Sirt1 Promoter Which Modulates Metainflammation in Diet-Induced Obesity Rats

Kristen Sparrow • July 05, 2020

Electroacupuncture: A Feasible Sirt1 Promoter Which Modulates Metainflammation in Diet-Induced Obesity Rats

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Ancient Medicine Made Modern: Scientific Solutions for Remarkable Results

I’ve never heard the term “metainflammation” before, but I understand the concept.  It refers to the global low-grade inflammation that can lead to so many issues, from heart disease, to cancer to cognitive decline.  Sirt1 is a target of anti-aging research so I like to flag articles concerning Sirt1.

Published online 2018 Oct 22. doi: 10.1155/2018/5302049
PMCID: PMC6217753
PMID: 30425749

Electroacupuncture: A Feasible Sirt1 Promoter Which Modulates Metainflammation in Diet-Induced Obesity Rats

Dan Luo, 1 Li Liu, 2 Feng-xia Liang, 3 Zhao-min Yu, 1 and Rui Chen 1

Associated Data

Data Availability Statement

Abstract

It is generally accepted that metainflammation, a state of chronic and low-grade inflammation in obesity, plays a great role in metabolic disorder like insulin resistance. To gain further insight into the mechanism of metainflammation and find feasible therapy of obesity, diet-induced obesity (DIO) rats model and Electroacupuncture (EA) treatment were established in this trail. The results indicated that rising Lee’s index, hyperlipidemia, insulin resistance, and increasing inflammation factors including NF-κB, TNF-α, and Macrophages 1 were determined in DIO rats while EA is exhibiting an effective intervention. Furthermore, to clarify this phenomenon and provide new recognition of alternative medicine for the treatment of metainflammation, we found that EA activating Sirt1 and Sirt1-dependent deacetylation of histone (H3K9) was the key of modulation. It should be noted that, while possible, the activating of Sirt1 could lead to deacetylation of NF-κB also. In this study, the deacetylation of NF-κB depended on higher level of Sirt1 than H3K9, which suggested that the deacetylation via Sirt1 in metainflammation could be specific and programmed.