Kristen Sparrow • May 26, 2020
This is a key article. Because Chinese Medicine has had longevity as part of its charter forever, this may be a piece of evidence that shows the science behind why this might be true. A brief description of the science behind Sirtuin1 follows in this abstract. There’s a caveat at the end of the wikipedia excerpt that any attempt to medically stimulate Sirt1 may lead to autoimmune phenomenon. A good reason to use acupuncture instead since it tends to employ feedback systems instead of directly stimulate one reaction or another.
To explore the effect of electroacupuncture (EA) on insulin sensitivity, adipose tissue inflammatory reaction and silent information regulation factor 1(SIRT1)/nuclear factor kappa B (NF-κB) signaling pathway in obese rats.
A total of 100 SPF-grade Wistar male rats were collected. Thirteen rats of them were selected randomly as the normal group and fed with common forage, and the rest rats were fed with high-fat forage. Eight weeks later, 39 rats that met the obesity criteria were randomized into a model group, an EA group and a sham-EA group, 13 rats in each one. In each group, 3 rats were collected randomly and the hyperinsulinemic-euglycemic clamp was exerted to record glucose infusion rate (GIR) so as to determine insulin sensitivity. Afterwards, in the EA group, EA was applied to “Zusanli” (ST 36), “Fenglong” (ST 40), “Zhongwan” (CV 12) and “Guanyuan” (CV 4), stimulated with continuous wave, 2 Hz in frequency, 1 mA in current intensity, for 15 min. The treatment was given once every 2 days, 3 times a week, for 8 weeks totally. In the sham-EA group, the needles were inserted shallowly at the sites, 5 mm lateral to each of the acupoints stimulated in the EA group, and the electrodes were attached to the needle handles, but without electric stimulation exerted. The rest management was the same as the EA group. Before and after intervention, the body mass and the insulin sensitivity were measured. After intervention, the white adipose tissue was collected from the kidney in the rats. Western blot was adopted to detect the relative protein expressions of SIRT1, interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and acetylated NF-κB (Ac-NFκB). The real-time fluorescence quantitative PCR was used to detect the mRNA expressions of SIRT1, IL-6 and TNF-α. The immunofluorescence double labeling method was applied to detect the co-expression of SIRT1 and Ac-NFκB in adipose tissue.
After fed with high-fat forage for 8 weeks, the body mass was significantly increased and GIR decreased in the rats of the model group as compared with the normal group (P<0.01), suggesting that the model of obese rat with insulin resistance was successfully established. After 8-week intervention, compared with the model group, the body mass was reduced and GIR increased in the rats of the EA group (P<0.01). The differences were not significant statistically in comparison between the sham-EA group and the model group (P>0.05). Compared with the normal group, in the model group, the protein and mRNA expressions of SIRT1 in adipose tissue were decreased, and the protein expression of Ac-NFκB increased, the protein and mRNA expressions of IL-6 and TNF-α increased (P<0.05, P<0.01). Compared with the model group, in the EA group, the protein and mRNA expressions of SIRT1 in adipose tissue were increased significantly, the protein expression of Ac-NFκB decreased, and the protein and mRNA expressions of IL-6 and TNF-α significantly decreased (P<0.05, P<0.01). There was no significant difference in each index between the sham-EA group and the model group (P>0.05). The results of immunofluorescence double labeling showed that SIRT1 and Ac-NFκB were co-expressed in adipose tissue.
Electroacupuncture significantly reduces the body mass, inflammatory reaction conditions of adipose tissue and improves insulin sensitivity in obese rats. Regarding the potential mechanism, after the activation of SIRT1/NF-κB signaling pathway by electroacupuncture, and down-regulates the transcription of downstream inflammatory factors.
Sirtuin 1 from Wikipedia
Sirtuin 1 is downregulated in cells that have high insulin resistance and inducing its expression increases insulin sensitivity, suggesting the molecule is associated with improving insulin sensitivity. Furthermore, SIRT1 was shown to de-acetylate and affect the activity of both members of the PGC1-alpha/ERR-alpha complex, which are essential metabolic regulatory transcription factors.
In mammals, SIRT1 has been shown to deacetylate and thereby deactivate the p53 protein. SIRT1 also stimulates autophagy by preventing acetylation of proteins (via deacetylation) required for autophagy as demonstrated in cultured cells and embryonic and neonatal tissues. This function provides a link between sirtuin expression and the cellular response to limited nutrients due to caloric restriction.
Human aging is characterized by a chronic, low-grade inflammation level, and NF-κB is the main transcriptional regulator of genes related to inflammation. SIRT1 inhibits NF-κB-regulated gene expression by deacetylating the RelA/p65 subunit of NF-κB at lysine 310.