Medical Acupuncture

Low-Frequency Electroacupuncture Improves Insulin Sensitivity in Obese Diabetic Mice through Activation of SIRT1/PGC-1α in Skeletal Muscle

Figure 4: Schematic model of electroacupuncture on insulin resistance in skeletal muscle. SIRT1-mediated deacetylation of PGC1α is required to activate genes that are associated with mitochondrial fatty acid oxidation in response to energy demands. The resultant increase in expression of mitochondrial genes, including NRF1, could exert positive effects on insulin signaling. eNOS: endothelial nitric oxide synthase; PGC1α: peroxisome proliferator-activated receptor γ coactivator 1α; SIRT1: Sirtuin 1; NRF1: nuclear respiratory factor 1.

This study suggested a preliminary mechanism of electroacupuncture. Specifically, low-frequency EA improved insulin sensitivity in a mouse model of genetic insulin resistance and diabetes, at least in part, via stimulation of SIRT1/PGC-1α in the skeletal muscle. Events involved in this mechanism are presented in Figure 4. This effect leads to a net switch in the metabolic program of the organism to an adaptation that may be of benefit in the face of disorders characterized by insulin resistance. The study introduces an effective and safe activator (electroacupuncture) for SIRT1, offering a basis for applying acupuncture in clinical practice in the treatment of diseases related to insulin resistance.

Low-Frequency Electroacupuncture Improves Insulin Sensitivity in Obese Diabetic Mice through Activation of SIRT1/PGC-1α in Skeletal Muscle

Evidence-Based Complementary and Alternative Medicine
Volume 2011

Integrative Cancer Care

Do not get so fat. Excessive adipose tissue can induce cancer.

Fibroblast growth factor receptor is a mechanistic link between visceral adiposity and cancer

Oncogene advance online publication 7 August 2017


Epidemiological evidence implicates excess adipose tissue in increasing cancer risk. Despite a steeply rising global prevalence of obesity, how adiposity contributes to transformation (stage a non-tumorigenic cell undergoes to become malignant) is unknown. To determine the factors in adipose tissue that stimulate transformation, we used a novel ex vivosystem of visceral adipose tissue (VAT)-condition medium-stimulated epithelial cell growth in soft agar. To extend this system in vivo, we used a murine lipectomy model of ultraviolet light B-induced, VAT-promoted skin tumor formation. We found that VAT from mice and obese human donors stimulated growth in soft agar of non-tumorigenic epithelial cells. The difference in VAT activity was associated with fibroblast growth factor-2 (FGF2) levels. Moreover, human and mouse VAT failed to stimulate growth in soft of agar in cells deficient in FGFR-1 (FGF2 receptor). We also demonstrated that circulating levels of FGF2 were associated with non-melanoma tumor formation in vivo. These data implicate FGF2 as a major factor VAT releases to transform epithelial cells—a novel, potential pathway of VAT-enhanced tumorigenesis. Strategies designed to deplete VAT stores of FGF2 or inhibit FGFR-1 in abdominally obese individuals may be important cancer prevention strategies as well as adjuvant therapies for improving outcomes.

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