Researchers Report that Rutin Supplementation Can Improve Muscle Mitochondrial Function in Obese Rats

A new study led by researchers at Ewha Womans University in Korea recently revealed that the consumption of rutin can improve obesity in rats through a positive effect on mitochondrial function in the skeletal muscle. The study was published in the journal Nutrients and is entitled “Rutin Increases Muscle Mitochondrial Biogenesis with AMPK Activation in High-Fat Diet-Induced Obese Rats”.

Mitochondria are small organelles within cells that are responsible for the production of energy through the process of respiration. Mitochondrial dysfunction can impair the cellular energy metabolism, potentially leading to cell death and neurodegeneration, and a harmful impact in several tissues organs. Mitochondrial dysfunction in skeletal muscle has been reported to be linked to obesity and obesity-associated metabolic disorders.

Obesity is considered a worldwide health epidemic being strongly associated with metabolic disorders like heart disease, hypertension and type 2 diabetes. It has been shown in obese humans that the skeletal muscle has a reduced number of mitochondria and a decreased mitochondrial function. Scientists believe that the study of obesity-induced mitochondrial changes in skeletal muscle may reveal possible targets to fight obesity and associated comorbidities.

Rutin (rutoside, quercetin-3-O-rutinoside and sophorin) is a bioflavanoid found in apples, figs, citrus fruits, buckwheat, green and black teas, which has strong antioxidant properties. Previous studies have shown that rutin, in addition to antioxidant properties, also has anti-inflammatory, anti-hypertensive, and anti-platelet properties through the regulation of inflammation, oxidative stress, and glucose and lipid metabolism.

In the study, researchers investigated the possible positive effect of rutin on obesity-induced mitochondrial dysfunction in skeletal muscle of high-fat diet-induced obese rats.

Researchers found that rutin supplementation induced a reduction in body weight and adipose tissue mass in the animals. Regarding mitochondria, rutin significantly increased the mitochondria size, the content in mitochondrial DNA, and the expression of genes linked to mitochondrial biogenesis in skeletal muscle, namely the nuclear respiratory factor-1 (NRF-1), sirtulin1 (SIRT1), peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) and transcription factor A (Tfam).

The team also reported that rutin supplementation increased the activity of the adenosine monophosphate-activated protein kinase (AMPK) by 40% in the muscle. AMPK is an important enzyme for cellular energy homeostasis and mitochondrial biogenesis.

The findings led the team to conclude, for the first time, that rutin supplementation has a beneficial effect on obesity that might be linked to mitochondria and AMPK activation in skeletal muscle. The authors suggest that further studies should be conducted in order to better understand the link between rutin, mitochondrial function, muscle fibers and obesity.