Anti-inflammatory Diet Reduces Heart, Skeletal Muscle Changes in PAH Mice

Joana Carvalho, PhD avatar

by Joana Carvalho, PhD |

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An anti-inflammatory diet with high amounts of protein, fish oil, the amino acid leucine, and oligosaccharides reduced changes in heart and skeletal muscle in a female mice model of pulmonary arterial hypertension (PAH), a study says.

The findings of the study, “Anti-inflammatory nutrition with high protein attenuates cardiac and skeletal muscle alterations in a pulmonary arterial hypertension model,” were published in the journal Scientific Reports.

PAH is a rare, life-threatening disorder caused by a narrowing of the arteries in the lungs, and morphological alterations in the heart’s right ventricle, leading to high blood pressure and progressive decline of heart and skeletal muscle function.

“Nutritional intervention with high protein, leucine, fish oil, and oligosaccharides has been shown to have beneficial effects on skeletal muscle atrophy in a mouse model of cancer. This provides evidence of a potential multi-organ treatment for PAH, where both cardiac and skeletal muscle impairments can be targeted in combination,” the researchers stated.

Leucine is an amino acid (the building blocks of proteins) found in protein-rich foods (meat, dairy products, and some legumes), and is known to slow muscle degradation; oligosaccharides are short sugar molecules found in many vegetables and play an important role in the health of the gastrointestinal tract.

In the study, a team of researchers from the Wageningen University, in the Netherlands, set out to evaluate the effects of an anti-inflammatory diet rich in protein, fish oil, leucine, and oligosaccharides on heart and skeletal muscle function in a female mice model of induced PAH.

To induce the development of PAH, researchers treated animals with weekly injections of monocrotaline (MCT) — a natural plant toxin normally used to trigger symptoms similar to those of humans with pulmonary hypertension — for eight weeks.

Female mice were randomly divided into three groups:

  • The sham group (control group), in which animals were not treated with MCT to develop PAH, and remained on a standard diet;
  • The MCT group, in which animals treated with MCT remained on a standard diet;
  • The MCT+NI group, in which animals treated with MCT were fed a diet rich in protein, fish oil, leucine, and oligosaccharides that had the same number of calories as the standard diet.

Results showed that mice treated with MCT had a 7% increase in heart weight, a 13% increase in the thickness of the heart’s right ventricle, and a 60% increase in the total amount of scarred tissue (fibrosis) in the heart compared to sham animals.

Importantly, the experimental anti-inflammatory diet attenuated the increase in heart weight, the thickness of the heart’s right ventricle, and the amount of scarred tissue found on the hearts of MCT-treated animals.

Microarray and quantitative real-time polymerase chain reaction (qRT-PCR) analyses — two techniques scientists use to measure the expression levels of genes — of the heart’s right ventricle revealed a significant increase in the expression levels of genes involved in tissue scarring in MCT-treated animals, compared to sham controls.

The increased expression levels of fibrotic genes seen in MCT-treated mice decreased significantly among animals fed the anti-inflammatory diet.

Researchers also found that while MCT-treated mice had a 22% increase in skeletal muscle atrophy (shrinkage), MCT-treated animals that had been fed the anti-inflammatory diet showed no signs of muscle atrophy.

Overall, “a multi-compound nutritional intervention providing higher amounts of protein, leucine, fish oil, and oligosaccharides significantly attenuated cardiac and skeletal muscle changes in a female mouse model of pulmonary hypertension,” the researchers said.

According to the team, “these results provide directions for further study to develop novel therapeutic strategies to prevent pathophysiological alterations in pulmonary hypertension.”


A Conversation With Rare Disease Advocates