A study coordinated by the research group of the Department of Clinical and Biological Sciences of the University of Turin has demonstrated how niacin, a form of vitamin B3improve the state of the mitochondria, counteract muscle atrophy and alterations of energy metabolism in cancer patients
The research group coordinated by Prof. Fabio Penna of the Department of Clinical and Biological Sciences dell’University of Turin has just published a scientific work in the prestigious journal ‘Nature Communications’ (https://rdcu.be/c82wc) in which it is demonstrated the efficacy of niacina form of the vitamin B3in countering the neoplastic cachexiaa multifactorial syndrome characterized by the progressive loss of muscle mass, with or without loss of fat mass, of a cancer patient.
Cancer growth and anticancer treatments generate harmful adaptations in patients, which often result in paraneoplastic syndromes, of which neoplastic cachexia is the most relevant and of negative impact. There cachexia it is characterized by inflammation and metabolic stress in various organs, with consequent compromised tissue function, reduced tolerance to chemotherapy and poor immune response: all factors that contribute to compromise the quality of life and reduce survival. In oncology practice, all attention is focused on cancer-targeted therapies, often ignoring the general state of the patient and missing the opportunity to treat cancer and associated syndromes as a single disease. In current research, aimed at considering the cancer-patient system as a whole, energy metabolism has been considered to find new anti-cachexia treatment options.
The identification of the specific target, i.e. the metabolism of NAD⁺ (nicotinamide adenine dinucleotide), occurred by studying preclinical research models (tumor-bearing mice) thanks to Juha Hulmi of Jyväskylä (Finland), whose analyzes showed theassociation between muscle wasting and NAD⁺ deficiency. Since NAD⁺ is essential for the proper functioning of the mitochondria, the ‘power plant’ of our cells, the loss of NAD⁺ can explain the energy deficit that occurs in the tissues of cancer patients, similarly to what happens in primary mitochondrial myopathy, where the enhancement of NAD⁺ with vitamin B3 counteracts dysmetabolism, as demonstrated by the pioneering work by Eija Pirinen (Finland).
The Turin contribution to the research was to characterize the metabolism of NAD⁺ in the context of neoplastic cachexia and to test the efficacy of NAD⁺ regeneration in tumor-bearing mice, animal models that Marc Beltra recently developed in the Turin laboratory. The intervention study was preceded by the work of Noora Pöllänen (Finland), whose screening of NAD⁺ metabolism disorders in novel models of cachexia confirmed that loss of NAD⁺ and reduced expression of associated genes is a common trait in experimental cachexia triggered by intestinal and pancreatic cancers. In an attempt to extend and validate this observation in the clinic, the group of Roberta Sartori(Department of Biomedical Sciences, University of Padua and VIMM Advanced Biomedical Research Foundation of Padua) joined the consortium and demonstrated the occurrence of NAD⁺ and energy metabolism alterations in the muscle of cancer patients affected by colorectal or of the pancreas. The patients were recruited at the UOC of General Surgery 1 Hospital – University of Padua in collaboration with a team of researchers from DiSCOG (Department of Oncological and Gastroenterological Surgical Sciences), University of Padua.
In order to demonstrate the importance of these alterations for the potential cure of cachexia, it was decided to test the efficacy of niacin (vitamin B3) in increasing NAD⁺ levels in tumor-bearing mice. Niacin prevented muscle NAD⁺ deficiency and improved the state of mitochondria, counteracting muscle atrophy and alterations in energy metabolism. Whereas niacin is inexpensive and has been used safely for the treatment of hypercholesterolemia in humans, its use is proposed for the management of cancer patients with impaired energy metabolism. In the future, targeting metabolic imbalance in the host will potentially reverse the vicious cycle of cachexia and unresponsiveness to cancer therapies, improving survival and quality of life for cancer patients.
NurseTimes editorial team
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