A new hope for the prevention and treatment of an increasingly widespread disease that is classified by the World Health Organization as the tenth cause of death of millions around the world
A team of University of Pennsylvania scientists has identified the role that an enzyme called nicotinamide adenine dinucleotide (NAD+) plays in kidney disease, opening the door to new ways to prevent and treat this increasingly prevalent and potentially fatal condition, according to New Atlas. New Atlas Quoted from Nature Metabolism.
According to the World Health Organization (WHO), kidney disease has risen from being the 13th leading cause of death to the 10th. In 2019, 1.3 million people died of kidney disease. But it is often possible to slow or stop kidney disease from progressing to kidney failure if it is caught and treated early.
Expressive
metabolic balance
NAD+ coenzyme nicotinamide adenine dinucleotide, a coenzyme, is found in every living cell where it regulates various metabolic pathways, as well as being involved in DNA repair and immune cell function. It is necessary to maintain metabolic balance through its effect on the mitochondria, which are the energy generators in the cell, and without sufficient levels of the enzyme, the cells of the body do not generate the energy necessary to carry out their metabolic functions.
The tubule cells in the kidneys require a lot of energy produced by the mitochondria to perform their function, reabsorb essential nutrients and excrete waste and toxins. When the mitochondria in these cells are damaged, an inflammatory response is triggered that can lead to kidney disease, leading to a buildup of fluid, electrolytes and waste products in the body.
human samples for the first time
In the new study, the researchers used metabolomics, the study of small molecules found in blood and urine, to map metabolic changes in human kidneys. It gives a measure of metabolites, which are very small molecules that are produced during metabolism; Insight into a person’s health status. This is the first time that human samples have been used in metabolic studies.
kidneys
The underlying disease mechanism
The researchers tested kidney samples from a healthy control group once morest samples from patients with diabetic kidney disease or kidney disease caused by high blood pressure. It turns out that NAD+ levels in diseased kidneys were significantly lower. To examine the disease mechanism underlying these differences, they performed RNA-sequencing of the samples.
Prevent kidney damage
The researchers sought to find a relationship between NAD+ levels and mitochondrial gene expression, and concluded that low NAD+ levels were a major feature of human kidney disease. Also, when lab rats were given over-the-counter supplementation of an NAD+ precursor, nicotinamide riboside or nicotinamide mononucleotide (NMN), to boost NAD+ levels, tubular cell mitochondria were protected from damage, thus preventing the development of kidney disease.
Developing treatment methods
The study’s lead researcher, Katalin Sostak, said she hoped “this research will lead to improved care in the future, so when patients have metabolite changes, they can receive treatment before kidney disorders become apparent.”
The researchers hope that their study will lead to further studies on the role of metabolites in kidney disease and the development of new approaches to prevention and treatment.
“Identification of NAD+-sensitive downstream mechanisms is critical to understanding conditions that may benefit from NAD+ supplementation,” said Joseph Bauer, co-author of the study.