Having shown that diet can affect gene expression, science is beginning to investigate more about how this happens.According to a recently published article Food and chemical toxicology A diet supplemented or deficient with methionine, an essential amino acid abundant in eggs, meat and seafood, is a coiled fiber composed of genes related to fat metabolism in hepatocytes and DNA and protein. It affects the expression of genes that modify chromatin. Intracellular chromosome.
In this study, we investigated how methionine affects DNA methylation. This is a biochemical process that involves the addition of methyl radicals to DNA molecules. This is an epigenetic change, meaning a change in the expression profile of a gene that defines an individual’s characteristics (phenotype). Epigenetic changes are repeated during cell division and can be transmitted to offspring, but they are not the same as changes in the DNA sequence (genotype). The relationship between methylation and disease is now being extensively studied by scientists.
To investigate the epigenetic mechanisms involved in liver cell changes, researchers fed mice with a methionine deficiency or methionine-supplemented diet and extracted cells from the liver for molecular analysis.
This study was fourth published by the Nutrigenomics Research Group at the Ribeirao Preto Pharmacy (FCFRP-USP), University of Sao Paulo, Brazil, and was generated during a FAPESP-sponsored Alexandre Ferro Aissa PhD study. It is based on. Through scholarships for doctoral programs and overseas research internships.
The study also included a collaborative study with a team led by Igor Pogribny, a researcher at the National Center for Toxicology, a branch of the US Food and Drug Administration (FDA). Pogribny has pioneered research on the role of methylation and methionine with a focus on fatty liver (non-alcoholic). Fatty liver disease), Currently considered epidemic. Pogribny himself suggested that Aissa investigate the effects of methionine on hepatocytes.
Previous studies by the FCFRP-USP group (such as those reported in 2014) Molecular nutrition and food research Showed that dietary methionine deficiency and supplementation can cause fatty liver-related molecular abnormalities, including changes in gene expression that lead to lipid accumulation in the liver. Researchers have found that fat accumulates in hepatocytes only when they are deficient in methionine, predisposing them to cirrhosis, cancer, and other illnesses. “But I still didn’t know how this would happen,” Aissa told Agência FAPESP.
The findings contribute to a better understanding of the effects of dietary compounds on gene regulation, including the effects of diet on microRNAs (or miRNAs, small RNA molecules that do not produce proteins but regulate gene function). increase.
We have observed that a diet with deficient levels of methionine, especially a diet deficient in amino acids, can cause dysregulation of some microRNAs that play an important role in liver homeostasis. “
Lusânia Maria Greggi Antunes, corresponding author of the article and coordinator of the FCFRP-USP nutritional genomics group.
“In our analysis, targets of these microRNAs associated with liver homeostasis, such as miR-190b-5p, miR-130b-3p, miR-376c-3p, miR-411-5p, miR-29c- A number of possible genes have been detected. At 3p, miR-295-3p, and miR-467d-5p, a methionine-deficient diet has a more substantial effect, “said Aissa. increase.
In the case of Antunes, “The specific contribution of this study is a list of several biomarkers associated with tissue changes, such as genes with altered methylation patterns and microRNAs associated with this process. All of these are used. And improve the diagnosis, prognosis. “
This group still has a large amount of data to analyze. For example, the latest study involved breeding female mice, which makes it possible to analyze the effects of methionine deficiency and supplementation on offspring. They also have data on methionine metabolism and its effects on the development of heart disease, including epigenetic mechanisms.