A new study by scientists at the Massachusetts Institute of Technology (MIT) and Harvard University delves into the complex relationship between nutrition, exercise, and the human body, yielding some interesting insights. This study explores the cellular dynamics of high-fat diets and physical activity, and how they steer cells and body systems in healthy or unhealthy directions.
The new study builds on previous research conducted by MIT researcher Manolis Kellis that focused on the FTO gene region associated with fat mass and obesity risk. This early study showed how genes in this region regulate signaling pathways that transform certain types of immature adipocytes into fat-burning or fat-storing cells.
Since then, Kellis has turned to exercise to explore what role it might play in this process. We performed single-cell RNA-seq of white adipose tissue that is packed in the skin, and subcutaneous white adipose tissue that underlies the skin.
These tissues were sourced from four different experimental groups of mice. After he fed two groups of mice either a normal diet or a high-fat diet for three weeks, he divided these groups into sedentary groups or exercise groups with access to a treadmill for an additional three weeks. After analyzing the four groups of tissues, the scientists were then able to identify genes that were either activated or repressed by exercise in 53 different cell types.
“One of the general points that our research has revealed is that a high-fat diet pushes all these cells and systems in one direction, and exercise pushes almost all of them in the opposite direction. It’s what it looks like,” Kelis said. “It’s been said that exercise can really have a big impact on the whole body.”
Analysis showed that some interesting changes occurred. At the heart of many of them were stem cells known as mesenchymal stem cells (MSCs). These cells can differentiate into adipocytes and other cells, such as fibroblasts, which connect tissues and organs, and scientists believe that a high-fat diet promotes their ability to differentiate into fat-storing cells. Conversely, exercise was shown to reverse this effect.
Furthermore, the high-fat diet caused mesenchymal stem cells to secrete factors that altered the supporting structure around the cells, called the extracellular matrix. This matrix remodeling created a more inflammatory environment and resulted in new support structures that were more accommodating for fat storage cells.
“When adipocytes (adipocytes) become overloaded with lipids, extreme stress can occur, leading to a systemic, long-lasting, low-grade inflammation,” Kelis said. It is one of the factors contributing to much of the negative impact.”
A growing body of research is unraveling how the body clock, or circadian rhythm, influences metabolism and adipocyte behavior, and this new research is also relevant in this area. The authors found that a high-fat diet suppressed genes that govern circadian rhythms, and exercise had the opposite effect, boosting them. and human genes associated with increased risk of obesity.
“There’s a lot of research showing that the time you eat during the day is very important in how you absorb calories,” Kelis said. We show that obesity and exercise do indeed directly affect circadian rhythms in peripheral organs, and may act systemically on peripheral clocks to regulate stem cell function and immunity.”
Scientists are now analyzing gut, liver and brain samples from mice to investigate changes in these tissues, and collecting blood and tissue samples from humans to investigate differences in human physiology. are carrying out this research. The authors believe that the findings are further evidence of how important healthy eating and exercise are to our health.
However, access to quality food and regular physical activity are not taken for granted and are not viable lifestyle interventions for everyone. believes this finding is also important in that it points to new targets for drugs that may one day replicate the effects of exercise.
“It is very important to understand the molecular mechanisms that drive the beneficial effects of exercise and the detrimental effects of a high-fat diet, so that we can understand how we can intervene and mimic the effects of exercise.” We can develop drugs, multiple organizations,” said Kellis.
A study was published in a journal cell metabolism.
Source: MIT
