A recent study has discovered that elevated blood fat levels in people with type 2 diabetes and obesity are more hazardous than previously thought.
Elevated fat levels in the blood cause stress in muscle cells in people with metabolic disorders, which is a response to changes outside the cell that harm its structure and function.
Researchers at the University of Leeds revealed that stressed-out cells emit a signal that can be passed on to other cells.
Because they are part of a mechanism designed to alleviate stress in the cell, the signals, known as ceramides, may have a protective advantage in the short term. However, in metabolic diseases, which are chronic illnesses, the signals can damage cells, exacerbate symptoms, and worsen the sickness.
Increased blood fat levels have long been known to harm tissues and organs, contributing to cardiovascular and metabolic illnesses such as type 2 diabetes. Obesity, which has nearly tripled in global rates since 1975, can induce the illness. Obesity affected more than 650 million people aged 18 and above in 2016.
Although this research is at an early stage, our discovery may form the basis of new therapies or therapeutic approaches to prevent the development of cardiovascular and metabolic diseases such as diabetes in people with elevated blood fats or obesity, said research supervisor Lee Roberts, Professor of Molecular Physiology and Metabolism at the University of Leeds’ School of Medicine.
By exposing skeletal muscle cells to a fatty acid called palmitate, the researchers were able to recreate the blood fat levels seen in individuals with metabolic illness in the lab. The ceramide signal began to be transmitted by the cells.
The researchers discovered that when these cells were mingled with others who hadn’t been exposed to fats before, they communicated with one another, carrying the signal in extracellular vesicles.
Human volunteers with metabolic illnesses were used in the experiment, and the results were similar. The discoveries shed light on how cells respond to stress in a whole new way, with crucial implications for our knowledge of metabolic illnesses like obesity.
“This discovery gives us a different perspective on how stress arises in the cells of obese patients, and it provides additional paths to examine when developing new treatments for metabolic illnesses,” Professor Roberts said.
“As the prevalence of obesity rises, so does the burden of accompanying chronic diseases like type 2 diabetes, necessitating innovative treatments.” We hope that the findings of our study here will pave the way for additional research to address this rising concern. “
The study was published in Nature Communications today and is titled “Long-chain ceramides are cell non-autonomous signals linking lipotoxicity to endoplasmic reticulum stress in skeletal muscle.”
Colleagues from the University of Cambridge, the University of Bonn, the University of Bari, Imperial College, and AstraZeneca made up the worldwide research team.
