New medical research flags the concern that higher blood fats are more harmful than first thought. The University of Leeds finding considers increased levels of blood fats in people with type 2 diabetes and obesity. These are established as more harmful than earlier research has suggested.
The reason for the worry is where the research shows that blood fats can kill cells, make symptoms more severe, and worsen the illness. Furthermore, increased fat in the blood has will damage tissues and organs, contribute to the development of cardiovascular and foster metabolic diseases including type 2 diabetes.
For the study, the researchers replicated the blood fat levels observed in humans with metabolic disease by exposing skeletal muscle cells to a fatty acid called palmitate. Here, the cells began to transmit the ceramide signal. When these cells were mixed with others (not been previously exposed to fats), the scientists noted that they communicated with each other, transporting the signal in packages called extracellular vesicles.
The process was next reproduced in human volunteers. The people in the study had previously been identified as having a metabolic disease. The data from the human studies gave comparable results.
According to the research team, these findings provide a completely new angle on how cells respond to stress, with important consequences for our understanding of certain metabolic diseases including obesity.
The research appears in the journal Nature Communications, titled “Long-chain ceramides are cell non-autonomous signals linking lipotoxicity to endoplasmic reticulum stress in skeletal muscle.”
In other medical news, activating a process that slows down as we age could be the basis for protecting individuals against atherosclerosis (which is a major cause of heart attacks and strokes).
As a proof-of-concept, scientists have successfully minimized an artery-narrowing plaque in mice. Left unattended, the condition would have led to the mice developing lesions. The researchers achieved this by boosting chaperone-mediated autophagy (CMA), which is described as ‘a cellular housekeeping process’.
Further details are provided in the Proceedings of the National Academy of Sciences, where the article is titled “Protective role of chaperone-mediated autophagy against atherosclerosis.”
