Researchers have discovered a new pathway by which endothelial cells boost the body’s metabolism.
According to researchers, vascular cells are key regulators of brown fat and energy metabolism.
A major risk factor for diabetes, insulin resistance occurs when the body’s cells do not respond to insulin and cannot use glucose (sugar) in the bloodstream. This condition is associated with an increased risk of cardiovascular disease and atherosclerosis, a buildup of fat within arteries that can restrict blood flow to body tissues. However, the precise mechanism by which insulin and the cells lining the vessel wall interact is unknown.
Scientists at the Joslin Diabetes Center describe in a paper a series of studies designed to explore the link between insulin, fat, and the vascular system. circulation researchLed by Dr. George King, Joslyn’s Chief Scientific Officer and Research Director, the group has discovered an entirely new way in which the body’s metabolism is controlled by the endothelial cells that line blood vessels. The results support scientific consensus by suggesting that vascular dysfunction may be the underlying cause of the undesirable metabolic changes that can lead to diabetes, contrary to what was previously believed. is challenging.
“In people with diabetes and insulin resistance, there has always been the notion that white fat and inflammation cause vascular dysfunction leading to the prevalence of heart, eye and kidney disease in this patient population,” said Dr. King. Thomas J. Beatson, Jr. Professor of Medicine in Diabetes Harvard Medical School“However, we discovered that blood vessels may have a large regulatory effect here, which was previously unknown.”
In addition to vascular problems, diabetes is associated with an undesirable decrease in the body’s brown fat stores, also known as brown adipose tissue. Brown fat, in contrast to white fat, burns energy, regulates weight and metabolism, and maintains body temperature. In a series of tests using a mouse model of diabetes, King and colleagues found that mice designed to increase insulin sensitivity solely by blood vessels weighed less than control animals, even when fed a high-fat diet. found that extra insulin-sensitive mice had more brown fat and reduced vascular injury than control animals.
Further investigation by the team revealed that insulin signals endothelial cells within blood vessels to produce nitric oxide, which triggers the production of brown fat cells. In the setting of insulin resistance, endothelial cell-produced nitric oxide is reduced, which is known to increase cardiovascular risk, thus reducing brown fat production. Because brown fat plays an essential role in regulating body weight and metabolism, low brown fat stores may be a risk factor rather than a symptom of diabetes.
“What we found here is that the endothelial cells lining the blood vessels can have a significant impact on the amount of brown fat produced.” It regulates the amount of brown fat.This finding is very interesting because it used to be thought that diabetes causes cardiovascular problems, but in this scenario the relationship seems to be reversed. I can see.”
The results of this study set the stage for using brown fat and the array of hormones and inflammatory proteins it regulates as biomarkers of atherosclerosis and cardiovascular disease—indications that doctors can test. . In the future, with future animal and clinical studies, this new information may open the door to entirely new weight management strategies by increasing brown adipose tissue through improved endothelial nitric oxide production. .
“Everything is connected,” said King. “We believe that blood vessels and endothelial cells play an important role not only in the regulation of brown fat, but also in the regulation of metabolism throughout the body. factors, and as other laboratories have shown, blood vessels also appear to be major regulators of brain function. “
References: “Endothelial cells induced progenitor cells into brown fat to alleviate atherosclerosis,” Kyungmin Park, Chien Lee, Matthew D. Lines, Hisashi Yokomizo, Ernesto Maddaloni, Takanori Arashiro, Ronald St. Louis, Ching Lee, Sayaka Katagiri, Jalyn Hu, Allen Clermont, Hyunseok Park, I-Hsien Wu, Marc Gregory Yu, Hetal Shah, Yu-Hua Tseng, George L. King, June 1, 2022 , circulation research.
DOI: 10.1161/CIRCRESAHA.121.319582
This study was funded by the National Institutes of Health and the NIDDK Center for Diabetes Research. Disclosures reported by the authors.
[Editor’s note: Previously the article said “nitrous” oxide when it should have been “nitric” oxide. Nitric oxide is NO, while nitrous oxide is N2O.]
