iRhom2 protein involved in obesity detection
The researchers have found in a study that the loss of iRhom2 protein in mice contributes to a reduction in fat in the body and increases energy intake of fatty deposits known as adipose.
Obesity is lately increasing in the global range, a disease that has been seen to be a serious public health issue. Nearly half of the population in Portugal is overweight and nearly 1 million adults have obesity. Known as a cardiovascular and diabetes risk factor, obesity is associated with chronic fat tissue inflammation.
The principal investigator says, during the research, we found that iRhom2 protein is strongly present in metabolic tissues and organs, which made us decide to study the role of iRhom2 in obesity in more detail.
The study demonstrates how the researchers reached the results. They used an animal model, comparing groups with iRhom2 deletion to controls, and feeding them with a normal diet versus a high-fat diet.
Surprisingly, they found that during obesity, iRhom2 protein levels increasae specifically in brown adipose tissue in obese animals compared to controls. Following up on this, they found that on a high-fat diet, the animals lacking iRhom2 protein were metabolically more healthy than their wild type counterparts.
The main author of the paper explained, that the deletion of iRhom2 led to enhanced energy consumption in adipose tissue, which protected animals from fat accumulation and inflammation, fatty liver and insulin resistance when the animals were placed on a diet that predisposed them to obesity.
Furthermore, the researchers found that at the cellular level deletion of iRhom2 leads to an increase in thermogenesis ( heat production) in brown adipose tissue. Thermogenesis in brown adipose tissue is an important physiological mechanism to consume excess body energy.
Interestingly no deleterious side effects were found in the animals with iRhom2 deletion, indicating that blocking iRhom2 may potentially be beneficial in the treatment of obesity and associated complications.
However, researchers intend to further explore the mechanisms and types of cells involved in obesity control iRhom2 and to identify the specific targets involved in the protection against obesity-associated with loss of iRhom2.
Obesity is lately increasing in the global range, a disease that has been seen to be a serious public health issue. Nearly half of the population in Portugal is overweight and nearly 1 million adults have obesity. Known as a cardiovascular and diabetes risk factor, obesity is associated with chronic fat tissue inflammation.
The principal investigator says, during the research, we found that iRhom2 protein is strongly present in metabolic tissues and organs, which made us decide to study the role of iRhom2 in obesity in more detail.
The study demonstrates how the researchers reached the results. They used an animal model, comparing groups with iRhom2 deletion to controls, and feeding them with a normal diet versus a high-fat diet.
Surprisingly, they found that during obesity, iRhom2 protein levels increasae specifically in brown adipose tissue in obese animals compared to controls. Following up on this, they found that on a high-fat diet, the animals lacking iRhom2 protein were metabolically more healthy than their wild type counterparts.
The main author of the paper explained, that the deletion of iRhom2 led to enhanced energy consumption in adipose tissue, which protected animals from fat accumulation and inflammation, fatty liver and insulin resistance when the animals were placed on a diet that predisposed them to obesity.
Furthermore, the researchers found that at the cellular level deletion of iRhom2 leads to an increase in thermogenesis ( heat production) in brown adipose tissue. Thermogenesis in brown adipose tissue is an important physiological mechanism to consume excess body energy.
Interestingly no deleterious side effects were found in the animals with iRhom2 deletion, indicating that blocking iRhom2 may potentially be beneficial in the treatment of obesity and associated complications.
However, researchers intend to further explore the mechanisms and types of cells involved in obesity control iRhom2 and to identify the specific targets involved in the protection against obesity-associated with loss of iRhom2.