An Increase In This Protein Level Can Make You Obese
KEY POINTS
- >650 million people obese people worldwide
- 2.8 million obesity-related deaths every year.
- Study points to a cellular mechanism related to obesity pave the way for a new treatment strategy
Over 650 million individuals throughout the world are obese, according to the World Health Organization. Obesity has reached epidemic proportions throughout the world causing a minimum of 2.8 million deaths every year. Identified as a major risk factor for several health conditions such as diabetes and heart diseases, new strategies are needed to combat obesity. Therefore, a deeper understanding of the cellular mechanisms pertaining to metabolic deregulation is important to approach the obesity epidemic.
"It is important to understand the fundamental mechanisms underlying how metabolic dysregulation occurs," News Medical quoted Colin Adrain, principal investigator of the research group. He added that, during the course of their research, it was evident 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 research, published in the Molecular Metabolism Journal, has demonstrated that. amongst obese individuals, the iRhom2 protein levels increase, particularly in the brown adipose tissues. Also, they found that while on a high-fat diet, those animals that lack iRhom2 protein were metabolically healthier when compared to their wild type counterparts.
The experts opined that the deletion of the protein iRhom2 can lead to enhanced energy consumption in adipose tissues that protect animals from inflammation, fatty liver, insulin resistance as well as fat accumulation when placed on a diet that put them at risk of becoming obese.
The researchers noted no side effects among animal models as a result of iRhom2 deletion. This paves the way towards treatment options for obesity by blocking the protein. They intended to develop the project to further understand the cell types and their mechanisms pertaining to iRhom2 control of obesity.
The findings of the study also demonstrated that deleting iRhom2 offered protection not only against weight gain but also from dyslipidemia, inflammation of the adipose tissues, hepatic stenosis and also improved insulin sensitivity. Another implication of the results that are worth noting is that iRhom2 is a negative regulator of thermogenesis and plays a vital role in controlling the homeostasis of adipose tissues during metabolic diseases.
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