Metabolic Dysfunction-inducing Protein in Obesity Revealed

The role of a protein that induces metabolic dysfunction leading to obesity has come to light in a new American study.

The findings of the research, conducted by Boston University School of Medicine (BUSM), have appeared online in the journal Science.

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The researchers discovered that Sfrp5 (secreted frizzled-related protein 5) is an anti-inflammatory adipokine whose expression is disrupted in animal models of obesity and type 2 diabetes.

Obesity is a predisposing factor for metabolic disorders such as type 2 diabetes, which is often associated with a low-grade inflammatory state in adipose tissue.

Adipose tissue secretes a variety of cytokines, referred to as adipokines.

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Most adipokines, such as tumour necrosis factor (TNF) a, interleukin (IL)-6 and leptin, are pro-inflammatory. One prominent exception is adiponectin, an anti-inflammatory adipokine that promotes insulin sensitization and protects cardiovascular tissue from ischemic injury.

According to the researchers, because adipokine dysregulation can contribute to the pathogenesis of obesity-linked disorders, they sought to identify new adipokines by comparing the gene expression profile of adipose tissue from lean mice with that from obese mice on a high calorie diet.

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Senior author Kenneth Walsh, director of the Whitaker Cardiovascular Institute at BUSM, said: "Our study shows that Sfrp5 is secreted by adipocytes and that it controls the microenvironment of white adipose tissue under conditions of obesity-induced metabolic stress. Whereas Sfrp5 deficient mice do not express a detectable phenotype when fed a normal diet, these animals displayed aggravated fat pad inflammation and systemic metabolic dysfunction when fed a high calorie diet."

Conversely, the BUSM researchers found the administration of Sfrp5 to models of obese and diabetic mice improved metabolic function and reduced adipose tissue inflammation.

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The researchers propose that Sfrp5 neutralizes noncanonical JNK activation by Wnt5a in macrophages and adipocytes via paracrine and autocrine mechanisms, respectively.

Walsh said: "The JNK signaling pathway in adipocytes and macrophages has emerged as an important mediator of adipose tissue inflammation that affects systemic metabolism. Thus, the Sfrp5-JNK1 regulatory axis in fat represents a potential target for the control of obesity-linked abnormalities in glucose homeostasis."

Source-ANI