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Protein Discovered to Cause Pre-Diabetes, Impaired Glucose Metabolism

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Protein Discovered to Cause Pre-Diabetes, Impaired Glucose Metabolism
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A new study led by researchers at Monash University in Clayton, Australia revealed the discovery of a protein called fetuin B linked to a fatty liver phenotype and that can cause pre-diabetes. The study was recently published in the journal Cell Metabolism and is entitled “Fetuin B Is a Secreted Hepatocyte Factor Linking Steatosis to Impaired Glucose Metabolism.

Obesity is a worldwide public health concern has been linked to the development of a relatively novel disease known as non-alcoholic fatty liver disease (NAFLD). It is estimated that around 60% of obese adults develop NAFLD.

NAFLD is characterized by an abnormal accumulation of fat in the liver (steatosis) in individuals who drink little or no alcohol. In some cases, the condition can become severe, causing inflammation and scarring of the liver, possibly leading to liver failure. NAFLD is also known to significantly increase the person’s risk of developing insulin resistance and diabetes.

In the study, researchers hypothesized that protein signals from liver cells can modulate metabolic phenotypes. The team found that factors secreted from steatotic hepatocytes (fatty liver cells) could induce inflammation and insulin resistance in vitro. When these secreted factors were analyzed in more detail, researchers found 32 to be differentially secreted between steatotic and non-steatotic liver cells. Of these, a protein was discovered to be increased in humans with liver steatosis and patients with type 2 diabetes – the fetuin B protein.

Interestingly, researchers reported that in their patient cohort, only obese patients who were also pre-diabetic or diabetic had high levels of fetuin B protein, but not obese individuals who were not diabetic.

Researchers found that fetuin B was able to impair insulin action and cause glucose intolerance in mice. The silencing of fetuin B expression in obese mice was found to improve glucose tolerance.

The findings led the team to propose that the protein secretory profile of hepatocytes is changed in the presence of steatosis, leading to inflammation and insulin resistance. Fetuin B protein, as one of the secreted factors from steatotic hepatocytes, could therefore be part of the link between NAFLD and the development of type 2 diabetes.

The research team suggests that fetuin B may represent a potential therapeutic target for the control of glucose metabolism and, consequently, for diabetes treatment. “By developing a drug that could block this protein, it may be possible to prevent the development of diabetes in patients with fatty liver,” concluded the study’s senior author Professor Matthew Watt in a news release.

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