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Archive - Jul 18, 2019

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Link Between Increased Expression of AEBP1 Gene and Severe Liver Disease Suggested by Study Results

Researchers have found that a gene known as AEBP1 may play a central role in the development, severity, and potential treatment of liver disease, according to a study by Temple University, the Geisinger Obesity Institute, and the Translational Genomics Research Institute (TGen), an affiliate of City of Hope. The findings are detailed in a study published online on July 12, 2019 in PLoS One. The open-access article is titled “AEBP1 Expression Increases with Severity of Fibrosis in NASH and Is Regulated by Glucose, Palmitate, and miR-372-3p.” The study results suggest that increased expression of AEBP1 correlates with the severity of liver fibrosis in patients with NASH (nonalcoholic steatohepatitis), which is a type of NAFLD (nonalcoholic fatty liver disease), the most common cause of liver damage. NASH indicates there is both inflammation and liver cell damage, along with fat in the liver. "Given the strong link between fibrosis and risk of liver-related mortality, efforts to identify and characterize the specific mechanisms contributing to NAFLD progression are critical for the development of effective therapeutic and preventative strategies," said Dr. Johanna DiStefano, Head of the Diabetes and Fibrotic Disease Unit at TGen and senior author of the PLoS article. One of the study's major findings is that AEBP1 regulates the expression of a network of at least nine genes related to fibrosis: AKR1B10, CCDC80, DPT, EFEMP1, ITGBL1, LAMC3, MOXD1, SPP1, and STMN2. "These findings indicate that AEBP1 may be a central regulator of a complex fibrosis gene expression network in the human liver," said Dr. DiStefano.

SIRT6 Over-Expression May Prevent Progression of Diabetes, Study Suggests

Targeting obesity through exercise and calorie restriction is often the first line of approach to treat diabetes and related cardiovascular disorders, such as cardiomyopathy. A recent animal study published in online on July 12, 2019 in The FASEB Journal explored an alternative sirtuin-based therapy to block the development of obesity and cardiomyopathy under conditions of excess nutrition, when diet restriction and regular exercise are not feasible. The article is titled “The Nuclear and Mitochondrial Sirtuins, Sirt6 and Sirt3, Regulate Each Other’s Activity and Protect the Heart from Developing Obesity-Mediated Diabetic Cardiomyopathy.” For this study, researchers assessed the potential of SIRT6 (image)- often considered a longevity factor - to protect the heart from developing diabetic cardiomyopathy. Prior research has shown that a deficiency of nuclear sirtuin SIRT6 can lead to the development of cardiomyopathy in mice. To conduct the experiment, researchers generated a group of whole-body SIRT6-overexpressing transgenic mice (Tg.SIRT6). The research team then observed the following groups of mice for 24 weeks: 1) control non-transgenic (N.Tg) mice fed a normal diet; 2) Tg.SIRT6 mice fed a normal diet; 3) control non-transgenic (N.Tg) mice fed a high-fat, high-sucrose (HF-HS) diet; and 4) Tg.SIRT6 mice fed a HF-HS diet. As expected, the control N.Tg mice fed a HF-HS diet developed obesity, compared to the N.Tg and Tg.SIRT6 mice fed a normal diet. Surprisingly, however, the Tg.SIRT6 mice fed a HF-HS diet did not develop obesity. This unexpected finding demonstrated that over-expression of SIRT6 can prevent the development of obesity under the conditions of excessive nutrition.