Adipose tissue and liver expression of SIRT1, 3, and 6 increase after extensive weight loss in morbid obesity

Moschen, Alexander R.; Wieser, Verena; Gerner, Romana R.; Bichler, A; Enrich, Barbara; Moser, Patrizia; Ebenbichler, Christoph; Kaser, Susanne; Tilg, Herbert

doi:10.1016/j.jhep.2013.07.027

Cited by 92 publications

(74 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Bariatric surgery and LAGB has been used to induce weight loss and to improve metabolic dysregulation in patients with severe obesity29 and we previously reported that LAGB improved glycaemic control along with a reduction in BMI 30 31. To explore a role of type I IFN signalling in metabolic dysregulation, we investigated the impact of weight loss on type I IFN responses in patients with severe obesity.…”

Section: Resultsmentioning

confidence: 99%

Adipose type I interferon signalling protects against metabolic dysfunction

Wieser

Adolph

Grander

et al. 2016

Gut

Self Cite

View full text Add to dashboard Cite

Objective Low-grade chronic inflammation emerges as a potent driver of insulin resistance and glucose dysregulation in obesity and associated non-alcoholic fatty liver disease (NAFLD). The liver, subcutaneous fat and the immune system participate in disturbances of metabolism. Type I interferon (IFN) signalling initiated by innate and adaptive immunity modulates inflammatory responses consequent to infection. However, little is known about the role of type I IFN signalling in metabolic diseases and the development of NAFLD. Design We determined the impact of type I IFN signalling by tissue-specific deletion of interferon (α and β) receptor 1 (Ifnar1) in hepatocytes (Ifnar1

show abstract

Section: Resultsmentioning

confidence: 99%

Adipose type I interferon signalling protects against metabolic dysfunction

Wieser

Adolph

Grander

et al. 2016

Gut

Self Cite

View full text Add to dashboard Cite

show abstract

“…This study included 55 individuals (34 females and 21 males), aged 9-95 years, divided into 8 age groups with 10-year intervals, with the exception of the 1st (9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19) and the 8th groups (80-95 years). Blood samples were collected at the Istanbul University Medico-Social Center, Turkey, with the written consent of the individuals who completed a form indicating their background regarding gender, age, inherited diseases, cancer, exposure to chemical or radioactive agents, permanent use of medicines, smoking habits and presence in the family of individuals aged >90 years.…”

Section: Methodsmentioning

confidence: 99%

“…Although studies on SIRT6 knockout mice reported a strong correlation between premature aging and the absence of the SIRT6 protein (10), the reports on the overexpression of sirtuin homologues on various model organisms have been controversial, from no effect (11) to expansion of lifespan only in male mice (12). Analyses at the mRNA and protein level revealed SIRT6 expression in the majority of mouse and human tissues, with particularly high protein levels in the thymus, skeletal muscle and brain (13,14). However, there is no sufficient data on SIRT6 promoter methylation levels and their correlation with human longevity.…”

Section: Introductionmentioning

confidence: 99%

Changes in human sirtuin 6 gene promoter methylation during aging

2014

View full text Add to dashboard Cite

Aging is a natural process during which changes at the cellular level increase death risk by developing susceptibility to a variety of diseases. Sirtuins have been shown to regulate lifespan in various organisms by deacetylating a number of important transcription factors. Of the 7 identified mammalian sirtuins (SIRT1-7), SIRT6 depletion is associated with severe symptoms of premature aging. In this study, we investigated the association between human longevity and promoter methylation. Genomic DNA from blood samples of 55 individuals (34 females and 21 males) was examined to detect methylation levels by quantitative polymerase chain reaction analysis following bisulfite treatment. While the results indicated 43.21% methylation in the 9-19 age group, this ratio was found to be increased up to 65.63% in the 20-79 age group and decreased to 52.15% in the 80-95 age group. Our results demonstrated that the gene is more active between 9-19 and 80-95 years compared to 20-79 years.

show abstract

“…126 127 In obese humans, liver expression of SIRT1 increased after extensive weight loss. 128 However, patients with NAFLD treated with 8 weeks of resveratrol did not improve hepatic steatosis (as measured by MRI) or insulin resistance, when compared with placebo. 129 Indeed, markers of hepatic inflammation such as alanine aminotransferases increased.…”

Section: Hdac Inhibitorsmentioning

confidence: 92%

Epigenetics in liver disease: from biology to therapeutics

Hardy

Mann

2016

Gut

126

140

View full text Add to dashboard Cite

Knowledge of the fundamental epigenetic mechanisms governing gene expression and cellular phenotype are sufficiently advanced that novel insights into the epigenetic control of chronic liver disease are now emerging. Hepatologists are in the process of shedding light on the roles played by DNA methylation, histone/chromatin modifications and non-coding RNAs in specific liver pathologies. Alongside these discoveries are advances in the technologies for the detection and quantification of epigenetic biomarkers, either directly from patient tissue or from body fluids. The premise for this review is to survey the recent advances in the field of liver epigenetics and to explore their potential for translation by industry and clinical hepatologists for the design of novel therapeutics and diagnostic/prognostic biomarkers. In particular, we present findings in the context of hepatocellular carcinoma, fibrosis and non-alcoholic fatty liver disease, where there is urgent unmet need for new clinical interventions and biomarkers.

show abstract

Adipose tissue and liver expression of SIRT1, 3, and 6 increase after extensive weight loss in morbid obesity

Cited by 92 publications

References 39 publications

Adipose type I interferon signalling protects against metabolic dysfunction

Adipose type I interferon signalling protects against metabolic dysfunction

Changes in human sirtuin 6 gene promoter methylation during aging

Epigenetics in liver disease: from biology to therapeutics

Contact Info

Product

Resources

About