Erratum: corrigendum: Sirt1 promotes fat mobilization in white adipocytes by repressing PPAR-γ

Picard, Frédéric; Kurtev, Martin V.; Chung, Namjin; Topark-Ngarm, Acharawan; Senawong, Thanaset; Oliveira, Rita Machado de; Leid, Mark; McBurney, Michael W.; Guarente, Leonard

doi:10.1038/nature02892

Cited by 175 publications

(233 citation statements)

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“…6 Finally, the effects of resveratrol were studied both in vitro and in vivo, demonstrating that the activation of Sirt1 influenced adipose tissue metabolism in rodents. 4 Differentiation of 3T3-L1 cells overexpressing Sirt1 resulted in cells with significantly less lipid accumulation compared to control cells. In contrast, using 3T3-L1 cells underexpressing Sirt1 resulted in differentiated adipocytes with significantly more lipid accumulation after differentiation.…”

Section: Introductionmentioning

confidence: 99%

“…3 In mammals, the SIR2 ortholog Sirt1 (Sirtulin 1) also seems to play a role for the changes in fat metabolism observed after calorie restriction. 4 Recently, small molecules capable of stimulating SIR2 in yeast were characterized. 5 Furthermore, it was demonstrated that the treatment with one of these compounds (resveratrol) induced SIR2 and thus mimicked calorie restriction.…”

Section: Introductionmentioning

confidence: 99%

“…In contrast, using 3T3-L1 cells underexpressing Sirt1 resulted in differentiated adipocytes with significantly more lipid accumulation after differentiation. 4 Furthermore, in vitro experiments revealed that resveratrol increased epinephrine-stimulated lipolysis. 4 Thus, caloric restriction seems to prolong lifespan through still not fully characterized pathways, which at least partly seem to involve activation of the Sirt1 enzyme.…”

Section: Introductionmentioning

confidence: 99%

“…4 Furthermore, in vitro experiments revealed that resveratrol increased epinephrine-stimulated lipolysis. 4 Thus, caloric restriction seems to prolong lifespan through still not fully characterized pathways, which at least partly seem to involve activation of the Sirt1 enzyme. At the other end of the spectrum lies the metabolic syndrome characterized by obesity, insulin resistance, cancer, cardiovascular disease, type 2 diabetes and premature death.…”

Section: Introductionmentioning

confidence: 99%

“…Furthermore, we studied whether Sirt1 expression is different in obese and lean individuals, and finally whether in vitro activation of the Sirt1 enzyme with resveratrol would influence epinephrine-induced lipolysis in a way similar to previously reported findings in rodent adipose tissue. 4 …”

Section: Introductionmentioning

confidence: 99%

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Low Sirt1 expression, which is upregulated by fasting, in human adipose tissue from obese women

et al. 2008

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Objective: Calorie restriction increases the life span in a number of different organisms. This effect is dependent upon activation of the Sirt1 enzyme, and many of the beneficial effects of calorie restriction can be mimicked using resveratrol, which activates the Sirt1 enzyme. Nothing is known about this system in human adipose tissue; therefore, we investigated this system in human adipose tissue. Design: Sirt1 mRNA was measured in adipose tissue biopsies from human volunteers before and after 6 days of total fasting. In addition, adipose tissue from lean and obese individuals was compared and in vitro investigations were performed. Results: Long-term total fasting (6 days) of nine human volunteers increased Sirt1 mRNA expression in subcutaneous adipose tissue more than twofold (0.197-0.454 arbitrary units, Po0.05). Likewise, lean women (n ¼ 12) had more than twofold higher Sirt1 expression in subcutaneous adipose tissue compared to obese women (n ¼ 12; 0.33-0.73 arbitrary units, Po0.05). Sirt1 was equally expressed in the stroma-vascular fraction and the isolated adipocyte fraction. Finally, in vitro, we demonstrated that resveratrol (a Sirt1 activator) significantly enhanced the lipolytic effect of epinephrine in human adipose tissue (Po0.05). Conclusion: Human adipose tissue contains Sirt1 and the expression of Sirt1 can be regulated by calorie restriction as in other species. Furthermore, we demonstrated that resveratrol affects human fat-cell metabolism similar to the effects in rodents (that is, increased epinephrine induced lipolysis). These findings indicated that the beneficial effects of calorie restriction in humans might involve the activation of Sirt1. Thus, based on these findings, we propose that Sirt1 might play important roles for the beneficial effects of calorie restriction in humans.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Low Sirt1 expression, which is upregulated by fasting, in human adipose tissue from obese women

et al. 2008

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Role of histone and transcription factor acetylation in diabetes pathogenesis

Gray

Meyts²

2005

Diabetes Metab. Res. Rev.

144

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Globally, diabetes (and, in particular, type 2 diabetes) represents a major challenge to world health. Currently in the United States, the costs of treating diabetes and its associated complications exceed 100 billion US dollars annually, and this figure is expected to soar in the near future. Despite decades of intense research efforts, the genetic basis of the events involved in the pathogenesis of diabetes is still poorly understood. Diabetes is a complex multigenic syndrome primarily due to beta-cell dysfunction associated with a variable degree of insulin resistance. Recent advances have led to exciting new developments with regard to our understanding of the mechanisms that regulate insulin transcription. These include data that implicate chromatin as a critical regulator of this event. The 'Histone Code' is a widely accepted hypothesis, whereby sequential modifications to the histones in chromatin lead to regulated transcription of genes. One of the modifications used in the histone code is acetylation. This is probably the best characterized modification of histones, which is carried out under the control of histone acetyltransferases (HATs) and histone deacetylases (HDACs). These enzymes also regulate the activity of a number of transcription factors through acetylation. Increasing evidence links possible dysregulation of these mechanisms in the pathogenesis of diabetes, with important therapeutic implications.

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Adiponectin and alcoholic fatty liver disease

2008

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Worldwide, one of the most prevalent forms of chronic disease is alcoholic fatty liver, which may progress to more severe forms of liver injury including steatohepatitis, fibrosis, and cirrhosis. The molecular mechanisms by which ethanol consumption causes accumulation of hepatic lipid are multiple and complex. Chronic ethanol exposure is thought to cause enhanced hepatic lipogenesis and impaired fatty acid oxidation by inhibiting key hepatic transcriptional regulators such as AMP‐activated kinase (AMPK), sirtuin 1 (SIRT1), PPAR‐gamma coactivator alpha (PGC‐1α), peroxisome proliferator‐activated receptor alpha (PPARα), and sterol regulatory element‐binding protein 1 (SREBP‐1). Adiponectin is an adipose‐derived hormone with a variety of beneficial biological functions. Increasing evidence suggests that altered adiponectin production in adipose tissue and impaired expression of hepatic adiponectin receptors (AdipoRs) are associated with the development of alcoholic liver steatosis in several rodent models. More importantly, studies have demonstrated a protective role of adiponectin against alcoholic liver steatosis. The hepato‐protective effect of adiponectin is largely mediated by the coordination of multiple signaling pathways in the liver, leading to enhanced fat oxidation, reduced lipid synthesis and prevention of hepatic steatosis. This review begins with an assessment of the current understanding of the role of adiponectin and its receptors in the regulation of lipid homeostasis in liver, with emphasis on their relationship to the development of alcoholic liver steatosis. Following sections will review hepatic signaling molecules involved in the protective actions of adiponectin against alcoholic fatty liver and summarize the current knowledge of regulatory mechanisms of adiponectin expression and secretion in response to chronic ethanol exposure. We will conclude with a discussion of potential strategies for treating human alcoholic fatty liver disease (AFLD), including nutritional and pharmacological modulation of adiponectin and its receptors. © 2008 IUBMB IUBMB Life, 60(12): 790–797, 2008

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Erratum: corrigendum: Sirt1 promotes fat mobilization in white adipocytes by repressing PPAR-γ

Cited by 175 publications

References 0 publications

Low Sirt1 expression, which is upregulated by fasting, in human adipose tissue from obese women

Low Sirt1 expression, which is upregulated by fasting, in human adipose tissue from obese women

Role of histone and transcription factor acetylation in diabetes pathogenesis

Adiponectin and alcoholic fatty liver disease

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