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

Pedersen, Steen B.; Ølholm, Jens; Paulsen, Søren K.; Bennetzen, Marianne; Richelsen, Bjørn

doi:10.1038/ijo.2008.78

Cited by 98 publications

(72 citation statements)

References 16 publications

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“…SIRT1 was not assayed in either study; however, it is noteworthy that, in another study, SIRT1 mRNA and AMPK activity were significantly increased (as was insulin sensitivity) in muscle of obese, insulin-resistant patients by 6 mo of caloric restriction that resulted in a 10% loss of body weight (12). Likewise, increased SIRT1 mRNA expression has been observed in subcutaneous adipose tissue of human volunteers after 6 days of total starvation, and in the same study, significantly greater SIRT1 expression was observed in lean compared with obese women (65).…”

Section: Ampk and Sirt1 Activity In The Setting Of The Metabolic Syndmentioning

confidence: 73%

“…With respect to the latter, concurrent decreases in AMPK and apparently SIRT1 activity have been observed in the liver of 48-h-starved rats 24 h after refeeding (48), and both molecules appear to be activated by starvation in adipose tissue (65,86). Likewise, in HepG2 cells (90), pyruvate activates and NAM inhibits both AMPK and SIRT1, and they do so within 1-2 h, suggesting that their interaction is much more rapid than in C 2 C 12 cells.…”

Section: The Putative Sirt1/ampk Cycle and Its Regulationmentioning

confidence: 96%

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AMPK and SIRT1: a long-standing partnership?

Ruderman

Nelson

et al. 2010

American Journal of Physiology-Endocrinology and Metabolism

720

590

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protein kinase (AMPK) and the histone/protein deacetylase SIRT1 are fuel-sensing molecules that have coexisted in cells throughout evolution. When a cell's energy state is diminished, AMPK activation restores energy balance by stimulating catabolic processes that generate ATP and downregulating anabolic processes that consume ATP but are not acutely needed for survival. SIRT1 in turn is best known historically for producing genetic changes that mediate the increase in longevity caused by calorie restriction. Although the two molecules have been studied intensively for many years, only recently has it become apparent that they have similar effects on diverse processes such as cellular fuel metabolism, inflammation, and mitochondrial function. In this review we will examine the evidence that these similarities occur because AMPK and SIRT1 both regulate each other and share many common target molecules. In addition, we will discuss the clinical relevance of these interactions and in particular the possibility that their dysregulation predisposes to disorders such as type 2 diabetes and atherosclerotic cardiovascular disease and is a target for their therapy.adenosine 5=-monophosphate-activated protein kinase; sirtuin 1; metabolic syndrome; mitochondrial function; insulin resistance; peroxisome proliferator-activated receptor-␥ coactivator-1␣; type 2 diabetes; atherosclerosis AMP-ACTIVATED PROTEIN KINASE (AMPK) is a fuel-sensing enzyme that is activated by decreases in a cell's energy state as reflected by an increased AMP/ATP ratio. When activated, it initiates metabolic and genetic events that restore ATP levels by stimulating processes that generate ATP (e.g., fatty acid oxidation) and inhibiting others that consume ATP but are not acutely required for survival (e.g., triglyceride and protein synthesis, cell proliferation) (40). In addition, AMPK sets in motion changes in mitochondrial biogenesis and function (37) that could more chronically increase the ability of a cell to generate ATP and diminish oxidative stress and other potentially adverse cellular events (78). The sirtuins are a family of evolutionarily conserved NAD ϩ -dependent histone/protein deacetylases that are also widely regarded as fuel-sensing molecules. They have many actions (see below) but are perhaps best known for their role in mediating the increase in longevity caused by caloric restriction in various species, including yeast, worms, and possibly mammals (21, 85). Seven sirtuins have been identified in mammalian cells. Of these the most studied and the focus of this review is silent information regulator T1 (SIRT1).AMPK and the sirtuins are present in all eukaryotic cells and probably have coexisted throughout evolution (7, 29). Although both molecules have been studied intensively, the similarities in their regulation and in their actions on such diverse processes as cellular metabolism, inflammation, and mitochondrial function have only recently become apparent. In this review we will examine the evidence that these similarities occur, ...

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Section: Ampk and Sirt1 Activity In The Setting Of The Metabolic Syndmentioning

confidence: 73%

Section: The Putative Sirt1/ampk Cycle and Its Regulationmentioning

confidence: 96%

AMPK and SIRT1: a long-standing partnership?

Ruderman

Nelson

et al. 2010

American Journal of Physiology-Endocrinology and Metabolism

720

590

View full text Add to dashboard Cite

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“…Conversely, SIRT1 levels are reduced in white fat in obese mice (Chalkiadaki and Guarente 2012) and obese humans (Pedersen et al 2008;Costa Cdos et al 2010). One possible mechanism for loss of SIRT1 in obese animals is suggested by the finding that a high-fat diet in mice triggers cleavage of SIRT1 in WAT by caspase 1 of the inflammasome (Chalkiadaki and Guarente 2012).…”

Section: Sirt1 and Nadmentioning

confidence: 99%

“…SIRT1 is also induced by CR in humans (Civitarese et al 2007). Reciprocally, a high-fat diet leads to the loss of SIRT1 in mice (Chalkiadaki and Guarente 2012), and obesity has the same effect in humans (Pedersen et al 2008;Costa Cdos et al 2010). Third, loss-of-function mutation of specific sirtuins ablates specific outputs of CR.…”

Section: Sirtuins and Cr In Micementioning

confidence: 99%

Calorie restriction and sirtuins revisited

2013

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Calorie or dietary restriction (CR) has attracted attention because it is the oldest and most robust way to extend rodent life span. The idea that the nutrient sensors, termed sirtuins, might mediate effects of CR was proposed 13 years ago and has been challenged in the intervening years. This review addresses these challenges and draws from a great body of new data in the sirtuin field that shows a systematic redirection of mammalian physiology in response to diet by sirtuins. The prospects for drugs that can deliver at least a subset of the benefits of CR seems very real.

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“…However, in addition to the weight loss effect, there is concern that activation of SIRT1 in all tissues may have undesirable effects. Some human studies have demonstrated a positive association between lower Body Mass Index (BMI) and variants of the SIRT1 gene, but the results differ between different populations [13][14][15][16][17][18][19][20] . Although the genetic variants of the SIRT1 gene are related to lower BMI and obesity reduction, the aim of this study was to investigate the association between the Single Nucleotide Polymorphism (SNP) rs7895833 of the SIRT1 gene and MetS.…”

Section: Introductionmentioning

confidence: 99%

Polymorphism in the SIRT1 gene and parameters of metabolic syndrome in a sample of the adult Brazilian population

et al. 2016

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Objective: To evaluate whether the single nucleotide polymorphism rs7895833 (A/G) of the gene SIRT1 is associated with metabolic syndrome criteria in a sample of Brazilian adults. Methods: Serum samples and oral mucosal cells were collected from 243 subjects aged 30 to 70 years. Biochemical, hormonal, and anthropometric data were obtained. The single nucleotide polymorphism rs7895833 (A/G) was analyzed by polymerase chain reaction using the amplification refractory mutation system. Results: Among the 243 study subjects, 100 (41.15%) were classified as non-metabolic syndrome and 143 (58.85%), as metabolic syndrome. The frequency of the single nucleotide polymorphism rs7895833 (A/G) did not differ between the groups. However, 111 patients (45.67%) were overweight (body mass index: 25-29.9 kg/m2). Blood glucose, total cholesterol, triglycerides, very low density lipoprotein, low density lipoprotein, waist and hip circumferences, and blood pressure were higher in the metabolic syndrome group than in the non-metabolic syndrome group. Free thyroxine 4, grown hormone, and insulin levels were within the normal range. The metabolic conditions of the patients with metabolic syndrome indicate biochemical, anthropometric, and hormonal changes characteristic of overweight and obesity. Conclusion: The SIRT1 polymorphism rs7895833 (A/G) is not associated with the metabolic syndrome in the adult Brazilian population.

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

Cited by 98 publications

References 16 publications

AMPK and SIRT1: a long-standing partnership?

AMPK and SIRT1: a long-standing partnership?

Calorie restriction and sirtuins revisited

Polymorphism in the SIRT1 gene and parameters of metabolic syndrome in a sample of the adult Brazilian population

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