SIRT1 and SIRT7 expression in adipose tissues of obese and normal-weight individuals is regulated by microRNAs but not by methylation status

Kuryłowicz, Alina; Owczarz, Magdalena; Połosak, Jacek; Jonas, Marta; Lisik, Wojciech; Jonas, Maurycy; Chmura, A.; Puzianowska-Kuźnicka, Monika

doi:10.1038/ijo.2016.131

Cited by 59 publications

(66 citation statements)

References 57 publications

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“…A recent study revealed that reduced Sirt1 mRNA level in adipose tissue of obese patients was correlated negatively with the level of miR-22 [33]. Interestingly, activation of Sirt1 induces the browning of white adipose tissue and promotes resistance to obesity [34], suggesting that factors that regulate Sirt1 might attenuate the metabolic disorders associated with obesity.…”

Section: Discussionmentioning

confidence: 99%

Loss of microRNA-22 prevents high-fat diet induced dyslipidemia and increases energy expenditure without affecting cardiac hypertrophy

et al. 2017

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Obesity is associated with development of diverse diseases, including cardiovascular diseases and dyslipidemia. MiRNA-22 (miR-22) is a critical regulator of cardiac function and targets genes involved in metabolic processes. Previously, we generated miR-22 null mice and we showed that loss of miR-22 blunted cardiac hypertrophy induced by mechanohormornal stress. In the present study, we examined the role of miR-22 in the cardiac and metabolic alterations promoted by high-fat (HF) diet. We found that loss of miR-22 attenuated the gain of fat mass and prevented dyslipidemia induced by HF diet, although the body weight gain, or glucose intolerance and insulin resistance did not seem to be affected. Mechanistically, loss of miR-22 attenuated the increased expression of genes involved in lipogenesis and inflammation mediated by HF diet. Similarly, we found that miR-22 mediates metabolic alterations and inflammation induced by obesity in the liver. However, loss of miR-22 did not appear to alter HF diet induced cardiac hypertrophy or fibrosis in the heart. Our study therefore establishes miR-22 as an important regulator of dyslipidemia and suggests it may serve as a potential candidate in the treatment of dyslipidemia associated with obesity.

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Section: Discussionmentioning

confidence: 99%

Loss of microRNA-22 prevents high-fat diet induced dyslipidemia and increases energy expenditure without affecting cardiac hypertrophy

et al. 2017

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“…Human studies have similarly shown that SIRT1 is expressed in both subcutaneous and visceral WAT and reduced by obesity [43], [69], [106], [107], [108], [109], [110]. The expressions of SIRT2, SIRT3 and SIRT5 were reported to be either reduced [43], [69], [102], or unaffected in obese subcutaneous WAT [108]. For SIRT7 results between different studies have also been varied: Rappou and colleagues [69] found decreased expression in obese subcutaneous WAT, whereas no expression difference [43] or increased expression [108] has also been reported.…”

Section: Sirts and Parps In Adipose Tissue Function In Basal And Obesmentioning

confidence: 99%

“…In contrast, caloric restriction increases Sirt1 and Sirt2 but reduces Sirt4 mRNA and protein level in WAT [85], [103], [104], [105]. Human studies have similarly shown that SIRT1 is expressed in both subcutaneous and visceral WAT and reduced by obesity [43], [69], [106], [107], [108], [109], [110]. The expressions of SIRT2, SIRT3 and SIRT5 were reported to be either reduced [43], [69], [102], or unaffected in obese subcutaneous WAT [108].…”

Section: Sirts and Parps In Adipose Tissue Function In Basal And Obesmentioning

confidence: 99%

“…The expressions of SIRT2, SIRT3 and SIRT5 were reported to be either reduced [43], [69], [102], or unaffected in obese subcutaneous WAT [108]. For SIRT7 results between different studies have also been varied: Rappou and colleagues [69] found decreased expression in obese subcutaneous WAT, whereas no expression difference [43] or increased expression [108] has also been reported. Caloric restriction and weight loss induced by gastric band operation increased the expression of SIRT1 , SIRT3 and SIRT6 in subcutaneous WAT in obese subjects [111], whereas long-term weight loss based on conventional caloric restriction diet regiment increased the mRNA levels of SIRT1 and SIRT7, but in contrast to gastric banding, SIRT3 expression was further reduced [69].

Fig.…”

Section: Sirts and Parps In Adipose Tissue Function In Basal And Obesmentioning

confidence: 99%

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Adipose tissue NAD+-homeostasis, sirtuins and poly(ADP-ribose) polymerases -important players in mitochondrial metabolism and metabolic health

et al. 2017

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Obesity, a chronic state of energy overload, is characterized by adipose tissue dysfunction that is considered to be the major driver for obesity associated metabolic complications. The reasons for adipose tissue dysfunction are incompletely understood, but one potential contributing factor is adipose tissue mitochondrial dysfunction. Derangements of adipose tissue mitochondrial biogenesis and pathways associate with obesity and metabolic diseases. Mitochondria are central organelles in energy metabolism through their role in energy derivation through catabolic oxidative reactions. The mitochondrial processes are dependent on the proper NAD+/NADH redox balance and NAD+ is essential for reactions catalyzed by the key regulators of mitochondrial metabolism, sirtuins (SIRTs) and poly(ADP-ribose) polymerases (PARPs). Notably, obesity is associated with disturbed adipose tissue NAD+ homeostasis and the balance of SIRT and PARP activities. In this review we aim to summarize existing literature on the maintenance of intracellular NAD+ pools and the function of SIRTs and PARPs in adipose tissue during normal and obese conditions, with the purpose of comprehending their potential role in mitochondrial derangements and obesity associated metabolic complications. Understanding the molecular mechanisms that are the root cause of the adipose tissue mitochondrial derangements is crucial for developing new effective strategies to reverse obesity associated metabolic complications.

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“…Thus, miR-133 targets this pathway at two different points [99]. In humans, Kurylowicz et al observed that the downregulation of SIRT1 negatively correlated with the expression of miR-22-3p in obese individuals and the upregulation of SIRT7 negatively correlated with miR-125a-5p levels in slim individuals [141]. Another study in humans showed the importance of the regulation of miR-199 as a modulator of SIRT1 and as a biomarker of atrial fibrillation after coronary artery bypass graft surgery [142].…”

Section: Miragings: What and Which Are They? How Can They Be Modulmentioning

confidence: 99%

NutrimiRAging: Micromanaging Nutrient Sensing Pathways through Nutrition to Promote Healthy Aging

Micó

Berninches

Tapia

et al. 2017

IJMS

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Current sociodemographic predictions point to a demographic shift in developed and developing countries that will result in an unprecedented increase of the elderly population. This will be accompanied by an increase in age-related conditions that will strongly impair human health and quality of life. For this reason, aging is a major concern worldwide. Healthy aging depends on a combination of individual genetic factors and external environmental factors. Diet has been proved to be a powerful tool to modulate aging and caloric restriction has emerged as a valuable intervention in this regard. However, many questions about how a controlled caloric restriction intervention affects aging-related processes are still unanswered. Nutrient sensing pathways become deregulated with age and lose effectiveness with age. These pathways are a link between diet and aging. Thus, fully understanding this link is a mandatory step before bringing caloric restriction into practice. MicroRNAs have emerged as important regulators of cellular functions and can be modified by diet. Some microRNAs target genes encoding proteins and enzymes belonging to the nutrient sensing pathways and, therefore, may play key roles in the modulation of the aging process. In this review, we aimed to show the relationship between diet, nutrient sensing pathways and microRNAs in the context of aging.

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SIRT1 and SIRT7 expression in adipose tissues of obese and normal-weight individuals is regulated by microRNAs but not by methylation status

Cited by 59 publications

References 57 publications

Loss of microRNA-22 prevents high-fat diet induced dyslipidemia and increases energy expenditure without affecting cardiac hypertrophy

Loss of microRNA-22 prevents high-fat diet induced dyslipidemia and increases energy expenditure without affecting cardiac hypertrophy

Adipose tissue NAD+-homeostasis, sirtuins and poly(ADP-ribose) polymerases -important players in mitochondrial metabolism and metabolic health

NutrimiRAging: Micromanaging Nutrient Sensing Pathways through Nutrition to Promote Healthy Aging

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