Resistin impairs SIRT1 function and induces senescence-associated phenotype in hepatocytes

An, Yu; Zheng, Yan; Zhang, Rongrong; Huang, Jianfeng; Zhu, Zhoujie; Zhou, Ronghua; Jin, Dan; Zhou, Yang

doi:10.1016/j.mce.2013.06.028

Cited by 18 publications

(9 citation statements)

References 39 publications

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“…Acetylation of p53 at Lys-382, a target of SIRT-1, was significantly higher in the OF group, suggesting an overall reduction in SIRT-1 activity 48 . Similar observations have been made in adipose tissue from OF mice 49 and in primary cultures of senescent mouse hepatocytes 50 . OS, and notably ROS, can modulate SIRT-1 expression and activity 51 .…”

Section: Discussionsupporting

confidence: 80%

Transient postnatal overfeeding causes liver stress-induced premature senescence in adult mice

Yzydorczyk

Chehade

et al. 2017

Sci Rep

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Unbalanced nutrition early in life is increasingly recognized as an important factor in the development of chronic, non-communicable diseases at adulthood, including metabolic diseases. We aimed to determine whether transient postnatal overfeeding (OF) leads to liver stress-induced premature senescence (SIPS) of hepatocytes in association with liver structure and hepatic function alterations. Litters sizes of male C57BL/6 mice were adjusted to 9 pups (normal feeding, NF) or reduced to 3 pups during the lactation period to induce transient postnatal OF. Compared to the NF group, seven-month-old adult mice transiently overfed during the postnatal period were overweight and developed glucose intolerance and insulin resistance. Their livers showed microsteatosis and fibrosis, while hepatic insulin signaling and glucose transporter protein expressions were altered. Increased hepatic oxidative stress (OS) was observed, with increased superoxide anion production, glucose-6-phosphate dehydrogenase protein expression, oxidative DNA damage and decreased levels of antioxidant defense markers, such as superoxide dismutase and catalase proteins. Hepatocyte senescence was characterized by increased p21WAF, p53, Acp53, p16INK4a and decreased pRb/Rb and Sirtuin-1 (SIRT-1) protein expression levels. Transient postnatal OF induces liver OS at adulthood, associated with hepatocyte SIPS and alterations in liver structure and hepatic functions, which could be mediated by a SIRT-1 deficiency.

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Section: Discussionsupporting

confidence: 80%

Transient postnatal overfeeding causes liver stress-induced premature senescence in adult mice

Yzydorczyk

Chehade

et al. 2017

Sci Rep

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“…In older adults, higher resistin levels have also been found to be associated with cardiovascular events [38] . An experimental study suggested that resistin may induce hepatocyte senescence [39] . Hence, the inverse relationship between serum levels of Klotho and resistin levels after a 6-month high-intensity training further supports the clinical improvements among COPD patients discussed above.…”

Section: Discussionmentioning

confidence: 99%

Benefits of High-Intensity Exercise Training to Patients with Chronic Obstructive Pulmonary Disease: A Controlled Study

et al. 2017

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Background: Various exercise training programs are used for patients with chronic obstructive pulmonary disease (COPD) of different severity. Objectives: To investigate the impact of individualized high-intensity training on exercise capacity with COPD. Methods: A total of 49 patients agreed to participate. Of these, 31 were assigned to the training group and 18 served as controls. The training group exercised twice a week for 90 min with consecutively increasing loads. At the time of enrollment (T₀), as well as after 3 (T₁) and 6 (T₂) months, a 6-min walk test (6-MWT) was performed and data on health-related quality of life, femoral muscle thickness, and various serum markers were obtained. Results: The training group improved in their 6-MWT results (T₀ = 407 ± 152 m vs. T₁ = 459 ± 127 m, p = 0.002, vs. T₂ = 483.2 ± 130.1 m, p = 0.004), in their cross-sectional area of the musculus rectus femoris (T₀ = 6.2 ± 1.2 cm² vs. T₁ = 6.9 ± 1.2 cm², p = 0.003, vs. 7.5 ± 1.6 cm², p = 0.002), and in their St. George's Respiratory Questionnaire (SGRQ) score (T₀ = 43.3 ± 18.0 vs. T₁ = 36.0 ± 18.4, p = 0.001, vs. T₂ = 34.7 ± 18. 0, p = 0.004). Serum levels of myostatin, irisin, resistin, and α-Klotho did not change significantly within the training period. Of note, the exercise group showed an inverse relationship between serum levels of resistin and those of α-Klotho after 6 months (r = -0.608, p = 0.021). Conclusions: COPD patients undergoing an individualized, structured, high-intensity training program improved their exercise capacity, gained muscle mass, and improved their quality of life.

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“…Indeed, in a genomewide coactivation study, PGC-1α was found to enhance the recruitment of 60 kDa BRG-1/Brm-associated factor subunit A (BAF60A) to the PPARα-binding sites (PPREs), which further activated PPARα-mediated peroxisomal and mitochondrial fat oxidation genes in the liver (Li et al 2008). Recently, resistin has been reported to weaken the interaction between SIRT1 and PPARα as well as PGC-1α (Yu et al 2013). Given that resistin was initially described as an adipokine increasing hepatic IR and glucose metabolism through an AMPK-dependent pathway, it is plausible that the activity of PGC-1α in the liver may be governed by a complex network of interactions among SIRT1, AMPK and PPARα.…”

Section: Sirtuins (Sirts)mentioning

confidence: 99%

PGC-1α, glucose metabolism and type 2 diabetes mellitus

Deng

Shi

et al. 2016

Journal of Endocrinology

139

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Type 2 diabetes mellitus (T2DM) is a chronic disease characterized by glucose metabolic disturbance. A number of transcription factors and coactivators are involved in this process. Peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α) is an important transcription coactivator regulating cellular energy metabolism. Accumulating evidence has indicated that PGC-1α is involved in the regulation of T2DM. Therefore, a better understanding of the roles of PGC-1α may shed light on more efficient therapeutic strategies. Here, we review the most recent progress on PGC-1α and discuss its regulatory network in major glucose metabolic tissues such as the liver, skeletal muscle, pancreas and kidney. The significant associations between PGC-1α polymorphisms and T2DM are also discussed in this review.

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Resistin impairs SIRT1 function and induces senescence-associated phenotype in hepatocytes

Cited by 18 publications

References 39 publications

Transient postnatal overfeeding causes liver stress-induced premature senescence in adult mice

Transient postnatal overfeeding causes liver stress-induced premature senescence in adult mice

Benefits of High-Intensity Exercise Training to Patients with Chronic Obstructive Pulmonary Disease: A Controlled Study

PGC-1α, glucose metabolism and type 2 diabetes mellitus

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