Evaluation of Plasma TRB3 and Sestrin 2 Levels in Obese and Normal-Weight Children

Nourbakhsh, Mitra; Sharifi, Roya; Ghorbanhosseini, Seyedeh Sara; Javad, Ali; Ahmadpour, Fatemeh; Azar, Maryam Razzaghy; Larijani, Bagher

doi:10.1089/chi.2017.0082

Cited by 29 publications

(22 citation statements)

References 40 publications

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“…The sensitivity was 64% and specificity was 44%. These results go with the results of the study conducted by Nourbakhsh et al [2017] which revealed low levels of sestrin 2 in obese children when compared to children with normal weight and these levels were negatively correlated with the BMI [17]. Also, Lee et al [2012] and chai et al…”

Section: Discussionsupporting

confidence: 88%

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Association of serum sestrin 2 and betatrophin with serum neutrophil gelatinase associated lipocalin levels in type 2 diabetic patients with diabetic nephropathy

Mohany

Rugaie

2020

J Diabetes Metab Disord

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Purpose Understanding the pathogenesis and the molecular mechanisms of diabetic nephropathy (DN) helps its timely detection and prevention. The current work aims tomeasure serum sestrin 2 and betatrophin levels in healthy and type diabetic (T2DM)subjects with/or without diabetic nephropathy (DN) and also to test their correlation with serum neutrophil gelatinase associated lipocalin (sNGAL); indicator of DN. Methods This study included 96 subjects; 20 healthy (G1) and 76 T2DM [22 normoalbuminuric (G2), 35 microalbuminuric (G3) and 19 macroalbuminuric (G4)]. Serum sestrin 2, betatrophin and NGAL were measured by their corresponding kits. Results Significant low levels of serum sestrin 2 andhigh levels of serum betatrophin were found in T2DM group when compared to G1 (p = 0.002,p > 0.001, respectively) and this difference is manifested in G4 followed, in order, by G3, G2 then G1 (p= > 0.001 for both). Also, serum sestrin2 levels showed significant negative correlations with sNGAL in G1 (r = −0.497, p = 0.026), G2 (r = −0.784, p > 0.001), G3 (r = −0.894, p > 0.001) and G4 (r = −0.896, pp. > 0.001) while serum betatrophin levels showed significant positive correlations with sNGAL in G2 (r = 0.681, p > 0.001), G3 (r = 0.518, p > 0.001) and G4 (r = 0.727, p > 0.001). Conclusion Serum sestrin 2 levels decrease significantly while betatrophin levels increase significantly in T2DM patients with DN especially those with macroalbuminuria. These levels have significant effect strengths on the indicator of diabetic nephropathy; sNGAL which might indicate theirvaluablerole in the timely detection and prevention of the development of DN. Keywords Serum sestrin2. Serum betatrophin. sNGAL. Diabetic nephropathy Abbreviations T2DM type 2 diabetes mellitus DN diabetic nephropathy sNGAL serum neutrophil gelatinase associated lipocalin KDa kilodalton ACR urinary albumn to creatinine ratio EDTA ethylendiaminetetraacetic acid ELISA enzyme-linked immunosorbant assay SPSS statistical package for social sciences ANOVA analysis of variance AMP adenosine monophosphate AMPK AMP-dependent protein kinase mTOR-C1 mammalian target of rapamycin complex 1 Dur duration of diabetes in years BMI body mass index s-FG serum fasting glucose s-Cr serum creatinine s-alb serum albumin GA% serum glycated albumin% HbA1c% glycosylated hemoglobin%.

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Section: Discussionsupporting

confidence: 88%

“…A decrease in the intracellular levels of sestrin 2 can lead many adverse sequelae such as oxidative damage, mitochondrial dysfunction, and insulin resistance [14,15]. The investigation of sestrin 2 levels in obese and/or T2DMpatients revealed controversial results [14,16,17].…”

Section: Introductionmentioning

confidence: 99%

Association of serum sestrin 2 and betatrophin with serum neutrophil gelatinase associated lipocalin levels in type 2 diabetic patients with diabetic nephropathy

Mohany

Rugaie

2020

J Diabetes Metab Disord

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“…In present study, the correlation between Sestrin2 and HDL might be associated with AMPK activation. Consistent with our view, Nourbakhsh et al [32] also revealed that there was a positive correlation between Sestrin2 and HDL.…”

Section: Discussionsupporting

confidence: 92%

Explorating the Involvement of Plasma Sestrin2 in Obstructive Sleep Apnea

Jiang

Wang

Zhai

et al. 2019

Canadian Respiratory Journal

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Obstructive sleep apnea (OSA) can lead to serious complications such as coronary heart disease and hypertension due to oxidative stress. Sestrin2 expression is upregulated under conditions of oxidative stress. This study aimed to explore whether Sestrin2 was involved in OSA. OSA and healthy control subjects were recruited and matched with age, gender, and body mass index (BMI). Plasma Sestrin2 levels were measured and compared. A multivariate stepwise regression model was used to detect the relationship between Sestrin2 and other variable factors. The Sestrin2 levels were compared between before and after four weeks treatment by nasal continuous positive airway pressure (nCPAP) in severe OSA patients. Fifty-seven subjects were divided into two groups: control group (39.33 ± 9.40 years, n = 21) and OSA group (38.81 ± 7.84 years, n = 36). Plasma Sestrin2 levels increased in the OSA group (control group 2.06 ± 1.76 ng/mL, OSA group 4.16 ± 2.37 ng/mL; P = 0.001). Sestrin2 levels decreased after four-week nCPAP treatment (pre-nCPAP 5.21 ± 2.32 ng/mL, post-nCPAP 4.01 ± 1.54 ng/mL; P = 0.004). Sestrin2 was positively correlated with apnea/hypopnea index (AHI) oxygen desaturation index, while negatively correlated with mean oxygen saturation. Moreover, these correlations remained unchanged after adjusting for gender, age, waist-to-hip ratio, and body mass index. Multiple regression analysis showed that there was an association between Sestrin2 and AHI. Our findings suggest that Sestrin2 is involved in OSA. The increase of plasma Sestrin2 is directly related to the severity of OSA. To some extent, Sestrin2 may be useful for determining the severity of OSA and monitoring the effect of CPAP. In addition, since some complications of OSA such as coronary heart disease and diabetes are usually related with oxidative stress, the role of Sestrin2 in those OSA complications needs further study.

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“…A recent study in rats induced to have diabesity showed that TRB3 is increased in the adipose tissue and that TRB3 silencing increased insulin response in this tissue and the systemic insulin sensitivity (Sun et al, 2017). Since TRB3 protein level is reported to be increased in the blood of patients with obesity (Nourbakhsh et al, 2017), this protein involvement in adipose tissue insulin resistance is likely. However, it is still needed to run studies in adipose tissue from subjects with diabesity.…”

Section: Adipose Tissuementioning

confidence: 99%

Endoplasmic reticulum stress and development of insulin resistance in adipose, skeletal, liver, and foetoplacental tissue in diabesity

Villalobos-Labra

Subiabre

Toledo

et al. 2019

Molecular Aspects of Medicine

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Diabesity is an abnormal metabolic condition shown by patients with obesity that develop type 2 diabetes mellitus. Patients with diabesity present with insulin resistance, reduced vascular response to insulin, and vascular endothelial dysfunction. Along with the several well-described mechanisms of insulin resistance, a state of endoplasmic reticulum (ER) stress, where the primary human targets are the adipose tissue, liver, skeletal muscle, and the foetoplacental vasculature, is apparent. ER stress characterises by the activation of the unfolded protein response via three canonical ER stress sensors, i.e., the protein kinase RNA-like endoplasmic reticulum kinase (PERK), inositol-requiring enzyme 1α (IRE1α), and activating transcription factor 6. Slightly different cell signalling mechanisms preferentially enable in diabesity in the ER stress-associated insulin resistance for adipose tissue (IRE1α/X-box binding protein 1 mRNA splicing/c-jun N-terminal kinase 1 activation), skeletal muscle (tribbles-like protein 3 (TRB3)/proinflammatory cytokines activation), and liver (PERK/activating transcription factor 4/TRB3 activation). There is no information in human subjects with diabesity in the foetoplacental vasculature. However, the available literature shows that pregnant women with pre-pregnancy obesity or overweight that develop gestational diabetes mellitus (GDM) and their newborn show insulin resistance. ER stress is recently reported to be triggered in endothelial cells from the human umbilical vein from mothers with pre-pregnancy obesity. However, whether a different metabolic alteration to obesity in pregnancy or GDM is present in women with pre-pregnancy obesity that develop GDM, is unknown. In this review, we summarised the findings on diabesity-associated mechanisms of insulin resistance with emphasis in the primary targets adipose, skeletal muscle, liver, and foetoplacental tissues. We also give evidence on the possibility of a new GDM-associated metabolic condition triggered in pregnancy by maternal obesity, i.e. gestational diabesity, leading to ER stress-associated insulin resistance in the human foetoplacental vasculature.

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Evaluation of Plasma TRB3 and Sestrin 2 Levels in Obese and Normal-Weight Children

Abstract: Both TRB3 and sestrin 2 may contribute to the development of obesity and its complications and can be considered interesting therapeutic target for the treatment of obesity.

Cited by 29 publications

References 40 publications

Association of serum sestrin 2 and betatrophin with serum neutrophil gelatinase associated lipocalin levels in type 2 diabetic patients with diabetic nephropathy

Association of serum sestrin 2 and betatrophin with serum neutrophil gelatinase associated lipocalin levels in type 2 diabetic patients with diabetic nephropathy

Explorating the Involvement of Plasma Sestrin2 in Obstructive Sleep Apnea

Endoplasmic reticulum stress and development of insulin resistance in adipose, skeletal, liver, and foetoplacental tissue in diabesity

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