Association of expression of selenoprotein P in mRNA and protein levels with metabolic syndrome in subjects with cardiovascular disease: Results of the Selenegene study

Gharipour, Mojgan; Sadeghi, Masoumeh; Salehi, Masoud; Behmanesh, Mehrdad; Khosravi, Elham; Dianatkhah, Minoo; Javanmard, Shaghayegh Haghjoo; Razavi, Rouzbeh; Gharipour, Amin

doi:10.1002/jgm.2945

Cited by 25 publications

(20 citation statements)

References 40 publications

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“…In the largest to-date study, liver fat content, evaluated with magnetic resonance imaging, showed a J-shaped association with SEPP, with the highest rates observed in individuals with low SEPP levels [19]. SEPP levels were also shown to be inversely associated with MetS [19,24]. These and our findings are contradictory to other 2 studies showing higher SEPP in NAFLD patients than controls [17,18].…”

Section: Discussioncontrasting

confidence: 99%

Selenoprotein P in Patients with Nonalcoholic Fatty Liver Disease

Polyzos

Mavrouli

Katsinelos

et al. 2019

Exp Clin Endocrinol Diabetes

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Objective Main aim of this study was to evaluate circulating selenoprotein P (SEPP) levels in patients with simple steatosis (SS) and nonalcoholic steatohepatitis (NASH) compared with healthy controls. Methods Thirty-one patients with biopsy-proven NAFLD (15 with SS, 10 with borderline NASH, 6 with definite NASH) and 27 matched controls without NAFLD were enrolled. Serum SEPP levels and liver function tests plus biochemical parameters were measured with ELISA and standard methods, respectively. Homeostatic model of assessment - insulin resistance (HOMA-IR) was calculated. Results SEPP levels were statistically different between groups (p-value for trend=0.043). In pairwise comparisons, SEPP was lower in definite NASH compared with controls (p=0.029), but not SS (p=0.18) or borderline NASH (p=0.35). SEPP was not different between controls, SS and borderline NASH. The unadjusted trend between the controls, SS and NASH patients remained essentially unchanged after adjustment for age, sex, log(ALT) and waist circumference, but it marginally lost significance when log(HOMA-IR) entered into the model. SEPP levels were not different between groups of different severity of steatosis, fibrosis, hepatocellular ballooning, lobular and portal inflammation. Conclusions Lower SEPP levels were observed in patients with definite NASH compared with controls, a finding warranting larger studies.

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Section: Discussioncontrasting

confidence: 99%

Selenoprotein P in Patients with Nonalcoholic Fatty Liver Disease

Polyzos

Mavrouli

Katsinelos

et al. 2019

Exp Clin Endocrinol Diabetes

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“…In our previous study, a significantly lower amount of SePP was shown in the MetS subjects compared with non‐MetS subjects. Therefore, it was concluded that the pathophysiology of MetS may be affected by SePP . Moreover, in this study, we found a significant increase in the amount of SePP following selenium supplementation in the MetS group.…”

Section: Discussionsupporting

confidence: 59%

“…Total RNA (2 µg) was treated with DNAse I and reverse transcribed using random hexamers and SuperScript II reverse transcriptase with a commercial kit (Rreverta‐L, Russia). Following this, the quality and concentration of the RNA samples were confirmed by electrophoresis on denaturized 1% agarose gel …”

Section: Methodsmentioning

confidence: 99%

Effects of selenium supplementation on expression of SEPP1 in mRNA and protein levels in subjects with and without metabolic syndrome suffering from coronary artery disease: Selenegene study a double‐blind randomized controlled trial

Gharipour

Ouguerram

Nazih

et al. 2018

J of Cellular Biochemistry

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Selenoprotein P (SePP) is involved in the protection against diseases. The present study is the first investigation of the effect of selenium supplementation on plasma selenium and expression of SEPP1 in mRNA and protein levels based on metabolic syndrome (MetS), in individuals suffering from coronary artery diseases. In this clinical trial, 160 patients with angiographically documented stenosis of more than 75% in each vessel were enrolled. Patients received either 200-mg selenium yeast tablets or placebo tablets orally after a meal, once daily for 60 days. The mRNA and protein levels of the selenium and SePP1 products were determined before and after the study. From the initial 160 participants, 145 subjects (71 MetS-affected individuals, 74 MetS-unaffected individuals) enrolled in this study. Comparing the selenium and placebo groups, no significant percentage changes of plasma selenium, △Ct SEPP1, or SePP were shown (P > 0.05). Moreover, beyond a significant difference for the expression of SePP in the selenium group compared to its baseline level (P < 0.05), no other significant differences were revealed for plasma selenium and △Ct SEPP1 after the intervention in either group (P > 0.05). Selenium supplementation did not affect plasma selenium or the mRNA or protein level of SePP in either groups after a 2-months intervention beyond a significant increase of SePP in the MetS group. This trial suggests that further studies should investigate the long-term use of selenium supplementation and the effect of a SePP increase on MetS as a potential therapeutic effect.

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“…The genome-wide significantly associated SNP rs78310016 is located in an intergenic region on chromosome 5q13, in close vicinity to SEPP1 and GHR . Both genes are involved in metabolism (Jørgensen et al, 2004) and have been linked to various metabolic phenotypes, such as diabetes mellitus, (Akbaba et al, 2018; Hellwege et al, 2014) weight and obesity, (Chen et al, 2017; Espinosa et al, 2019; Gao et al, 2011), and metabolic syndrome (Gharipour et al, 2017). Interestingly, for rs78310016 we showed a chromatin interaction with HMGCS1.…”

Section: Discussionmentioning

confidence: 99%

A new genetic locus for antipsychotic-induced weight gain: A genome-wide study of first-episode psychosis patients using amisulpride (from the OPTiMiSE cohort)

et al. 2020

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Background: Antipsychotic-induced weight gain is a common and debilitating side effect of antipsychotics. Although genome-wide association studies of antipsychotic-induced weight gain have been performed, few genome-wide loci have been discovered. Moreover, these genome-wide association studies have included a wide variety of antipsychotic compounds. Aims: We aim to gain more insight in the genomic loci affecting antipsychotic-induced weight gain. Given the variable pharmacological properties of antipsychotics, we hypothesized that targeting a single antipsychotic compound would provide new clues about genomic loci affecting antipsychoticinduced weight gain. Methods: All subjects included for this genome-wide association study (n=339) were first-episode schizophrenia spectrum disorder patients treated with amisulpride and were minimally medicated (defined as antipsychotic use <2 weeks in the previous year and/or <6 weeks lifetime). Weight gain was defined as the increase in body mass index from before until approximately 1 month after amisulpride treatment. Results: Our genome-wide association analyses for antipsychotic-induced weight gain yielded one genome-wide significant hit (rs78310016; β=1.05; p=3.66 × 10 -08 ; n=206) in a locus not previously associated with antipsychotic-induced weight gain or body mass index. Minor allele carriers had an odds ratio of 3.98 (p=1.0 × 10 −03 ) for clinically meaningful antipsychotic-induced weight gain (⩾7% of baseline weight). In silico analysis elucidated a chromatin interaction with 3-Hydroxy-3-Methylglutaryl-CoA Synthase 1. In an attempt to replicate single-nucleotide polymorphisms previously associated with antipsychotic-induced weight gain, we found none were associated with amisulpride-induced weight gain. Conclusion: Our findings suggest the involvement of rs78310016 and possibly 3-Hydroxy-3-Methylglutaryl-CoA Synthase 1 in antipsychotic-induced weight gain. In line with the unique binding profile of this atypical antipsychotic, our findings furthermore hint that biological mechanisms underlying amisulpride-induced weight gain differ from antipsychotic-induced weight gain by other atypical antipsychotics.

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Association of expression of selenoprotein P in mRNA and protein levels with metabolic syndrome in subjects with cardiovascular disease: Results of the Selenegene study

Abstract: We have demonstrated a significant decrease in circulating SeP levels according to MetS status in patients with documented cardiovascular disease.

Cited by 25 publications

References 40 publications

Selenoprotein P in Patients with Nonalcoholic Fatty Liver Disease

Selenoprotein P in Patients with Nonalcoholic Fatty Liver Disease

Effects of selenium supplementation on expression of SEPP1 in mRNA and protein levels in subjects with and without metabolic syndrome suffering from coronary artery disease: Selenegene study a double‐blind randomized controlled trial

A new genetic locus for antipsychotic-induced weight gain: A genome-wide study of first-episode psychosis patients using amisulpride (from the OPTiMiSE cohort)

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