Pub Date : 2024-05-03DOI: 10.1186/s12263-024-00744-7
Mohammad Hassan Sohouli, Ghazaleh Eslamian, Seyed Hossein Ardehali, Seyed Ahmad Raeissadat, Ghazaleh Shimi, Katayoun Pourvali, Hamid Zand
Evidences have shown that obesity is influenced by various factors, including various hormones such as thyroid hormones and the body’s metabolism rate. It seems that practical solutions such as weight loss diets and common drugs can affect these potential disorders. In this study, we investigate one of these common drugs, N-Acetylcysteine (NAC), on expressions of UCP1 and factors related to thyroid function in adults with obesity. The current investigation was carried out as a randomized clinical trial (RCT) including 43 adults with obesity who were potential candidates for bariatric surgery. These individuals were randomly divided into two groups: 600 mg of NAC (n = 22) or placebo (n = 21) for a duration of 8 weeks. Visceral adipose tissue was utilized in the context of bariatric surgery to investigate the gene expression of UCP1 and thyroid function. Polymerase chain reaction (PCR) was performed in duplicate for UCP1, DIO2, DIO3, THRα and β, and 18s RNA (as an internal control) using the provided instructions to investigate the expression of the respective genes. Our findings revealed that after 8 weeks compared to placebo, NAC caused a significant decrease in the expression of the DIO3 gene as one of the genes related to thyroid function and metabolism. However, regarding other related genes, no statistically significant was found (despite the increase in UCP1, DIO2, and THRα expression and decrease in THRβ expression). In addition, after adjustment of possible confounders, no significant effect was observed on anthropometric factors and serum levels of thyroid hormones. The results of this study indicate that, following an 8-week period, NAC effectively decreases the expression of the DIO3 gene in the visceral fat tissue, in comparison to the placebo.
{"title":"Effects of N-acetylcysteine on the expressions of UCP1 and factors related to thyroid function in visceral adipose tissue of obese adults: a randomized, double-blind clinical trial","authors":"Mohammad Hassan Sohouli, Ghazaleh Eslamian, Seyed Hossein Ardehali, Seyed Ahmad Raeissadat, Ghazaleh Shimi, Katayoun Pourvali, Hamid Zand","doi":"10.1186/s12263-024-00744-7","DOIUrl":"https://doi.org/10.1186/s12263-024-00744-7","url":null,"abstract":"Evidences have shown that obesity is influenced by various factors, including various hormones such as thyroid hormones and the body’s metabolism rate. It seems that practical solutions such as weight loss diets and common drugs can affect these potential disorders. In this study, we investigate one of these common drugs, N-Acetylcysteine (NAC), on expressions of UCP1 and factors related to thyroid function in adults with obesity. The current investigation was carried out as a randomized clinical trial (RCT) including 43 adults with obesity who were potential candidates for bariatric surgery. These individuals were randomly divided into two groups: 600 mg of NAC (n = 22) or placebo (n = 21) for a duration of 8 weeks. Visceral adipose tissue was utilized in the context of bariatric surgery to investigate the gene expression of UCP1 and thyroid function. Polymerase chain reaction (PCR) was performed in duplicate for UCP1, DIO2, DIO3, THRα and β, and 18s RNA (as an internal control) using the provided instructions to investigate the expression of the respective genes. Our findings revealed that after 8 weeks compared to placebo, NAC caused a significant decrease in the expression of the DIO3 gene as one of the genes related to thyroid function and metabolism. However, regarding other related genes, no statistically significant was found (despite the increase in UCP1, DIO2, and THRα expression and decrease in THRβ expression). In addition, after adjustment of possible confounders, no significant effect was observed on anthropometric factors and serum levels of thyroid hormones. The results of this study indicate that, following an 8-week period, NAC effectively decreases the expression of the DIO3 gene in the visceral fat tissue, in comparison to the placebo.","PeriodicalId":54337,"journal":{"name":"Genes and Nutrition","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140829867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-03-19DOI: 10.1186/s12263-024-00743-8
Marzieh Nemati, Bahareh Ebrahimi, Nima Montazeri-Najafabady
Probiotics has offered a new prospect to treat and manage a variety of endocrine disorders such as obesity, diabetes, non- alcoholic fatty liver disease and metabolic syndrome. The precise mechanisms by which probiotics exert their beneficial effects on endocrine disorders and its associated problems are still indecisive. It seems that regulating the immune system and suppressing pro-inflammatory pathways like tumor necrosis factor-α and interleukin-6 or triggering anti-inflammatory pathways like interleukin-4 and 10 may be one of the potential mechanisms in the managing of endocrine disorders. In this systematic review, we hypothesized that various probiotic strains (Lactobacillus, Biofidiobacteria, Streptococcus, Entrococcus, Clostridium, and Bacillus) alone or in combination with each other could manage endocrine disorders via modulating inflammatory pathways such as suppressing pro-inflammatory cytokines (IL-6, IL-12, TNF-α, TNF-β, NFκB, and MCP-1), stimulating anti-inflammatory cytokines (IL-4,IL-6, IL-22, IL-23, IL-33, and TGF-β) and maintaining other factors like C-reactive protein, Toll like receptors, LPS, and NK cells. Data source this search was performed in PubMed and Scopus. Both human and animal studies were included. Among more than 15,000 papers, 25 studies were identified as eligible for more assessments. Quality assessment of the studies was cheeked by two researchers independently by title and abstract screening, then article which have inclusion criteria were included, and data retrieved from the included full text studies as the authors had originally reported. Results specified that Lactobacillus has been the most widely used probiotic as well as which one exhibiting the extend of the therapeutic effects on endocrine disorders, especially obesity by modulating immune responses. Also, most studies have revealed that probiotics through suppressing pro-inflammatory pathways specially via reducing levels TNF-α cytokine exhibited protective or beneficial effects on endocrine diseases particularly obesity as well as through decreasing level of IL-6 induced therapeutic effects in diabetes. This systematic review suggests that probiotics could ameliorate endocrine disorders via their immunomodulatory effects.
{"title":"Probiotics ameliorate endocrine disorders via modulating inflammatory pathways: a systematic review","authors":"Marzieh Nemati, Bahareh Ebrahimi, Nima Montazeri-Najafabady","doi":"10.1186/s12263-024-00743-8","DOIUrl":"https://doi.org/10.1186/s12263-024-00743-8","url":null,"abstract":"Probiotics has offered a new prospect to treat and manage a variety of endocrine disorders such as obesity, diabetes, non- alcoholic fatty liver disease and metabolic syndrome. The precise mechanisms by which probiotics exert their beneficial effects on endocrine disorders and its associated problems are still indecisive. It seems that regulating the immune system and suppressing pro-inflammatory pathways like tumor necrosis factor-α and interleukin-6 or triggering anti-inflammatory pathways like interleukin-4 and 10 may be one of the potential mechanisms in the managing of endocrine disorders. In this systematic review, we hypothesized that various probiotic strains (Lactobacillus, Biofidiobacteria, Streptococcus, Entrococcus, Clostridium, and Bacillus) alone or in combination with each other could manage endocrine disorders via modulating inflammatory pathways such as suppressing pro-inflammatory cytokines (IL-6, IL-12, TNF-α, TNF-β, NFκB, and MCP-1), stimulating anti-inflammatory cytokines (IL-4,IL-6, IL-22, IL-23, IL-33, and TGF-β) and maintaining other factors like C-reactive protein, Toll like receptors, LPS, and NK cells. Data source this search was performed in PubMed and Scopus. Both human and animal studies were included. Among more than 15,000 papers, 25 studies were identified as eligible for more assessments. Quality assessment of the studies was cheeked by two researchers independently by title and abstract screening, then article which have inclusion criteria were included, and data retrieved from the included full text studies as the authors had originally reported. Results specified that Lactobacillus has been the most widely used probiotic as well as which one exhibiting the extend of the therapeutic effects on endocrine disorders, especially obesity by modulating immune responses. Also, most studies have revealed that probiotics through suppressing pro-inflammatory pathways specially via reducing levels TNF-α cytokine exhibited protective or beneficial effects on endocrine diseases particularly obesity as well as through decreasing level of IL-6 induced therapeutic effects in diabetes. This systematic review suggests that probiotics could ameliorate endocrine disorders via their immunomodulatory effects.","PeriodicalId":54337,"journal":{"name":"Genes and Nutrition","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140167690","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-03-02DOI: 10.1186/s12263-023-00736-z
Kimya Khaledi, Rastegar Hoseini, Ahmad Gharzi
The protein tyrosine phosphatase 1B (PTP1B) plays a crucial role in the development of insulin resistance. Aerobic training (AT) and vitamin D (Vit D) supplementation have been shown to individually improve glucose tolerance and diabetes-related factors. However, the impact of their combined effect on PTP1B gene expression and serum irisin in the visceral adipose tissue remains unknown. This study aims to investigate whether 8 weeks of combined AT with Vit D supplementation can improve the expression of PTP1B in adipose tissue and serum irisin in obese rats with type 2 diabetes (T2D). Fifty male Wistar rats were divided into two groups: diabetic (n = 40) and non-diabetic (ND; n = 10). The diabetic rats were further divided into four groups: aerobic training with vitamin D supplementation (D + AT + Vit D; n = 10), aerobic training only (D + AT; n = 10), vitamin D supplementation only (D + Vit D; n = 10), and control (D + C; n = 10). The D + Vit D and D + AT + Vit D groups received 5000 IU of vitamin D via injection once a week, while the D + AT and D + C groups received sesame oil. Diabetes was induced in all groups except the nondiabetic group by intraperitoneal (IP) injection of streptozotocin. At the end of the intervention, blood and adipose tissue samples were collected, and RNA was extracted from adipose tissue for real-time PCR analysis of PPTP1B gene expression. There was an increase in serum Vit D and irisin levels and a decrease in HOMA-IR and PTP1B gene expression in the diabetic rat model treated with D + AT and injected with 50,000 IU/kg/week of Vit D. Comparatively, when treated with D + AT + Vit D, the downregulation of PTP1B was significantly higher (p = 0.049; p = 0.004), and there was a significant increase in irisin (p = 0.010; p = 0.001). The present study shows that the combined AT and Vit D supplementation positively impacts the expression of PTP1B in adipose tissue and serum irisin in rats with T2D. These findings suggest that combining AT with Vit D supplementation can provide a new and effective strategy to improve glucose tolerance and diabetes-related factors in individuals with T2D by regulating the expression of PTP1B in adipose tissue and promoting the synthesis of beneficial irisin protein.
蛋白酪氨酸磷酸酶 1B (PTP1B)在胰岛素抵抗的形成过程中起着至关重要的作用。有氧训练（AT）和维生素 D（Vit D）补充剂已被证明可单独改善葡萄糖耐量和糖尿病相关因素。然而，它们的联合作用对内脏脂肪组织中 PTP1B 基因表达和血清鸢尾素的影响仍然未知。本研究的目的是探讨联合服用 AT 和维生素 D 8 周能否改善肥胖的 2 型糖尿病（T2D）大鼠脂肪组织中 PTP1B 基因的表达和血清鸢尾素。50 只雄性 Wistar 大鼠分为两组：糖尿病组（n = 40）和非糖尿病组（n = 10）。糖尿病大鼠又分为四组：进行有氧训练并补充维生素 D（D + AT + Vit D；n = 10）、仅进行有氧训练（D + AT；n = 10）、仅补充维生素 D（D + Vit D；n = 10）和对照组（D + C；n = 10）。D + 维生素 D 组和 D + AT + 维生素 D 组每周注射一次 5000 IU 维生素 D，而 D + AT 组和 D + C 组则服用芝麻油。除非糖尿病组外，其他各组均通过腹腔注射链脲佐菌素诱发糖尿病。干预结束后，收集血液和脂肪组织样本，并从脂肪组织中提取 RNA 进行 PPTP1B 基因表达的实时 PCR 分析。在使用 D + AT 和注射 50,000 IU/kg/week Vit D 治疗的糖尿病大鼠模型中，血清 Vit D 和鸢尾素水平增加，HOMA-IR 和 PTP1B 基因表达下降；相比之下，在使用 D + AT + Vit D 治疗时，PTP1B 的下调幅度明显更高（p = 0.049；p = 0.004），而鸢尾素则显著增加（p = 0.010；p = 0.001）。本研究表明，联合补充 AT 和维生素 D 会对 T2D 大鼠脂肪组织中 PTP1B 的表达和血清鸢尾素产生积极影响。这些研究结果表明，通过调节 PTP1B 在脂肪组织中的表达和促进有益鸢尾素蛋白的合成，将 AT 与维生素 D 补充剂结合使用可为改善 T2D 患者的葡萄糖耐量和糖尿病相关因素提供一种新的有效策略。
{"title":"The impact of vitamin D on type 2 diabetes management: boosting PTP1B gene expression and physical activity benefits in rats","authors":"Kimya Khaledi, Rastegar Hoseini, Ahmad Gharzi","doi":"10.1186/s12263-023-00736-z","DOIUrl":"https://doi.org/10.1186/s12263-023-00736-z","url":null,"abstract":"The protein tyrosine phosphatase 1B (PTP1B) plays a crucial role in the development of insulin resistance. Aerobic training (AT) and vitamin D (Vit D) supplementation have been shown to individually improve glucose tolerance and diabetes-related factors. However, the impact of their combined effect on PTP1B gene expression and serum irisin in the visceral adipose tissue remains unknown. This study aims to investigate whether 8 weeks of combined AT with Vit D supplementation can improve the expression of PTP1B in adipose tissue and serum irisin in obese rats with type 2 diabetes (T2D). Fifty male Wistar rats were divided into two groups: diabetic (n = 40) and non-diabetic (ND; n = 10). The diabetic rats were further divided into four groups: aerobic training with vitamin D supplementation (D + AT + Vit D; n = 10), aerobic training only (D + AT; n = 10), vitamin D supplementation only (D + Vit D; n = 10), and control (D + C; n = 10). The D + Vit D and D + AT + Vit D groups received 5000 IU of vitamin D via injection once a week, while the D + AT and D + C groups received sesame oil. Diabetes was induced in all groups except the nondiabetic group by intraperitoneal (IP) injection of streptozotocin. At the end of the intervention, blood and adipose tissue samples were collected, and RNA was extracted from adipose tissue for real-time PCR analysis of PPTP1B gene expression. There was an increase in serum Vit D and irisin levels and a decrease in HOMA-IR and PTP1B gene expression in the diabetic rat model treated with D + AT and injected with 50,000 IU/kg/week of Vit D. Comparatively, when treated with D + AT + Vit D, the downregulation of PTP1B was significantly higher (p = 0.049; p = 0.004), and there was a significant increase in irisin (p = 0.010; p = 0.001). The present study shows that the combined AT and Vit D supplementation positively impacts the expression of PTP1B in adipose tissue and serum irisin in rats with T2D. These findings suggest that combining AT with Vit D supplementation can provide a new and effective strategy to improve glucose tolerance and diabetes-related factors in individuals with T2D by regulating the expression of PTP1B in adipose tissue and promoting the synthesis of beneficial irisin protein.","PeriodicalId":54337,"journal":{"name":"Genes and Nutrition","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140017208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-02-27DOI: 10.1186/s12263-024-00742-9
Nur Aliah Natasha Md Shahrulnizam, Mohd Danial Mohd Efendy Goon, Sharaniza Ab Rahim, Sook Weih Lew, Siti Hamimah Sheikh Abdul Kadir, Effendi Ibrahim
Tocotrienol-rich fraction (TRF) has been reported to protect the heart from oxidative stress-induced inflammation. It is, however, unclear whether the protective effects of TRF against oxidative stress involve the activation of farnesoid X receptor (fxr), a bile acid receptor, and the regulation of bile acid metabolites. In the current study, we investigated the effects of TRF supplementation on antioxidant activities, expression of fxr and its target genes in cardiac tissue, and serum untargeted metabolomics of high-fat diet-fed mice. Mice were divided into high-fat diet (HFD) with or without TRF supplementation (control) for 6 weeks. At the end of the intervention, body weight (BW), waist circumference (WC), and random blood glucose were measured. Heart tissues were collected, and the gene expression of sod1, sod2, gpx, and fxr and its target genes shp and stat3 was determined. Serum was subjected to untargeted metabolomic analysis using UHPLC-Orbitrap. In comparison to the control, the WC of the TRF-treated group was higher (p >0.05) than that of the HFD-only group, in addition there was no significant difference in weight or random blood glucose level. Downregulation of sod1, sod2, and gpx expression was observed in TRF-treated mice; however, only sod1 was significant when compared to the HFD only group. The expression of cardiac shp (fxr target gene) was significantly upregulated, but stat3 was significantly downregulated in the TRF-treated group compared to the HFD-only group. Biochemical pathways found to be influenced by TRF supplementation include bile acid secretion, primary bile acid biosynthesis, and biotin and cholesterol metabolism. In conclusion, TRF supplementation in HFD-fed mice affects antioxidant activities, and more interestingly, TRF also acts as a signaling molecule that is possibly involved in several bile acid-related biochemical pathways accompanied by an increase in cardiac fxr shp expression. This study provides new insight into TRF in deregulating bile acid receptors and metabolites in high-fat diet-fed mice.
{"title":"Palm-based tocotrienol-rich fraction (TRF) supplementation modulates cardiac sod1 expression, fxr target gene expression, and tauro-conjugated bile acid levels in aleptinemic mice fed a high-fat diet","authors":"Nur Aliah Natasha Md Shahrulnizam, Mohd Danial Mohd Efendy Goon, Sharaniza Ab Rahim, Sook Weih Lew, Siti Hamimah Sheikh Abdul Kadir, Effendi Ibrahim","doi":"10.1186/s12263-024-00742-9","DOIUrl":"https://doi.org/10.1186/s12263-024-00742-9","url":null,"abstract":"Tocotrienol-rich fraction (TRF) has been reported to protect the heart from oxidative stress-induced inflammation. It is, however, unclear whether the protective effects of TRF against oxidative stress involve the activation of farnesoid X receptor (fxr), a bile acid receptor, and the regulation of bile acid metabolites. In the current study, we investigated the effects of TRF supplementation on antioxidant activities, expression of fxr and its target genes in cardiac tissue, and serum untargeted metabolomics of high-fat diet-fed mice. Mice were divided into high-fat diet (HFD) with or without TRF supplementation (control) for 6 weeks. At the end of the intervention, body weight (BW), waist circumference (WC), and random blood glucose were measured. Heart tissues were collected, and the gene expression of sod1, sod2, gpx, and fxr and its target genes shp and stat3 was determined. Serum was subjected to untargeted metabolomic analysis using UHPLC-Orbitrap. In comparison to the control, the WC of the TRF-treated group was higher (p >0.05) than that of the HFD-only group, in addition there was no significant difference in weight or random blood glucose level. Downregulation of sod1, sod2, and gpx expression was observed in TRF-treated mice; however, only sod1 was significant when compared to the HFD only group. The expression of cardiac shp (fxr target gene) was significantly upregulated, but stat3 was significantly downregulated in the TRF-treated group compared to the HFD-only group. Biochemical pathways found to be influenced by TRF supplementation include bile acid secretion, primary bile acid biosynthesis, and biotin and cholesterol metabolism. In conclusion, TRF supplementation in HFD-fed mice affects antioxidant activities, and more interestingly, TRF also acts as a signaling molecule that is possibly involved in several bile acid-related biochemical pathways accompanied by an increase in cardiac fxr shp expression. This study provides new insight into TRF in deregulating bile acid receptors and metabolites in high-fat diet-fed mice.","PeriodicalId":54337,"journal":{"name":"Genes and Nutrition","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139978492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-19DOI: 10.1186/s12263-024-00737-6
Yanru Zhang, Ruike Ding, Yulin Zhang, Jia Qi, Wenbin Cao, Lijun Deng, Lin Zhou, Yun Ye, Ying Xue, Enqi Liu
Obese patients have been found to be susceptible to iron deficiency, and malabsorption of dietary iron is the cause of obesity-related iron deficiency (ORID). Divalent metal transporter 1 (DMT1) and ferroportin (FPN), are two transmembrane transporter proteins expressed in the duodenum that are closely associated with iron absorption. However, there have been few studies on the association between these two proteins and the increased susceptibility to iron deficiency in obese patients. Chronic inflammation is also thought to be a cause of obesity-related iron deficiency, and both conditions can have an impact on spermatogenesis and impair male reproductive function. Based on previous studies, transgenerational epigenetic inheritance through gametes was observed in obesity. Our results showed that obese mice had decreased blood iron levels (p < 0.01), lower protein and mRNA expression for duodenal DMT1 (p < 0.05), but no statistically significant variation in mRNA expression for duodenal FPN (p > 0.05); there was an increase in sperm miR-135b expression (p < 0.05). Bioinformatics revealed ninety overlapping genes and further analysis showed that they were primarily responsible for epithelial cilium movement, fatty acid beta-oxidation, protein dephosphorylation, fertilization, and glutamine transport, which are closely related to spermatogenesis, sperm development, and sperm viability in mice. In obese mice, we observed downregulation of DMT1 in the duodenum and upregulation of miR-135b in the spermatozoa.
{"title":"Dysfunction of DMT1 and miR-135b in the gut-testis axis in high-fat diet male mice","authors":"Yanru Zhang, Ruike Ding, Yulin Zhang, Jia Qi, Wenbin Cao, Lijun Deng, Lin Zhou, Yun Ye, Ying Xue, Enqi Liu","doi":"10.1186/s12263-024-00737-6","DOIUrl":"https://doi.org/10.1186/s12263-024-00737-6","url":null,"abstract":"Obese patients have been found to be susceptible to iron deficiency, and malabsorption of dietary iron is the cause of obesity-related iron deficiency (ORID). Divalent metal transporter 1 (DMT1) and ferroportin (FPN), are two transmembrane transporter proteins expressed in the duodenum that are closely associated with iron absorption. However, there have been few studies on the association between these two proteins and the increased susceptibility to iron deficiency in obese patients. Chronic inflammation is also thought to be a cause of obesity-related iron deficiency, and both conditions can have an impact on spermatogenesis and impair male reproductive function. Based on previous studies, transgenerational epigenetic inheritance through gametes was observed in obesity. Our results showed that obese mice had decreased blood iron levels (p < 0.01), lower protein and mRNA expression for duodenal DMT1 (p < 0.05), but no statistically significant variation in mRNA expression for duodenal FPN (p > 0.05); there was an increase in sperm miR-135b expression (p < 0.05). Bioinformatics revealed ninety overlapping genes and further analysis showed that they were primarily responsible for epithelial cilium movement, fatty acid beta-oxidation, protein dephosphorylation, fertilization, and glutamine transport, which are closely related to spermatogenesis, sperm development, and sperm viability in mice. In obese mice, we observed downregulation of DMT1 in the duodenum and upregulation of miR-135b in the spermatozoa.","PeriodicalId":54337,"journal":{"name":"Genes and Nutrition","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139498643","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-06-02DOI: 10.1186/s12263-022-00710-1
de Sousa, Bruno Rafael Virginio, de Lima Tavares Toscano, Lydiane, de Almeida Filho, Eder Jackson Bezerra, Sena, Klécia Farias, Costa, Matheus Silveira, de Souza Cunha, Rebeka Correia, de Souza Siqueira Quintans, Jullyana, Heimfarth, Luana, Marques, Aline Telles Biasoto, da Silva, Darcilene Fiuza, de Campos, Luis Felipe Castelli Correia, Persuhn, Darlene Camati, Silva, Alexandre Sérgio
We examined the influence of superoxide dismutase 3 (SOD3) Arg213Gly and Peroxisome Proliferator-Activated α-Receptor (PPARα) 7G/C polymorphisms to a single dose of purple grape juice supplementation on time-to-exhaustion running test, redox balance and muscle damage in recreational runners. Forty-seven male recreational runners performed a running test until exhaustion after supplementation with grape juice or a control drink. Serum total antioxidant capacity (TAC), malondialdehyde (MDA), plasma nitrite (NO), creatine kinase (CK) and lactate dehydrogenase (LDH) were measured pre and post exercise. Also, polymorphisms were analyzed in DNA extracted from the oral mucosa. Grape juice improved the time-to-exhaustion. When analyzed by genotype, the recreational runners with GG+CG genotypes of the SOD3 gene had greater time-to-exhaustion than the CC genotype, but was no different for the PAPRα gene. A slight difference was noted in TAC, since the CC genotype of the SOD3 gene showed higher TAC values in the post-exercise compared to the baseline and with pre-exercise, but these values did not increase compared to the CG+GG group, respectively. The SOD3 and PPARα genes were similar at all times for the other biochemical variables. The ergogenic effect of grape juice was genotype-dependent for SOD3 Arg213Gly. However, biochemical redox balance markers did not explain this difference.
{"title":"Purple grape juice improves performance of recreational runners, but the effect is genotype dependent: a double blind, randomized, controlled trial","authors":"de Sousa, Bruno Rafael Virginio, de Lima Tavares Toscano, Lydiane, de Almeida Filho, Eder Jackson Bezerra, Sena, Klécia Farias, Costa, Matheus Silveira, de Souza Cunha, Rebeka Correia, de Souza Siqueira Quintans, Jullyana, Heimfarth, Luana, Marques, Aline Telles Biasoto, da Silva, Darcilene Fiuza, de Campos, Luis Felipe Castelli Correia, Persuhn, Darlene Camati, Silva, Alexandre Sérgio","doi":"10.1186/s12263-022-00710-1","DOIUrl":"https://doi.org/10.1186/s12263-022-00710-1","url":null,"abstract":"We examined the influence of superoxide dismutase 3 (SOD3) Arg213Gly and Peroxisome Proliferator-Activated α-Receptor (PPARα) 7G/C polymorphisms to a single dose of purple grape juice supplementation on time-to-exhaustion running test, redox balance and muscle damage in recreational runners. Forty-seven male recreational runners performed a running test until exhaustion after supplementation with grape juice or a control drink. Serum total antioxidant capacity (TAC), malondialdehyde (MDA), plasma nitrite (NO), creatine kinase (CK) and lactate dehydrogenase (LDH) were measured pre and post exercise. Also, polymorphisms were analyzed in DNA extracted from the oral mucosa. Grape juice improved the time-to-exhaustion. When analyzed by genotype, the recreational runners with GG+CG genotypes of the SOD3 gene had greater time-to-exhaustion than the CC genotype, but was no different for the PAPRα gene. A slight difference was noted in TAC, since the CC genotype of the SOD3 gene showed higher TAC values in the post-exercise compared to the baseline and with pre-exercise, but these values did not increase compared to the CG+GG group, respectively. The SOD3 and PPARα genes were similar at all times for the other biochemical variables. The ergogenic effect of grape juice was genotype-dependent for SOD3 Arg213Gly. However, biochemical redox balance markers did not explain this difference.","PeriodicalId":54337,"journal":{"name":"Genes and Nutrition","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2022-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138507721","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-05-30DOI: 10.1186/s12263-022-00708-9
Wang, Tianyi, Cheng, Jun, Wang, Yanggan
Atrial fibrillation is the most common arrhythmia disease. Animal and observational studies have found a link between iron status and atrial fibrillation. However, the causal relationship between iron status and AF remains unclear. The purpose of this investigation was to use Mendelian randomization (MR) analysis, which has been widely applied to estimate the causal effect, to reveal whether systemic iron status was causally related to atrial fibrillation. Single nucleotide polymorphisms (SNPs) strongly associated (P < 5 × 10−8) with four biomarkers of systemic iron status were obtained from a genome-wide association study involving 48,972 subjects conducted by the Genetics of Iron Status consortium. Summary-level data for the genetic associations with atrial fibrillation were acquired from the AFGen (Atrial Fibrillation Genetics) consortium study (including 65,446 atrial fibrillation cases and 522,744 controls). We used a two-sample MR analysis to obtain a causal estimate and further verified credibility through sensitivity analysis. Genetically instrumented serum iron [OR 1.09; 95% confidence interval (CI) 1.02–1.16; p = 0.01], ferritin [OR 1.16; 95% CI 1.02–1.33; p = 0.02], and transferrin saturation [OR 1.05; 95% CI 1.01–1.11; p = 0.01] had positive effects on atrial fibrillation. Genetically instrumented transferrin levels [OR 0.90; 95% CI 0.86–0.97; p = 0.006] were inversely correlated with atrial fibrillation. In conclusion, our results strongly elucidated a causal link between genetically determined higher iron status and increased risk of atrial fibrillation. This provided new ideas for the clinical prevention and treatment of atrial fibrillation.
心房颤动是最常见的心律失常疾病。动物和观察性研究已经发现了铁状态和房颤之间的联系。然而，铁状态与房颤之间的因果关系尚不清楚。本研究的目的是使用孟德尔随机化(MR)分析来揭示全身铁状态是否与房颤有因果关系，孟德尔随机化(MR)分析已被广泛应用于估计因果关系。在一项涉及48,972名受试者的全基因组关联研究中，由遗传铁状态联盟(Genetics of iron status consortium)获得了与四种全身铁状态生物标志物密切相关(P < 5 × 10−8)的单核苷酸多态性(SNPs)。房颤遗传关联的概要数据来自AFGen(房颤遗传学)联合研究(包括65,446例房颤病例和522,744例对照)。我们使用双样本MR分析获得因果估计，并通过敏感性分析进一步验证可信性。基因检测血清铁[OR 1.09;95%置信区间(CI) 1.02 ~ 1.16;p = 0.01]，铁蛋白[OR 1.16;95% ci 1.02-1.33;p = 0.02]，转铁蛋白饱和度[OR 1.05;95% ci 1.01-1.11;P = 0.01]对房颤有积极作用。基因检测转铁蛋白水平[OR 0.90;95% ci 0.86-0.97;P = 0.006]与房颤呈负相关。总之，我们的研究结果有力地阐明了基因决定的高铁状态和房颤风险增加之间的因果关系。这为房颤的临床防治提供了新的思路。
{"title":"Genetic support of a causal relationship between iron status and atrial fibrillation: a Mendelian randomization study","authors":"Wang, Tianyi, Cheng, Jun, Wang, Yanggan","doi":"10.1186/s12263-022-00708-9","DOIUrl":"https://doi.org/10.1186/s12263-022-00708-9","url":null,"abstract":"Atrial fibrillation is the most common arrhythmia disease. Animal and observational studies have found a link between iron status and atrial fibrillation. However, the causal relationship between iron status and AF remains unclear. The purpose of this investigation was to use Mendelian randomization (MR) analysis, which has been widely applied to estimate the causal effect, to reveal whether systemic iron status was causally related to atrial fibrillation. Single nucleotide polymorphisms (SNPs) strongly associated (P < 5 × 10−8) with four biomarkers of systemic iron status were obtained from a genome-wide association study involving 48,972 subjects conducted by the Genetics of Iron Status consortium. Summary-level data for the genetic associations with atrial fibrillation were acquired from the AFGen (Atrial Fibrillation Genetics) consortium study (including 65,446 atrial fibrillation cases and 522,744 controls). We used a two-sample MR analysis to obtain a causal estimate and further verified credibility through sensitivity analysis. Genetically instrumented serum iron [OR 1.09; 95% confidence interval (CI) 1.02–1.16; p = 0.01], ferritin [OR 1.16; 95% CI 1.02–1.33; p = 0.02], and transferrin saturation [OR 1.05; 95% CI 1.01–1.11; p = 0.01] had positive effects on atrial fibrillation. Genetically instrumented transferrin levels [OR 0.90; 95% CI 0.86–0.97; p = 0.006] were inversely correlated with atrial fibrillation. In conclusion, our results strongly elucidated a causal link between genetically determined higher iron status and increased risk of atrial fibrillation. This provided new ideas for the clinical prevention and treatment of atrial fibrillation.","PeriodicalId":54337,"journal":{"name":"Genes and Nutrition","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2022-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138507665","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-05-05DOI: 10.1186/s12263-022-00709-8
Khamis, Abeer A., Ibrahim, Rana M., El-hefnawy, Gad B., Ibrahim, Wafaa M., Ali, Ehab M.
Genetic instability leads to genome mutations, changes in nucleotide sequences, rearrangements, and gains or losses of part of the chromosomes. This instability can initiate and develop cancer. This study evaluated genomic stability in methotrexate and anthocyanin-treated mammary adenocarcinoma model. Seventy albino mice were divided into seven groups: negative control, anthocyanin, methotrexate, Ehrlich’s solid tumor; Ehrlich’s solid tumor and methotrexate; Ehrlich’s solid tumor and anthocyanin; and Ehrlich’s solid tumor, methotrexate, and anthocyanin groups. Tumor weight and size were evaluated. Serum arylesterase activity was low in all the induced tumors and those treated with anthocyanin, methotrexate, or both. Poly[adenosine diphosphate (ADP)-ribose] polymerase activity was high, and glutathione S-transferase activity was low in the tumors treated with anthocyanin, methotrexate, or both, compared with that of the untreated tumor. There was an increase in DNA damage in the mice with solid tumors and those injected with methotrexate or methotrexate and anthocyanin, compared with that in the untreated mice. There was a decrease in genetic instability and DNA damage in the tumor-bearing mice treated with anthocyanin, with a concomitant increase in nuclear poly[adenosine diphosphate (ADP)-ribose] polymerase activity, compared with those of the untreated group. Anthocyanin exerted positive effects in the treatment of mammary adenocarcinoma.
{"title":"Impact of anthocyanin on genetic stability in mammary adenocarcinoma-induced mice treated with methotrexate","authors":"Khamis, Abeer A., Ibrahim, Rana M., El-hefnawy, Gad B., Ibrahim, Wafaa M., Ali, Ehab M.","doi":"10.1186/s12263-022-00709-8","DOIUrl":"https://doi.org/10.1186/s12263-022-00709-8","url":null,"abstract":"Genetic instability leads to genome mutations, changes in nucleotide sequences, rearrangements, and gains or losses of part of the chromosomes. This instability can initiate and develop cancer. This study evaluated genomic stability in methotrexate and anthocyanin-treated mammary adenocarcinoma model. Seventy albino mice were divided into seven groups: negative control, anthocyanin, methotrexate, Ehrlich’s solid tumor; Ehrlich’s solid tumor and methotrexate; Ehrlich’s solid tumor and anthocyanin; and Ehrlich’s solid tumor, methotrexate, and anthocyanin groups. Tumor weight and size were evaluated. Serum arylesterase activity was low in all the induced tumors and those treated with anthocyanin, methotrexate, or both. Poly[adenosine diphosphate (ADP)-ribose] polymerase activity was high, and glutathione S-transferase activity was low in the tumors treated with anthocyanin, methotrexate, or both, compared with that of the untreated tumor. There was an increase in DNA damage in the mice with solid tumors and those injected with methotrexate or methotrexate and anthocyanin, compared with that in the untreated mice. There was a decrease in genetic instability and DNA damage in the tumor-bearing mice treated with anthocyanin, with a concomitant increase in nuclear poly[adenosine diphosphate (ADP)-ribose] polymerase activity, compared with those of the untreated group. Anthocyanin exerted positive effects in the treatment of mammary adenocarcinoma.","PeriodicalId":54337,"journal":{"name":"Genes and Nutrition","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2022-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138507740","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-04-25DOI: 10.1186/s12263-022-00707-w
Choi, Woo Jeong, Shin, Dayeon
Metabolic syndrome (MetS) is characterized by the coexistence of disorders such as diabetes, hypertension, hyperlipidemia, and obesity and is affected by genetic factors. Previous genome-wide association studies (GWAS) suggested that APOA5 gene variants were significantly associated with MetS and its components. Dietary factors such as red and processed meat consumption can cause chronic diseases, including hypertension, diabetes, and vascular depression. The aim of this study was to investigate the modulation of the incidence of MetS by the interaction between APOA5 rs662799 polymorphism and red and processed meat consumption. In this prospective cohort study, 3266 participants were collected from the Korea Association REsource (KARE) cohort of the Korean Genome and Epidemiology Study (KoGES) from 2001 to 2016. APOA5 rs662799 polymorphism was extracted by GWAS using the Korean Chip. Red and processed meat consumption data were assessed using a semi-quantitative food frequency questionnaire. The incidence of MetS in carriers of the minor G allele of rs662799 (AG + GG) and the third tertile of red and processed meat consumption (serving/day) was higher than those with the major allele of rs662799 (AA) and the first tertile of red and processed meat consumption (HR 1.70, 95% CI 1.30–2.22, p interaction = 0.002). An association between the presence of the minor alleles of rs662799 and high red and processed meat consumption and the incidence of MetS was observed in Korean adults.
{"title":"Interactions between red and processed meat consumption and APOA5 gene variants associated with the incidence of metabolic syndrome in Korean adults","authors":"Choi, Woo Jeong, Shin, Dayeon","doi":"10.1186/s12263-022-00707-w","DOIUrl":"https://doi.org/10.1186/s12263-022-00707-w","url":null,"abstract":"Metabolic syndrome (MetS) is characterized by the coexistence of disorders such as diabetes, hypertension, hyperlipidemia, and obesity and is affected by genetic factors. Previous genome-wide association studies (GWAS) suggested that APOA5 gene variants were significantly associated with MetS and its components. Dietary factors such as red and processed meat consumption can cause chronic diseases, including hypertension, diabetes, and vascular depression. The aim of this study was to investigate the modulation of the incidence of MetS by the interaction between APOA5 rs662799 polymorphism and red and processed meat consumption. In this prospective cohort study, 3266 participants were collected from the Korea Association REsource (KARE) cohort of the Korean Genome and Epidemiology Study (KoGES) from 2001 to 2016. APOA5 rs662799 polymorphism was extracted by GWAS using the Korean Chip. Red and processed meat consumption data were assessed using a semi-quantitative food frequency questionnaire. The incidence of MetS in carriers of the minor G allele of rs662799 (AG + GG) and the third tertile of red and processed meat consumption (serving/day) was higher than those with the major allele of rs662799 (AA) and the first tertile of red and processed meat consumption (HR 1.70, 95% CI 1.30–2.22, p interaction = 0.002). An association between the presence of the minor alleles of rs662799 and high red and processed meat consumption and the incidence of MetS was observed in Korean adults.","PeriodicalId":54337,"journal":{"name":"Genes and Nutrition","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2022-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138543238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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