Pub Date : 2024-09-18DOI: 10.1016/j.jnutbio.2024.109771
Pin-Yu Chen , Mao-Shin Lin , Chin-Chuan Chen , Yann-Lii Leu , Shu-Huei Wang
Abnormal vascular smooth muscle cell (VSMC) proliferation and migration play crucial roles in neointimal hyperplasia and restenosis progression in response to stimulation with various inflammatory cytokines, such as platelet-derived growth factor-BB (PDGF-BB) and tumour necrosis factor-α (TNF-α). Hydroxygenkwanin (HGK) exerts remarkable anti-inflammatory, antitumour, antiproliferative and antimigratory effects. The aim of the study was to elucidate the therapeutic effect and regulatory mechanism of HGK on neointimal hyperplasia. The results showed that HGK inhibited the abnormal proliferation, migration, and inflammation of PDGF-BB- or TNF-α-treated VSMCs through regulation of the PDK1/AKT/mTOR pathway. In addition, HGK promoted circulating endothelial progenitor cell (EPC) chemotaxis. In an in vivo assay, HGK dramatically enhanced re-endothelization and reduced neointimal hyperplasia after femoral artery denudation with a guide wire in mice. These results suggest that HGK can serve as a therapeutic target drug or a functional food supplement for the treatment of restenosis.
{"title":"The flavonoid hydroxygenkwanin reduces inflammation and neointimal formation","authors":"Pin-Yu Chen , Mao-Shin Lin , Chin-Chuan Chen , Yann-Lii Leu , Shu-Huei Wang","doi":"10.1016/j.jnutbio.2024.109771","DOIUrl":"10.1016/j.jnutbio.2024.109771","url":null,"abstract":"<div><div>Abnormal vascular smooth muscle cell (VSMC) proliferation and migration play crucial roles in neointimal hyperplasia and restenosis progression in response to stimulation with various inflammatory cytokines, such as platelet-derived growth factor-BB (PDGF-BB) and tumour necrosis factor-α (TNF-α). Hydroxygenkwanin (HGK) exerts remarkable anti-inflammatory, antitumour, antiproliferative and antimigratory effects. The aim of the study was to elucidate the therapeutic effect and regulatory mechanism of HGK on neointimal hyperplasia. The results showed that HGK inhibited the abnormal proliferation, migration, and inflammation of PDGF-BB- or TNF-α-treated VSMCs through regulation of the PDK1/AKT/mTOR pathway. In addition, HGK promoted circulating endothelial progenitor cell (EPC) chemotaxis. In an in vivo assay, HGK dramatically enhanced re-endothelization and reduced neointimal hyperplasia after femoral artery denudation with a guide wire in mice. These results suggest that HGK can serve as a therapeutic target drug or a functional food supplement for the treatment of restenosis.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"135 ","pages":"Article 109771"},"PeriodicalIF":4.8,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142289539","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-14DOI: 10.1016/j.jnutbio.2024.109767
Hongkun Lin , Xiaoping Guo , Jingjing Liu , Li Chen , Huimin Chen , Ying Zhao , Hongxia Li , Shuang Rong , Ping Yao
Iron overload is a common feature of alcoholic liver disease (ALD) and contributes significantly to disease progression. Quercetin, a flavonoid known for its iron-chelating properties, has emerged as a potential protective compound against ALD. However, research on quercetin's regulatory effects on iron levels in ALD is limited. To address this, we conducted a study using male C57BL/6J mice were subjected to a Lieber De Carli liquid diet containing ethanol (28% energy replacement) with or without quercetin supplementation (100 mg/kg.BW) for 12 weeks. Additionally, HepG2 cells, after transfection with the CYP2E1 plasmid, were incubated with ethanol and/or quercetin. Our findings revealed that ethanol consumption led to iron overload in both hepatocytes and lysosomes. Interestingly, despite the increase in iron levels, cells exhibited impaired iron utilization, disrupting normal iron metabolism. Further analysis identified a potential mechanism involving the Rab7-V1G1 (V-ATPase subunit) axis. Inhibition of V-ATPase by Concanamycin A caused elevated ROS levels, impaired lysosomal and mitochondria function, and increased expression of HIF1α and IRP2. Ultimately, this disruption in cellular processes led to iron overload and mitochondrial iron deficiency. Quercetin supplementation mitigated ethanol-induced hepatocyte damage by reversing iron overload through modulation of the Rab7-V1G1 axis and improving the interaction between lysosomes and mitochondria. In conclusion, this study elucidates a novel pathophysiological mechanism by which quercetin protects against ALD through its regulation of iron homeostasis.
{"title":"Refining the Rab7-V1G1 axis to mitigate iron deposition: Protective effects of quercetin in alcoholic liver disease","authors":"Hongkun Lin , Xiaoping Guo , Jingjing Liu , Li Chen , Huimin Chen , Ying Zhao , Hongxia Li , Shuang Rong , Ping Yao","doi":"10.1016/j.jnutbio.2024.109767","DOIUrl":"10.1016/j.jnutbio.2024.109767","url":null,"abstract":"<div><div>Iron overload is a common feature of alcoholic liver disease (ALD) and contributes significantly to disease progression. Quercetin, a flavonoid known for its iron-chelating properties, has emerged as a potential protective compound against ALD. However, research on quercetin's regulatory effects on iron levels in ALD is limited. To address this, we conducted a study using male C57BL/6J mice were subjected to a Lieber De Carli liquid diet containing ethanol (28% energy replacement) with or without quercetin supplementation (100 mg/kg.BW) for 12 weeks. Additionally, HepG2 cells, after transfection with the CYP2E1 plasmid, were incubated with ethanol and/or quercetin. Our findings revealed that ethanol consumption led to iron overload in both hepatocytes and lysosomes. Interestingly, despite the increase in iron levels, cells exhibited impaired iron utilization, disrupting normal iron metabolism. Further analysis identified a potential mechanism involving the Rab7-V1G1 (V-ATPase subunit) axis. Inhibition of V-ATPase by Concanamycin A caused elevated ROS levels, impaired lysosomal and mitochondria function, and increased expression of HIF1α and IRP2. Ultimately, this disruption in cellular processes led to iron overload and mitochondrial iron deficiency. Quercetin supplementation mitigated ethanol-induced hepatocyte damage by reversing iron overload through modulation of the Rab7-V1G1 axis and improving the interaction between lysosomes and mitochondria. In conclusion, this study elucidates a novel pathophysiological mechanism by which quercetin protects against ALD through its regulation of iron homeostasis.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"135 ","pages":"Article 109767"},"PeriodicalIF":4.8,"publicationDate":"2024-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142289537","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-14DOI: 10.1016/j.jnutbio.2024.109770
Xinlei Guo , Honggui Li , Bilian Zhu , Xiaoxiao Wang , Qian Xu , Eduardo Aquino , Minji Koo , Qingsheng Li , James Cai , Shannon Glaser , Chaodong Wu
Stimulator of interferon genes (STING) is positively correlated with the degrees of liver inflammation in human metabolic dysfunction-associated steatotic liver disease (MASLD). In addition, STING disruption alleviates MASLD in mice fed a high-fat diet (HFD) for 3 months (3-m-HFD). Here we investigated the role of the duration of dietary feeding in regulating MASLD in mice and explored the involvement of STING in sex differences in MASLD. Both male and female STING-disrupted (STINGgt) and wild-type C57BL/6J mice were fed an HFD for 3 or 7 months (7-m-HFD). Additionally, female STINGgt mice upon ovariectomy (OVX) and 3-m-HFD were analyzed for MASLD. Upon 3-m-HFD, STINGgt mice exhibited decreased severity of MASLD compared to control. However, upon 7-m-HFD, STINGgt mice were comparable with wild-type mice in body weight, fat mass, and MASLD. Regarding regulating the liver RNA transcriptome, 7-m-HFD increased the expression of genes indicating proinflammatory activation of various liver cells. Interestingly, the severity of MASLD in female mice was much lighter than in male mice, regardless of STING disruption. Upon OVX, female STINGgt mice showed significantly increased severity of MASLD relative to sham control but were comparable with male STINGgt mice. Upon treatment with 17-beta estradiol (E2), hepatocytes revealed decreased fat deposition while macrophages displayed decreases in lipopolysaccharide-induced phosphorylation of Nfkb p65 and Jnk p46 independent of STING. These results suggest that 7-m-HFD, without altering female sex-based protection, abolishes STING disruption-driven protection of MASLD, likely through causing proinflammatory activation of multiple types of liver cells to offset the effect of STING disruption.
{"title":"HFD feeding for seven months abolishes STING disruption-driven but not female sex-based protection against hepatic steatosis and inflammation in mice","authors":"Xinlei Guo , Honggui Li , Bilian Zhu , Xiaoxiao Wang , Qian Xu , Eduardo Aquino , Minji Koo , Qingsheng Li , James Cai , Shannon Glaser , Chaodong Wu","doi":"10.1016/j.jnutbio.2024.109770","DOIUrl":"10.1016/j.jnutbio.2024.109770","url":null,"abstract":"<div><div>Stimulator of interferon genes (STING) is positively correlated with the degrees of liver inflammation in human metabolic dysfunction-associated steatotic liver disease (MASLD). In addition, STING disruption alleviates MASLD in mice fed a high-fat diet (HFD) for 3 months (3-m-HFD). Here we investigated the role of the duration of dietary feeding in regulating MASLD in mice and explored the involvement of STING in sex differences in MASLD. Both male and female STING-disrupted (STING<sup>gt</sup>) and wild-type C57BL/6J mice were fed an HFD for 3 or 7 months (7-m-HFD). Additionally, female STING<sup>gt</sup> mice upon ovariectomy (OVX) and 3-m-HFD were analyzed for MASLD. Upon 3-m-HFD, STING<sup>gt</sup> mice exhibited decreased severity of MASLD compared to control. However, upon 7-m-HFD, STING<sup>gt</sup> mice were comparable with wild-type mice in body weight, fat mass, and MASLD. Regarding regulating the liver RNA transcriptome, 7-m-HFD increased the expression of genes indicating proinflammatory activation of various liver cells. Interestingly, the severity of MASLD in female mice was much lighter than in male mice, regardless of STING disruption. Upon OVX, female STING<sup>gt</sup> mice showed significantly increased severity of MASLD relative to sham control but were comparable with male STING<sup>gt</sup> mice. Upon treatment with 17-beta estradiol (E2), hepatocytes revealed decreased fat deposition while macrophages displayed decreases in lipopolysaccharide-induced phosphorylation of Nfkb p65 and Jnk p46 independent of STING. These results suggest that 7-m-HFD, without altering female sex-based protection, abolishes STING disruption-driven protection of MASLD, likely through causing proinflammatory activation of multiple types of liver cells to offset the effect of STING disruption.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"135 ","pages":"Article 109770"},"PeriodicalIF":4.8,"publicationDate":"2024-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142289535","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Inflammation is a common feature of neurological disorders that alters cell function in microglia and astrocytes as well as other neuronal cell types. Astrocytes modulate blood flow, regulate glutamate metabolism, and exert antioxidant protection. When responding to inflammatory damage, astrocytes enhance immune cell infiltration and amplify inflammatory responses via the upregulation of cytokine production. Several molecules have been proposed to attenuate neuroinflammation and control neurological diseases. Curcumin gained attention due to its capacity to cross the blood-brain barrier and its well-described anti-inflammatory and antioxidant activities. Our study aimed to understand if oral curcumin administration could protect against central nervous system inflammatory damage induced by intracerebroventricular injection of LPS while focusing on astrocyte function. Despite its poor bioavailability, we found that curcumin reaches the central nervous system, prevents the locomotory damage caused by LPS, and reduces inflammatory signaling via IL-1β and COX-2. Furthermore, we observed that curcumin was protective against LPS-induced S100B secretion in the cerebrospinal fluid and GSH reduction in the hippocampal tissue. However, curcumin could not protect the animals from anhedonia, assessed by the sucrose preference test, and weight loss induced by LPS. Our results indicate that oral curcumin administration exerts a protective anti-inflammatory action in the central nervous system, attenuating the sickness behavior induced by ICV LPS. This work demonstrates that curcumin has an important modulative effect on astrocytes, thus suggesting that astrocytes are critical to the anti-inflammatory effects of curcumin.
{"title":"Curcumin attenuates neuroinflammatory damage induced by LPS: Implications for the role of S100B","authors":"Marina Seady , Gabriel Schirmbeck , Jéssica Taday , Fernanda Telles Fróes , Jéfeli Vasques Baú , Jeferson Jantsch , Renata Padilha Guedes , Carlos-Alberto Gonçalves , Marina Concli Leite","doi":"10.1016/j.jnutbio.2024.109768","DOIUrl":"10.1016/j.jnutbio.2024.109768","url":null,"abstract":"<div><div>Inflammation is a common feature of neurological disorders that alters cell function in microglia and astrocytes as well as other neuronal cell types. Astrocytes modulate blood flow, regulate glutamate metabolism, and exert antioxidant protection. When responding to inflammatory damage, astrocytes enhance immune cell infiltration and amplify inflammatory responses via the upregulation of cytokine production. Several molecules have been proposed to attenuate neuroinflammation and control neurological diseases. Curcumin gained attention due to its capacity to cross the blood-brain barrier and its well-described anti-inflammatory and antioxidant activities. Our study aimed to understand if oral curcumin administration could protect against central nervous system inflammatory damage induced by intracerebroventricular injection of LPS while focusing on astrocyte function. Despite its poor bioavailability, we found that curcumin reaches the central nervous system, prevents the locomotory damage caused by LPS, and reduces inflammatory signaling via IL-1β and COX-2. Furthermore, we observed that curcumin was protective against LPS-induced S100B secretion in the cerebrospinal fluid and GSH reduction in the hippocampal tissue. However, curcumin could not protect the animals from anhedonia, assessed by the sucrose preference test, and weight loss induced by LPS. Our results indicate that oral curcumin administration exerts a protective anti-inflammatory action in the central nervous system, attenuating the sickness behavior induced by ICV LPS. This work demonstrates that curcumin has an important modulative effect on astrocytes, thus suggesting that astrocytes are critical to the anti-inflammatory effects of curcumin.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"135 ","pages":"Article 109768"},"PeriodicalIF":4.8,"publicationDate":"2024-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142289533","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-12DOI: 10.1016/j.jnutbio.2024.109769
Kun Jia, Peng Shi, Lei Zhang, Xiaojun Yan, Jilin Xu, Kai Liao
Obesity-related chronic kidney disease (CKD) poses a significant risk to individuals' health and wellbeing, but the pathological mechanisms and treatment strategies are currently limited. Trans-cinnamic acid (CA) is a key active monomer found in cinnamon bark and is known for its diverse pharmacological activities. However, its effect on obesity-related renal injury remains unknown. In the current study, the in vitro and in vivo experiments were combined to investigate the beneficial effect of CA on renal injury induced by HFD or PA. We found that CA significantly reduced the obesity of zebrafish body and the accumulation of fat in kidney tissues. The histopathological changes and dysfunction induced by HFD were effectively mitigated by CA administration, as evidenced by the detection of Hematoxylin-Eosin straining, NAG activity, creatinine level, and expression of functional-related genes, respectively. Additionally, the in vitro and in vivo findings demonstrated that CA dramatically reduced the oxidative stress, inflammatory, and apoptosis in HFD-induced kidney tissues or PA-treated HEK293T and HK-2 cells. Finally, the results regarding ERK, JNK, and P38 proteins phosphorylation confirmed that CA may alleviate HFD-induced renal injury by inhibiting the phosphorylation of ERK, JNK, and P38 MAPK proteins. This theory was further supported by the results of co-treatment with anisomycin (a JNK activator) or lipopolysaccharide and CA in HEK293T cells. This study proves that CA alleviates the obesity-related CKD probably through inhibition of MAPK signaling pathway.
{"title":"Trans-cinnamic acid alleviates high-fat diet-induced renal injury via JNK/ERK/P38 MAPK pathway","authors":"Kun Jia, Peng Shi, Lei Zhang, Xiaojun Yan, Jilin Xu, Kai Liao","doi":"10.1016/j.jnutbio.2024.109769","DOIUrl":"10.1016/j.jnutbio.2024.109769","url":null,"abstract":"<div><div>Obesity-related chronic kidney disease (CKD) poses a significant risk to individuals' health and wellbeing, but the pathological mechanisms and treatment strategies are currently limited. Trans-cinnamic acid (CA) is a key active monomer found in cinnamon bark and is known for its diverse pharmacological activities. However, its effect on obesity-related renal injury remains unknown. In the current study, the <em>in vitro</em> and <em>in vivo</em> experiments were combined to investigate the beneficial effect of CA on renal injury induced by HFD or PA. We found that CA significantly reduced the obesity of zebrafish body and the accumulation of fat in kidney tissues. The histopathological changes and dysfunction induced by HFD were effectively mitigated by CA administration, as evidenced by the detection of Hematoxylin-Eosin straining, NAG activity, creatinine level, and expression of functional-related genes, respectively. Additionally, the <em>in vitro</em> and <em>in vivo</em> findings demonstrated that CA dramatically reduced the oxidative stress, inflammatory, and apoptosis in HFD-induced kidney tissues or PA-treated HEK293T and HK-2 cells. Finally, the results regarding ERK, JNK, and P38 proteins phosphorylation confirmed that CA may alleviate HFD-induced renal injury by inhibiting the phosphorylation of ERK, JNK, and P38 MAPK proteins. This theory was further supported by the results of co-treatment with anisomycin (a JNK activator) or lipopolysaccharide and CA in HEK293T cells. This study proves that CA alleviates the obesity-related CKD probably through inhibition of MAPK signaling pathway.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"135 ","pages":"Article 109769"},"PeriodicalIF":4.8,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142289541","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-12DOI: 10.1016/j.jnutbio.2024.109759
Blanca Gavilán-Carrera , Vivianna Aguilera-Fernández , Francisco J. Amaro-Gahete , Antonio Rosales-Castillo , Alberto Soriano-Maldonado , José Antonio Vargas-Hitos
Patients with systemic lupus erythematosus (SLE) face increased cardiovascular risk not fully explained by traditional cardiovascular risk factors. Arterial stiffness, inflammation and disease-related therapies may be contributors to augmented cardiovascular risk, whereas healthy dietary habits could help in their management. The aim of the present study was to analyze the association of the adherence to the Mediterranean Diet with arterial stiffness, inflammation, and disease-related medication in women with SLE. A total of 76 women with SLE were included in this cross-sectional exploratory study. The adherence to the Mediterranean Diet was assessed using the Mediterranean Diet Score. Arterial stiffness was measured through pulse wave velocity (PWV). Inflammatory profile was evaluated through high-sensitivity C-reactive protein (hsCRP). The use (yes / no) and doses (mg /day and cumulative dose over the last 3 years) of corticosteroids and immunosuppressants were also registered. No association of the overall adherence to the Mediterranean Diet with PWV, hsCRP or medication use was found (all P>.05). Lower intake of full dairy products was related to greater odds of corticosteroids use (odds=1.72; P=.004), and both higher current (β=0.29; P=.024) and cumulative (β=0.21; P=.040) doses. Lower intake of red wine was associated with lower odds of immunosuppressants use (odds=0.63; P=.008). No association of the adherence to the Mediterranean Diet with arterial stiffness, inflammation or disease-related medication was observed in women with SLE with mild disease activity. However, higher dairy products and lower red wine consumption were related to lower use of disease-related medication. Future intervention studies are needed to better understand how nutritional education promoting Mediterranean Diet food groups can complement conventional SLE treatments.
背景：系统性红斑狼疮（SLE）患者的心血管风险增加，而传统的心血管风险因素并不能完全解释这一现象。动脉僵化、炎症或与疾病相关的疗法可能是导致心血管风险增加的因素，而健康的饮食习惯则有助于控制这些因素：本研究旨在分析系统性红斑狼疮女性患者坚持地中海饮食与动脉僵化、炎症和疾病相关药物治疗之间的关系：这项横断面探索性研究共纳入了 76 名女性系统性红斑狼疮患者。这项横断面探索性研究共纳入了 76 名患有系统性红斑狼疮的女性患者，采用地中海饮食评分法对其是否坚持地中海饮食进行了评估。动脉僵化通过脉搏波速度（PWV）进行测量。通过高敏 C 反应蛋白（hsCRP）评估炎症情况。此外，还登记了皮质类固醇和免疫抑制剂的使用情况（是/否）和剂量（毫克/天和过去三年的累积剂量）：结果：总体上坚持地中海饮食与脉搏波速度、hsCRP或药物使用均无关联（P>0.05）。全乳制品摄入量较低与使用皮质类固醇的几率较大有关（几率=1.72；P=0.004），与当前剂量（β=0.29；P=0.024）和累积剂量（β=0.21；P=0.040）较高有关。红葡萄酒摄入量较低与使用免疫抑制剂的几率较低有关（几率=0.63；P=0.008）：结论：在病情活动轻微的系统性红斑狼疮女性患者中，没有观察到坚持地中海饮食与动脉僵化、炎症或与疾病相关的药物治疗有关。然而，较多的乳制品和较少的红葡萄酒摄入量与较少使用疾病相关药物有关。未来需要进行干预研究，以更好地了解推广地中海饮食食物群的营养教育如何与传统的系统性红斑狼疮治疗方法相辅相成。
{"title":"Association of the Mediterranean diet with arterial stiffness, inflammation, and medication use in women with systemic lupus erythematosus: An exploratory study","authors":"Blanca Gavilán-Carrera , Vivianna Aguilera-Fernández , Francisco J. Amaro-Gahete , Antonio Rosales-Castillo , Alberto Soriano-Maldonado , José Antonio Vargas-Hitos","doi":"10.1016/j.jnutbio.2024.109759","DOIUrl":"10.1016/j.jnutbio.2024.109759","url":null,"abstract":"<div><div>Patients with systemic lupus erythematosus (SLE) face increased cardiovascular risk not fully explained by traditional cardiovascular risk factors. Arterial stiffness, inflammation and disease-related therapies may be contributors to augmented cardiovascular risk, whereas healthy dietary habits could help in their management. The aim of the present study was to analyze the association of the adherence to the Mediterranean Diet with arterial stiffness, inflammation, and disease-related medication in women with SLE. A total of 76 women with SLE were included in this cross-sectional exploratory study. The adherence to the Mediterranean Diet was assessed using the Mediterranean Diet Score. Arterial stiffness was measured through pulse wave velocity (PWV). Inflammatory profile was evaluated through high-sensitivity C-reactive protein (hsCRP). The use (yes / no) and doses (mg /day and cumulative dose over the last 3 years) of corticosteroids and immunosuppressants were also registered. No association of the overall adherence to the Mediterranean Diet with PWV, hsCRP or medication use was found (all <em>P</em>>.05). Lower intake of full dairy products was related to greater odds of corticosteroids use (odds=1.72; <em>P</em>=.004), and both higher current (β=0.29; <em>P</em>=.024) and cumulative (β=0.21; <em>P</em>=.040) doses. Lower intake of red wine was associated with lower odds of immunosuppressants use (odds=0.63; <em>P</em>=.008). No association of the adherence to the Mediterranean Diet with arterial stiffness, inflammation or disease-related medication was observed in women with SLE with mild disease activity. However, higher dairy products and lower red wine consumption were related to lower use of disease-related medication. Future intervention studies are needed to better understand how nutritional education promoting Mediterranean Diet food groups can complement conventional SLE treatments.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"134 ","pages":"Article 109759"},"PeriodicalIF":4.8,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142289519","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-12DOI: 10.1016/j.jnutbio.2024.109766
Qingqing Zhu , Xinyi Lu , Ting Zhang , Mengsha Shi , Rongrong Gao , Yanli Zhou , Haifeng Zhang , Wenming Yao , Changyong Qi , Shengen Liao , Xinli Li
Long-term dysfunction of glucose metabolism causes cardiac dysfunction called diabetic cardiomyopathy (DCM). To investigate the effect and underlying mechanism of RS on the process of DCM, mouse models induced by a high-fat diet (HFD) and streptozotocin (STZ) were fed RS (2 g/kg/day) and vehicle treatment (by oral gavage) for 14 weeks. Various analyses, including qRT-PCR, western blot, immunofluorescence staining, histology staining, cardiac function, and diversity detection of intestinal microbiota were performed. RS intervention could directly improve myocardial fibrosis, hypertrophy, apoptosis, and cardiac insufficiency in DCM. These beneficial effects may be achieved by elevating the expression of IGF-1, activating the ERK phosphorylation. Furthermore, by carrying out nano LC-MS/MS analyses and 16S rDNA sequencing, we found RS might primarily affect proteins in the cytoplasm involved in post-translational modification, protein conversion, and signal transduction mechanisms. RS altered intestinal microbiota and improved intestinal mucosal permeability towards a favorable direction in DCM. This multidimensional assessment of RS suggests that might be a promising approach towards the treatment of DCM.
{"title":"Resistant starch confers protection of dietary against diabetic cardiomyopathy","authors":"Qingqing Zhu , Xinyi Lu , Ting Zhang , Mengsha Shi , Rongrong Gao , Yanli Zhou , Haifeng Zhang , Wenming Yao , Changyong Qi , Shengen Liao , Xinli Li","doi":"10.1016/j.jnutbio.2024.109766","DOIUrl":"10.1016/j.jnutbio.2024.109766","url":null,"abstract":"<div><div>Long-term dysfunction of glucose metabolism causes cardiac dysfunction called diabetic cardiomyopathy (DCM). To investigate the effect and underlying mechanism of RS on the process of DCM, mouse models induced by a high-fat diet (HFD) and streptozotocin (STZ) were fed RS (2 g/kg/day) and vehicle treatment (by oral gavage) for 14 weeks. Various analyses, including qRT-PCR, western blot, immunofluorescence staining, histology staining, cardiac function, and diversity detection of intestinal microbiota were performed. RS intervention could directly improve myocardial fibrosis, hypertrophy, apoptosis, and cardiac insufficiency in DCM. These beneficial effects may be achieved by elevating the expression of IGF-1, activating the ERK phosphorylation. Furthermore, by carrying out nano LC-MS/MS analyses and 16S rDNA sequencing, we found RS might primarily affect proteins in the cytoplasm involved in post-translational modification, protein conversion, and signal transduction mechanisms. RS altered intestinal microbiota and improved intestinal mucosal permeability towards a favorable direction in DCM. This multidimensional assessment of RS suggests that might be a promising approach towards the treatment of DCM.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"134 ","pages":"Article 109766"},"PeriodicalIF":4.8,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142289538","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-08DOI: 10.1016/j.jnutbio.2024.109765
Mi-Jeong Kim , Taeyeon Hwang , Sugyeong Ha , Hyerin Kim , Jeongwon Kim , Doyeon Kim , Ji-an Yoo , Byeong Moo Kim , Hae Young Chung , Donghwan Kim , Jaewon Lee , Haeseung Lee , Sangok Kim , Ki Wung Chung
Calorie restriction (CR) is known to confer health benefits, including longevity and disease prevention. Although CR is promising in preventing chronic kidney disease (CKD), its potential impact on the progression of kidney fibrosis from acute kidney injury (AKI) to CKD remains unclear. Here, we present evidence that CR exacerbates renal damage in a mouse model of folic acid (FA)-induced renal fibrosis by altering mitochondrial metabolism and inflammation. Mice subjected to CR (60% of ad libitum) for three days were subjected to high dose of FA (250 mg/kg) injection and maintained under CR for an additional week before being sacrificed. Biochemical analyses showed that CR mice exhibited increased kidney injury and fibrosis. RNA sequencing analysis demonstrated decreased electron transport and oxidative phosphorylation (OXPHOS) in CR kidneys with injury, heightened inflammatory, and fibrotic responses. CR significantly decreased OXPHOS gene and protein levels and reduced β-oxidation-associated proteins in the kidney. To determine whether defects in mitochondrial metabolism is associated with inflammation in the kidney, further in vitro experiments were performed. NRK52E kidney epithelial cells were treated with antimycin A to induce mitochondrial damage. Antimycin A treatment significantly increased chemokine expression via a STING-dependent pathway. Serum restriction in NRK49F kidney fibroblasts was observed to enhance the fibrotic response induced by TGFβ under in vitro conditions. In summary, our results indicate that CR exacerbates fibrosis and inflammatory responses in the kidney by altering mitochondrial metabolism, highlighting the importance of adequate energy supply for an effective response to AKI and fibrosis development.
众所周知，卡路里限制（CR）对健康有益，包括延年益寿和预防疾病。尽管卡路里限制在预防慢性肾脏病（CKD）方面大有可为，但它对肾脏纤维化从急性肾损伤（AKI）发展到慢性肾脏病的潜在影响仍不清楚。在这里，我们提出证据表明，在叶酸（FA）诱导的肾脏纤维化小鼠模型中，CR会通过改变线粒体代谢和炎症加剧肾脏损伤。对小鼠进行为期3天的CR治疗（60%的自由饮食）后，对其注射高剂量的叶酸（250毫克/千克），并在CR治疗下再维持一周后将其处死。生化分析表明，CR 小鼠的肾损伤和纤维化加剧。RNA测序分析表明，CR肾脏中的电子传递和氧化磷酸化（OXPHOS）功能降低，并伴有损伤、炎症和纤维化反应加重。CR 肾脏中的 OXPHOS 基因和蛋白水平明显降低，β-氧化相关蛋白也有所减少。为了确定线粒体代谢缺陷是否与肾脏炎症有关，我们进行了进一步的体外实验。用抗霉素 A 处理 NRK52E 肾上皮细胞以诱导线粒体损伤。抗霉素 A 可通过 STING 依赖性途径显著增加趋化因子的表达。在体外条件下，观察到 NRK49F 肾成纤维细胞的血清限制增强了 TGFβ 诱导的纤维化反应。总之，我们的研究结果表明，CR 通过改变线粒体代谢加剧了肾脏的纤维化和炎症反应，突出了充足的能量供应对于有效应对 AKI 和纤维化发展的重要性。
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Glucosamine (GlcN) is one of the dietary supplements used in the treatment of osteoarthritis. Endogenously, GlcN is synthesized from glucose through the hexosamine pathway. In addition to ameliorating arthritis, several biological functions of GlcN have been reported, including insulin resistance in skeletal muscle. However, the regulatory role of GlcN in skeletal muscle development is not clear. We therefore investigated the effect of GlcN on myoblast proliferation, differentiation, and myotube development and their underlying mechanisms in C2C12 cells. Myoblast proliferation was measured by MTT assay. The expressions of MyoD, myogenin (MyoG), and myosin heavy chain (MyHC) were identified as determinants of myoblast differentiation. Expressions of atrogin-1 and muscle RING-finger protein-1 (MuRF-1) were identified as markers of myotube atrophy. The results show that treatment with GlcN significantly reduced myoblast proliferation and phosphorylation of Stat3 and S6K. These findings suggest that GlcN can inhibit growth of myoblasts through inhibiting phosphorylation of Stat3 and S6K. In addition, GlcN significantly suppressed the expression of MyoD, MyoG, and MyHC, as well as myotube formation. Pretreatment of C2C12 myoblast cells with ER stress inhibitors significantly blocked GlcN-inhibited MyHC expression and myotube formation. It can be concluded that GlcN suppressed myogenic differentiation via a pathway that involved ER stress. Moreover, GlcN decreased myotube diameter and expression of MyHC, as well as increased MuRF-1 in C2C12 myotubes. Meanwhile, GlcN also reduced the expressions of phosphorylated Akt and mTOR were stimulated after GlcN treatment in C2C12 myotubes. Thus, GlcN induced skeletal muscle atrophy by inhibiting the protein synthesis pathway. Chronic GlcN infusion also caused skeletal muscle atrophy in mice. In conclusion, GlcN regulated important stages of skeletal muscle development through different signaling pathways.
{"title":"Glucosamine inhibits myoblast proliferation and differentiation, and stimulates myotube atrophy through distinct signal pathways","authors":"Shui-Yu Liu , Luen-Kui Chen , Yi-Ting Chung , Chien-Wei Chen , Guan-Lin Wu , Yi-Chieh Chang , Pin-Rong Chen , Yuan-I Chang , Heng-Fu Lin , Liang-Yi Wu , Chi-Chang Juan","doi":"10.1016/j.jnutbio.2024.109762","DOIUrl":"10.1016/j.jnutbio.2024.109762","url":null,"abstract":"<div><div>Glucosamine (GlcN) is one of the dietary supplements used in the treatment of osteoarthritis. Endogenously, GlcN is synthesized from glucose through the hexosamine pathway. In addition to ameliorating arthritis, several biological functions of GlcN have been reported, including insulin resistance in skeletal muscle. However, the regulatory role of GlcN in skeletal muscle development is not clear. We therefore investigated the effect of GlcN on myoblast proliferation, differentiation, and myotube development and their underlying mechanisms in C2C12 cells. Myoblast proliferation was measured by MTT assay. The expressions of MyoD, myogenin (MyoG), and myosin heavy chain (MyHC) were identified as determinants of myoblast differentiation. Expressions of atrogin-1 and muscle RING-finger protein-1 (MuRF-1) were identified as markers of myotube atrophy. The results show that treatment with GlcN significantly reduced myoblast proliferation and phosphorylation of Stat3 and S6K. These findings suggest that GlcN can inhibit growth of myoblasts through inhibiting phosphorylation of Stat3 and S6K. In addition, GlcN significantly suppressed the expression of MyoD, MyoG, and MyHC, as well as myotube formation. Pretreatment of C2C12 myoblast cells with ER stress inhibitors significantly blocked GlcN-inhibited MyHC expression and myotube formation. It can be concluded that GlcN suppressed myogenic differentiation via a pathway that involved ER stress. Moreover, GlcN decreased myotube diameter and expression of MyHC, as well as increased MuRF-1 in C2C12 myotubes. Meanwhile, GlcN also reduced the expressions of phosphorylated Akt and mTOR were stimulated after GlcN treatment in C2C12 myotubes. Thus, GlcN induced skeletal muscle atrophy by inhibiting the protein synthesis pathway. Chronic GlcN infusion also caused skeletal muscle atrophy in mice. In conclusion, GlcN regulated important stages of skeletal muscle development through different signaling pathways.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"135 ","pages":"Article 109762"},"PeriodicalIF":4.8,"publicationDate":"2024-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142289534","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-07DOI: 10.1016/j.jnutbio.2024.109761
Margaret J. Morris , Kyoko Hasebe , Arya L. Shinde , Michael K. H Leong , Md. Mustahsan Billah , Sonia Hesam-Shariati , Michael D. Kendig
Time-restricted feeding (TRF) is a popular dietary strategy whereby daily food intake is limited to a <12h window. As little is known about the effects of TRF on cognitive and behavioral measures, the present study examined the effects of time-restricted (8h/day; zeitgeber time [ZT]12–20) or continuous access to a high-fat, high-sugar cafeteria-style diet (Caf; Caf and Caf-TRF groups; n=12 adult male Sprague-Dawley rats) or standard chow (Chow and Chow-TRF groups) on short-term memory, anxiety-like behavior, adiposity and gut microbiota composition over 13-weeks with daily food intake measures. TRF significantly reduced daily energy intake in Caf- but not chow-fed groups. In Caf-fed groups, TRF reduced the proportion of energy derived from sugar while increasing that derived from protein. Caf diet significantly increased weight gain, adiposity and fasting glucose within 4 weeks; TRF partially reduced these effects. Caf diet increased anxiety-like behavior in the Elevated Plus Maze in week 3 but not week 12, and impaired hippocampal-dependent place recognition memory in week 11; neither measure was affected by TRF. Global microbiota composition differed markedly between chow and Caf groups, with a small effect of TRF in rats fed chow. In both chow and Caf diet groups, TRF reduced microbiota alpha diversity measures of Shannon diversity and evenness relative to continuous access. Results indicate only limited benefits of TRF access to an obesogenic diet under these conditions, suggesting that more severe time restriction may be required to offset adverse metabolic and cognitive effects when using highly palatable diets.
限时喂养（TRF）是一种流行的饮食策略，即把每天的食物摄入量限制在一定的范围内。
{"title":"Time-restricted feeding does not prevent adverse effects of palatable cafeteria diet on adiposity, cognition and gut microbiota in rats","authors":"Margaret J. Morris , Kyoko Hasebe , Arya L. Shinde , Michael K. H Leong , Md. Mustahsan Billah , Sonia Hesam-Shariati , Michael D. Kendig","doi":"10.1016/j.jnutbio.2024.109761","DOIUrl":"10.1016/j.jnutbio.2024.109761","url":null,"abstract":"<div><div>Time-restricted feeding (TRF) is a popular dietary strategy whereby daily food intake is limited to a <12h window. As little is known about the effects of TRF on cognitive and behavioral measures, the present study examined the effects of time-restricted (8h/day; zeitgeber time [ZT]12–20) or continuous access to a high-fat, high-sugar cafeteria-style diet (Caf; Caf and Caf-TRF groups; <em>n</em>=12 adult male Sprague-Dawley rats) or standard chow (Chow and Chow-TRF groups) on short-term memory, anxiety-like behavior, adiposity and gut microbiota composition over 13-weeks with daily food intake measures. TRF significantly reduced daily energy intake in Caf- but not chow-fed groups. In Caf-fed groups, TRF reduced the proportion of energy derived from sugar while increasing that derived from protein. Caf diet significantly increased weight gain, adiposity and fasting glucose within 4 weeks; TRF partially reduced these effects. Caf diet increased anxiety-like behavior in the Elevated Plus Maze in week 3 but not week 12, and impaired hippocampal-dependent place recognition memory in week 11; neither measure was affected by TRF. Global microbiota composition differed markedly between chow and Caf groups, with a small effect of TRF in rats fed chow. In both chow and Caf diet groups, TRF reduced microbiota alpha diversity measures of Shannon diversity and evenness relative to continuous access. Results indicate only limited benefits of TRF access to an obesogenic diet under these conditions, suggesting that more severe time restriction may be required to offset adverse metabolic and cognitive effects when using highly palatable diets.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"134 ","pages":"Article 109761"},"PeriodicalIF":4.8,"publicationDate":"2024-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142289540","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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