{"title":"Pharmacological benefits of <i>Acacia</i> against metabolic diseases: intestinal-level bioactivities and favorable modulation of gut microbiota.","authors":"Manas Ranjan Saha, Priyankar Dey","doi":"10.1080/13813455.2021.1966475","DOIUrl":"10.1080/13813455.2021.1966475","url":null,"abstract":"<p><strong>Context: </strong>Obesity-associated chronic metabolic disease is a leading contributor to mortality globally. Plants belonging to the genera <i>Acacia</i> are routinely used for the treatment of diverse metabolic diseases under different ethnomedicinal practices around the globe.</p><p><strong>Objective: </strong>The current review centres around the pharmacological evidence of intestinal-level mechanisms for metabolic health benefits by <i>Acacia</i> spp.</p><p><strong>Results: </strong><i>Acacia</i> spp. increase the proportions of gut commensals (<i>Bifidobacterium</i> and <i>Lactobacillus</i>) and reduces the population of opportunistic pathobionts (<i>Escherichia coli</i> and <i>Clostridium</i>). <i>Acacia</i> gum that is rich in fibre, can also be a source of prebiotics to improve gut health. The intestinal-level anti-inflammatory activities of <i>Acacia</i> are likely to contribute to improvements in gut barrier function that would prevent gut-to-systemic endotoxin translocation and limit \"low-grade\" inflammation associated with metabolic diseases.</p><p><strong>Conclusion: </strong>This comprehensive review for the first time has emphasised the intestinal-level benefits of <i>Acacia</i> spp. which could be instrumental in limiting the burden of metabolic disease.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39326061","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Abrogation of cardiomyopathy in diabetic rats by escin - possible role of NF-κβ and MCP-1.","authors":"Sachin V Suryavanshi, Yogesh A Kulkarni","doi":"10.1080/13813455.2021.1963782","DOIUrl":"10.1080/13813455.2021.1963782","url":null,"abstract":"<p><strong>Objective: </strong>Diabetic cardiomyopathy is one of the most common complications of diabetes. Escin may significantly inhibit myocardial damage through its NF-κβ inhibitory, antidiabetic, neuroprotective, and potent anti-inflammatory activity. Hence, the study was carried out to evaluate the effect of escin in diabetic cardiomyopathy.</p><p><strong>Methods: </strong>Diabetes induction was done in rats with streptozotocin. After six weeks of induction, diabetic animals were administered with escin (5, 10, and 20 mg/kg) for the next four weeks.</p><p><strong>Results: </strong>Escin prevented the progression of abnormalities in the biochemical, hemodynamic parameters and electrocardiogram. Escin also prevented the progression of abnormality in the oxidative stress parameters. The expression of NF-κβ and MCP-1 was significantly reduced with escin treatment. Furthermore, escin also prevented damage to myocardial cells and reduced collagen deposition in the cardiomyocytes.</p><p><strong>Conclusion: </strong>Escin prevented the progression of cardiomyopathy in diabetic rats. Hence escin can be an alternative option for the management of diabetic cardiomyopathy.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39314895","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Elham Karimi-Sales, Gisou Mohaddes, Mohammad Reza Alipour
{"title":"Hepatoprotection of capsaicin in alcoholic and non-alcoholic fatty liver diseases.","authors":"Elham Karimi-Sales, Gisou Mohaddes, Mohammad Reza Alipour","doi":"10.1080/13813455.2021.1962913","DOIUrl":"10.1080/13813455.2021.1962913","url":null,"abstract":"<p><p>Alcoholic liver disease (ALD) and non-alcoholic fatty liver disease (NAFLD) are common causes of chronic liver disease that share the range of steatosis, steatohepatitis, fibrosis, cirrhosis, and finally, hepatocellular carcinoma. They are identified by the dysregulation of disease-specific signalling pathways and unique microRNAs. Capsaicin is an active ingredient of chilli pepper that acts as an agonist of transient receptor potential vanilloid subfamily 1. It seems that the protective role of capsaicin against NAFLD and ALD is linked to its anti-steatotic, antioxidant, anti-inflammatory, and anti-fibrotic effects. Capsaicin-induced inhibiting metabolic syndrome and gut dysbiosis and increasing bile acids production are also involved in its anti-NAFLD role. This review summarises the different molecular mechanisms underlying the protective role of capsaicin against NAFLD and ALD. More experimental studies are needed to clarify the effects of capsaicin on the expression of genes involved in hepatic lipid metabolism and hepatocytes apoptosis in NAFLD and ALD.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39326624","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The triggering pathway, the metabolic amplifying pathway, and cellular transduction in regulation of glucose-dependent biphasic insulin secretion.","authors":"Shradha Bisht, Mamta F Singh","doi":"10.1080/13813455.2023.2299920","DOIUrl":"https://doi.org/10.1080/13813455.2023.2299920","url":null,"abstract":"<p><p><b>Introduction:</b> Insulin secretion is a highly regulated process critical for maintaining glucose homeostasis. This abstract explores the intricate interplay between three essential pathways: The Triggering Pathway, The Metabolic Amplifying Pathway, and Cellular Transduction, in orchestrating glucose-dependent biphasic insulin secretion.<b>Mechanism:</b> During the triggering pathway, glucose metabolism in pancreatic beta-cells leads to ATP production, closing ATP-sensitive potassium channels and initiating insulin exocytosis. The metabolic amplifying pathway enhances insulin secretion via key metabolites like NADH and glutamate, enhancing calcium influx and insulin granule exocytosis. Additionally, the cellular transduction pathway involves G-protein coupled receptors and cyclic AMP, modulating insulin secretion.<b>Result and Conclusion:</b> These interconnected pathways ensure a dynamic insulin response to fluctuating glucose levels, with the initial rapid phase and the subsequent sustained phase. Understanding these pathways' complexities provides crucial insights into insulin dysregulation in diabetes and highlights potential therapeutic targets to restore glucose-dependent insulin secretion.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2024-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139401617","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Tomatidine ameliorates high-fat-diet/streptozocin (HFD/STZ)-induced type 2 diabetes mellitus in mice.","authors":"Li Cai, Baojian Hou, Juping Hu","doi":"10.1080/13813455.2023.2298404","DOIUrl":"https://doi.org/10.1080/13813455.2023.2298404","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the effects of tomatidine (Td) on the progression of type 2 diabetes mellitus (T2DM) in mice and uncover the mechanism.</p><p><strong>Methods: </strong>T2DM mice model was induced by high-fat diet (HFD) and intrabitoneal injection of streptozotocin (STZ). The mice were grouped as follows: 1, control; 2, T2D; 3, T2D + tomatidine (5 mg/kg); 4, T2D + tomatidine (10 mg/kg); 5, T2D + tomatidine (20 mg/kg). Fasting blood glucose was detected by glucose metre and fasting insulin was detected by the kit to determine the effect of Td on T2DM mice. ELISA, qPCR, and Immunoblot assays were performed to detect the effects of Td on the hepatic glucose homeostasis and inflammation of mice. Immunoblot assays further confirmed the mechanism.</p><p><strong>Results: </strong>Td improved blood glucose and insulin resistance in T2DM mice. In addition, Td improved liver function and lipid metabolism disorder in T2DM mice. Td also affected the liver glucose homeostasis related genes in T2DM mice. Td alleviated serum inflammation in T2DM mice. We further found that Td activated AMPK pathway, therefore ameliorating T2DM.</p><p><strong>Conclusion: </strong>Td ameliorated HFD/STZ-induced T2DM in mice, suggesting that it could serve as a drug of T2DM.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2024-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139377147","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The oral microbial odyssey influencing chronic metabolic disease.","authors":"Upasana Gupta, Priyankar Dey","doi":"10.1080/13813455.2023.2296346","DOIUrl":"https://doi.org/10.1080/13813455.2023.2296346","url":null,"abstract":"<p><strong>Introduction: </strong>Since the oral cavity is the gateway to the gut, oral microbes likely hold the potential to influence metabolic disease by affecting the gut microbiota.</p><p><strong>Method: </strong>A thorough review of literature has been performed to link the alterations in oral microbiota with chronic metabolic disease by influencing the gut microbiota.</p><p><strong>Result: </strong>A strong correlation exists between abnormalities in oral microbiota and several systemic disorders, such as cardiovascular disease, diabetes, and obesity, which likely initially manifest as oral diseases. Ensuring adequate oral hygiene practices and cultivating diverse oral microflora are crucial for the preservation of general well-being. Oral bacteria have the ability to establish and endure in the gastrointestinal tract, leading to the development of prolonged inflammation and activation of the immune system. Oral microbe-associated prophylactic strategies could be beneficial in mitigating metabolic diseases.</p><p><strong>Conclusion: </strong>Oral microbiota can have a profound impact on the gut microbiota and influence the pathogenesis of metabolic diseases.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2023-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139032120","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Zaida Zakaria, Zaidatul Akmal Othman, Victor Udo Nna, Mahaneem Mohamed
{"title":"The promising roles of medicinal plants and bioactive compounds on hepatic lipid metabolism in the treatment of non-alcoholic fatty liver disease in animal models: molecular targets.","authors":"Zaida Zakaria, Zaidatul Akmal Othman, Victor Udo Nna, Mahaneem Mohamed","doi":"10.1080/13813455.2021.1939387","DOIUrl":"10.1080/13813455.2021.1939387","url":null,"abstract":"<p><p>Imbalance in hepatic lipid metabolism can lead to an abnormal triglycerides deposition in the hepatocytes which can cause non-alcoholic fatty liver disease (NAFLD). Four main mechanisms responsible for regulating hepatic lipid metabolism are fatty acid uptake, de novo lipogenesis, lipolysis and fatty acid oxidation. Controlling the expression of transcription factors at molecular level plays a crucial role in NAFLD management. This paper reviews various medicinal plants and their bioactive compounds emphasising mechanisms involved in hepatic lipid metabolism, other important NAFLD pathological features, and their promising roles in managing NAFLD through regulating key transcription factors. Although there are many medicinal plants popularly investigated for NAFLD treatment, there is still little information and scientific evidence available and there has been no research on clinical trials scrutinised on this matter. This review also aims to provide molecular information of medicinal plants in NALFD treatment that might have potentials for future scientifically controlled studies.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/13813455.2021.1939387","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39253937","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"<i>Securidaca inappendiculata</i> stem extract confers robust antioxidant and antidiabetic effects against high fructose/streptozotocin induced type 2 diabetes in rats. Exploration of bioactive compounds using UHPLC-ESI-QTOF-MS.","authors":"Opeyemi Joshua Olatunji, Jian Zuo, Oladipupo Odunayo Olatunde","doi":"10.1080/13813455.2021.1921811","DOIUrl":"10.1080/13813455.2021.1921811","url":null,"abstract":"<p><p>Diabetes mellitus is the most deadly and most prevalent metabolic disease of contemporary times. This study evaluated the antidiabetic, antioxidant, and pancreato-protective effects of <i>Securidaca inappendiculata</i> extract (SIE) in high-fructose/streptozotocin-induced type 2 diabetes. SIE (50, 100, and 200 mg/kg) was administered to diabetic rats for 8 weeks, thereafter glycaemic parameters, pancreatic β cell function, lipid profile, hepatorenal function, and antioxidant parameters were evaluated in diabetic rats treated SIE. The results indicated that treatment with SIE markedly lowered blood glucose, lipid parameters, hepatorenal function parameters, and lipid peroxidation at the end of the intervention. Additionally, serum insulin levels were significantly increased as supported by restoration of pancreatic β-cell cells in the H&E staining. Moreover, SIE also upregulated serum antioxidant enzyme activities in the treated diabetic rats. The results revealed that SIE possesses potent antihyperglycemic and antihyperlipidemic and antioxidant effects with the considerable restoration of pancreatic β-cells function.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/13813455.2021.1921811","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38977918","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Li Zheng, Yalan Wang, Yanhong Li, Li Li, Xiaohong Wang, Yan Li
{"title":"miR-765 targeting PDX1 impairs pancreatic β-cell function to induce type 2 diabetes.","authors":"Li Zheng, Yalan Wang, Yanhong Li, Li Li, Xiaohong Wang, Yan Li","doi":"10.1080/13813455.2021.1946561","DOIUrl":"10.1080/13813455.2021.1946561","url":null,"abstract":"<p><p>Type 2 diabetes (T2DM) is a chronic metabolism disorder with a symptom as pancreatic β-cell dysfunction. In this study, the bioinformatics analysis identified the key regulators (PDX1 and miR-765) in T2DM. By qRT-PCR and western blotting, miR-765 with high expression and PDX1 with low expression were observed in blood samples from T2DM patients and the T2DM cell model. Together with GSIS assay, CCK-8, TUNEL assay, glycolysis assay, and mitochondrial respiration assay, miR-765 overexpression impaired insulin secretion cell viability, glycolysis, and mitochondrial respiration, while enhanced cell apoptosis in pancreatic β-cell. The Luciferase reporter, RIP, and RNA pull-down assays showed that PDX1 was the target gene of miR-765 in pancreatic β-cell. Besides, the negative effect of miR-765 on pancreatic β-cell could be overturned by PDX1 overexpression. In conclusion, we confirmed that miR-765 could cause a detrimental effect on pancreatic β-cell survival and function by targeting PDX1, which might provide new insight for T2DM therapy.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/13813455.2021.1946561","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39283368","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yonghong Zhang, Shujuan Han, Tian Li, Li Zhu, Feng Wei
{"title":"Bisphenol A induces non-alcoholic fatty liver disease by promoting the O-GlcNAcylation of NLRP3.","authors":"Yonghong Zhang, Shujuan Han, Tian Li, Li Zhu, Feng Wei","doi":"10.1080/13813455.2023.2288533","DOIUrl":"10.1080/13813455.2023.2288533","url":null,"abstract":"<p><p>Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease. The mechanism by which bisphenol A (BPA) promots NAFLD remains unclear. Palmitic acid (PA) and lipopolysaccharide (LPS) were used to simulate NAFLD in HepG2 cells <i>in vitro</i>. Total cholesterol (TC), triglyceride (TG) content, and lipid accumulation were measured to evaluate lipid metabolism. The caspase-1-stained cells and NLRP3 inflammasome-associated proteins were evaluated for pyroptosis. Western blot analysis was used to detect protein levels and co-immunoprecipitation (Co-IP) was used to detect the association between the proteins. Cycloheximide (CHX) treatment combined with western blot was performed to access protein stability. This data have shown that BPA induces lipid metabolism dysfunction and pyroptosis by upregulating O-GlcNAc transferase (OGT) level. NLRP3 directly interacts with OGT, and elevated OGT enhanced the stability of NLRP3 protein. BPA promoted OGT-mediated O-GlcNAcylation to stabilised NLRP3, thus accelerating NAFLD progress <i>in vitro</i>. Our study reveals that BPA, as an environmental factor, may be involved in the promotion of NAFLD, and that targeting NLRP3 and OGT may inhibit BPA's induction of NAFLD.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138457563","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}