Archives of Physiology and Biochemistry最新文献

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Leptin Rs7799039 polymorphism is associated with type 2 diabetes mellitus Egyptian patients. 瘦素Rs7799039多态性与埃及2型糖尿病患者相关。
IF 3 4区 医学
Archives of Physiology and Biochemistry Pub Date : 2023-10-15 DOI: 10.1080/13813455.2023.2265078
Amal Ahmed Mohamed, Dina M Abo-Elmatty, Alaa S Wahba, Omnia Ezzat Esmail, Hadeer Saied Mahmoud Salim, Wafaa Salah Mohammed Hegab, Mona Mostafa Farid Ghanem, Nadia Youssef Riad, Doaa Ghaith, Lamiaa I Daker, Shorouk Issa, Noha Hassan Radwan, Eman Sultan, Omar Mohamoud Azzam, Ehab A M El-Shoura
{"title":"Leptin Rs7799039 polymorphism is associated with type 2 diabetes mellitus Egyptian patients.","authors":"Amal Ahmed Mohamed,&nbsp;Dina M Abo-Elmatty,&nbsp;Alaa S Wahba,&nbsp;Omnia Ezzat Esmail,&nbsp;Hadeer Saied Mahmoud Salim,&nbsp;Wafaa Salah Mohammed Hegab,&nbsp;Mona Mostafa Farid Ghanem,&nbsp;Nadia Youssef Riad,&nbsp;Doaa Ghaith,&nbsp;Lamiaa I Daker,&nbsp;Shorouk Issa,&nbsp;Noha Hassan Radwan,&nbsp;Eman Sultan,&nbsp;Omar Mohamoud Azzam,&nbsp;Ehab A M El-Shoura","doi":"10.1080/13813455.2023.2265078","DOIUrl":"https://doi.org/10.1080/13813455.2023.2265078","url":null,"abstract":"<p><strong>Background: </strong>Leptin (LEP) is an anti-obesity hormone that regulates food intake, energy expenditure, and glucose metabolism. The genetic variants in LEP and the LEP receptor (LEPR) gene may play an important role in the pathogenesis of type 2 diabetes mellitus (T2DM) and obesity. The current study aimed to investigate the association of serum LEP levels, and LEP polymorphisms in LEP (rs7799039, 2548 G/A) with T2DM in Egyptian patients.</p><p><strong>Methods: </strong>A total of 205 subjects were included in the present case-control study, consisting of 100 T2DM patients and 105 healthy controls. The anthropometric, psychometric, and biochemical measurements were taken from all the subjects. The genotyping of LEP gene variants was carried out by polymerase chain reaction TaqMan technology. Serum LEP levels were measured by the ELISA technique.</p><p><strong>Results: </strong>T2DM patients had significantly elevated levels of glycated haemoglobin (HbA1c), fasting blood sugar (FBS), postprandial blood sugar (PPBS), international normalisation ratio (INR), creatinine, urea, cholesterol, triglyceride (TG), and low-density lipoproteins (LDL) and significantly decreased high-density lipoprotein (HDL) compared to healthy subjects. serum LEP levels were significantly decreased <i>p</i> (<0.001) as compared to the control group. LEP gene SNP rs7799039 was associated with an increased diabetic risk with A allele being more frequent in T2DM patients than control subjects. The distribution of the AA genotype and GA genotype of LEP SNP rs7799039 was higher in the diabetic group than control one. In addition, AA + GA genotype carriers had significantly elevated HbA1c, FBS, PPBS, TG, and LDL levels and on the contrary, decreased serum LEP levels compared to GG homozygotes.</p><p><strong>Conclusion: </strong>The genetic polymorphism rs7799039 showed a highly significant correlation with blood LEP. The co-dominant and dominant models of the LEP genetic polymorphism (rs7799039, 2548 G/A) were shown to have a significant correlation with complicated and uncomplicated diabetes individuals, but we have found that serum LEP levels were inversely related with control and diabetes patients. A positive significant association was found between LEP genetic polymorphism (rs7799039, 2548 G/A) and serum LEP in patients and controls. LEP levels and its rs7799039 genetic variant may play a vital role in increasing T2DM susceptibility.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2023-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41231912","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}
引用次数: 0
Intermittent fasting in health and disease. 健康和疾病方面的间歇性禁食。
IF 3 4区 医学
Archives of Physiology and Biochemistry Pub Date : 2023-10-13 DOI: 10.1080/13813455.2023.2268301
Anubhav Mishra, Devika Sobha, Dimple Patel, Padmanaban S Suresh
{"title":"Intermittent fasting in health and disease.","authors":"Anubhav Mishra,&nbsp;Devika Sobha,&nbsp;Dimple Patel,&nbsp;Padmanaban S Suresh","doi":"10.1080/13813455.2023.2268301","DOIUrl":"https://doi.org/10.1080/13813455.2023.2268301","url":null,"abstract":"<p><strong>Context: </strong>Intermittent fasting, a new-age dietary concept derived from an age-old tradition, involves repetitive cycles of fasting/calorie restriction and eating.</p><p><strong>Objective: </strong>We aim to take a deep dive into the biological responses to intermittent fasting, delineate the disease-modifying and cognitive effects of intermittent fasting, and also shed light on the possible side effects.</p><p><strong>Methods: </strong>Numerous <i>in vitro</i> and <i>in vivo</i> studies were reviewed, followed by an in-depth analysis, and compilation of their implications in health and disease.</p><p><strong>Results: </strong>Intermittent fasting improves the body's stress tolerance, which is further amplified with exercise. It impacts various pathological conditions like cancer, obesity, diabetes, cardiovascular disease, and neurodegenerative diseases.</p><p><strong>Conclusion: </strong>During dietary restriction, the human body experiences a metabolic switch due to the depletion of liver glycogen, which promotes a shift towards utilising fatty acids and ketones in the system, thereby significantly impacting adiposity, ageing and the immune response to various diseases.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2023-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41189552","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}
引用次数: 1
Ellagic acid reduces hepatic lipid contents through regulation of SIRT1 and AMPK in old rats. Ellagic酸通过调节SIRT1和AMPK降低老年大鼠肝脏脂质含量。
IF 3 4区 医学
Archives of Physiology and Biochemistry Pub Date : 2023-10-10 DOI: 10.1080/13813455.2023.2262165
Mahdis Rahimi Naiini, Beydolah Shahouzehi, Mohammad Khaksari, Shahrzad Azizi, Niloufar Naghibi, Mahdieh Nazari-Robati
{"title":"Ellagic acid reduces hepatic lipid contents through regulation of SIRT1 and AMPK in old rats.","authors":"Mahdis Rahimi Naiini,&nbsp;Beydolah Shahouzehi,&nbsp;Mohammad Khaksari,&nbsp;Shahrzad Azizi,&nbsp;Niloufar Naghibi,&nbsp;Mahdieh Nazari-Robati","doi":"10.1080/13813455.2023.2262165","DOIUrl":"https://doi.org/10.1080/13813455.2023.2262165","url":null,"abstract":"<p><strong>Objective: </strong>Ellagic acid is used in traditional medicine for the treatment of lipid disorders. In this study, the effects of ellagic acid on key regulators of lipid metabolism, and histopathological alterations in aged liver were examined.</p><p><strong>Methods: </strong>A total of 21 male Wistar rats were divided into three groups, including young control, old control, and old ellagic acid. After one month of treatment with ellagic acid, the expression levels of hepatic SIRT1, AMPK, SREBP-1c, PPAR-α, and phosphorylated AMPK (p-AMPK) were evaluated. The levels of several serum biochemical factors, and hepatic triglyceride, and cholesterol contents were assessed.</p><p><strong>Results: </strong>Ellagic acid elevated the levels of SIRT1, p-AMPK, and PPAR-α and reduced SREBP-1c level in the liver of old rats. It decreased triglyceride and cholesterol contents in the aged liver and improved histopathological changes.</p><p><strong>Conclusions: </strong>The results demonstrated that ellagic acid can exert protective effects against hepatic lipid metabolism disorders induced by ageing.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2023-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41181909","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}
引用次数: 0
The role of astrocytes response triggered by hyperglycaemia during spinal cord injury. 高血糖引发的星形胶质细胞反应在脊髓损伤中的作用。
IF 3 4区 医学
Archives of Physiology and Biochemistry Pub Date : 2023-10-05 DOI: 10.1080/13813455.2023.2264538
C Sámano, G L Mazzone
{"title":"The role of astrocytes response triggered by hyperglycaemia during spinal cord injury.","authors":"C Sámano,&nbsp;G L Mazzone","doi":"10.1080/13813455.2023.2264538","DOIUrl":"https://doi.org/10.1080/13813455.2023.2264538","url":null,"abstract":"<p><p><b>Objective:</b> This manuscript aimed to provide a comprehensive overview of the physiological, molecular, and cellular mechanisms triggered by reactive astrocytes (RA) in the context of spinal cord injury (SCI), with a particular focus on cases involving hyperglycaemia.<b>Methods:</b> The compilation of articles related to astrocyte responses in neuropathological conditions, with a specific emphasis on those related to SCI and hyperglycaemia, was conducted by searching through databases including Science Direct, Web of Science, and PubMed.<b>Results and Conclusions:</b> This article explores the dual role of astrocytes in both neurophysiological and neurodegenerative conditions within the central nervous system (CNS). In the aftermath of SCI and hyperglycaemia, astrocytes undergo a transformation into RA, adopting a distinct phenotype. While there are currently no approved therapies for SCI, various therapeutic strategies have been proposed to alleviate the detrimental effects of RAs following SCI and hyperglycemia. These strategies show promising potential in the treatment of SCI and its likely comorbidities.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2023-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41098429","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}
引用次数: 0
Tumour necrosis factor α-308 G/a and -238 G/a polymorphisms as predicator of diabetic retinopathy in Egyptians. 肿瘤坏死因子α-308 G/a和-238 G/a多态性作为埃及人糖尿病视网膜病变的预测因子。
IF 3 4区 医学
Archives of Physiology and Biochemistry Pub Date : 2023-10-01 Epub Date: 2021-04-29 DOI: 10.1080/13813455.2021.1908365
Leqaa Abd Al Azeem Moemen, Mohamed El Shahat Ebeid, Amira A Abdelazeem, Mahmoud Kenawy M Kenawy, Zeinab M Osman
{"title":"Tumour necrosis factor α-308 G/a and -238 G/a polymorphisms as predicator of diabetic retinopathy in Egyptians.","authors":"Leqaa Abd Al Azeem Moemen,&nbsp;Mohamed El Shahat Ebeid,&nbsp;Amira A Abdelazeem,&nbsp;Mahmoud Kenawy M Kenawy,&nbsp;Zeinab M Osman","doi":"10.1080/13813455.2021.1908365","DOIUrl":"10.1080/13813455.2021.1908365","url":null,"abstract":"<p><strong>Background: </strong>Diabetic retinopathy (DR) is a duration dependent serious micro vascular insult of diabetes mellitus. Inflammation has a critical role in the development of early and late stage of DR. Tumour necrosis factor alpha (TNF-α) is an inflammatory cytokine that promoteup regulation of adhesion molecule expression, leukocyte recruitment and monocyte attraction. TNF-α levels are increased in retinas or vitreous of diabetic animals. A cross-sectional, observational study was performed in a sample of diabetic patients who attend diabetes polyclinic of RIO Hospital, Giza, Egypt, between October 2016 and December 2019. Three hundred diabetic patients were studied (150 males and 150 females). 100 diabetic patients without retinopathy, 100 diabetic patients with proliferative retinopathy (PDR), 100diabetic patients with non-proliferative retinopathy (NPDR), also 100 healthy subjects as a control group All patients and subjects were analysed for serum TNF-α levels by ELISA assay and -308 G/A and -238 G/A polymorphism by using Restriction fragment length polymorphisms.</p><p><strong>Aim: </strong>Evaluating the role of tumour necrosis factor α and -308 G/A, -238 G/A polymorphisms in the pathogenesis of proliferative diabetic retinopathy among Egyptian patients.</p><p><strong>Results: </strong>A statistically significant increase in TNF-α levels was detected in diabetic without retinopathy, NPDR and PDR groups compared to control group (<i>p</i> > .001). There were no significant different in Genotype and allele frequencies of the -308G/A, and -238 G/A, polymorphisms in both NPDR and PDR. However, the G/G genotype of the -308 G/A polymorphism occurred more frequently in PDR patients with than NPDR patients (0.74% vs 0.68%).</p><p><strong>Conclusion: </strong>The present study clearly demonstrated increased levels of TNF-α, in diabetic patients with diabetic without retinopathy, NPDR and PDR. Furthermore, this study suggested that TNF-α assay could be used as diagnostic tools to predict the initiation and progression of diabetic retinopathy. They could serve as biomarkers not only for an early detection of the disease, but also to monitor the effects of therapy. Also, the G/G genotype of the -308 G/A polymorphism and the G allele of TNF-α gene were more frequent in PDR patients than with NPDR.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/13813455.2021.1908365","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10620638","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}
引用次数: 0
Exploring plant-based alpha-glucosidase inhibitors: promising contenders for combatting type-2 diabetes. 探索植物性α-葡萄糖苷酶抑制剂:对抗2型糖尿病的有力竞争者。
IF 3 4区 医学
Archives of Physiology and Biochemistry Pub Date : 2023-09-28 DOI: 10.1080/13813455.2023.2262167
Sonali Kumari, Ravi Saini, Aditi Bhatnagar, Abha Mishra
{"title":"Exploring plant-based alpha-glucosidase inhibitors: promising contenders for combatting type-2 diabetes.","authors":"Sonali Kumari,&nbsp;Ravi Saini,&nbsp;Aditi Bhatnagar,&nbsp;Abha Mishra","doi":"10.1080/13813455.2023.2262167","DOIUrl":"https://doi.org/10.1080/13813455.2023.2262167","url":null,"abstract":"<p><p><b>Objective:</b> This systematic review aimed to provide comprehensive details on the α-G inhibitory potential of various bioactive compounds derived from natural sources.<b>Methods:</b> A comprehensive literature search was conducted using various databases and search engines, including Science Direct, Google Scholar, SciFinder, Web of Science, and PubMed until May, 2023.<b>Results and conclusions:</b> The enzyme alpha-glucosidase (α-G) is found in the brush border epithelium of the small intestine and consists of duplicated glycoside hydrolase (GH31) domain. It involves the conversion of disaccharides and oligosaccharides into monosaccharides by acting on alpha (1 → 4) and (1 → 6) linked glucose residue. Once absorbed, glucose enters the bloodstream and elevates postprandial glucose, which is associated with the development of type 2 Diabetes (T2D). Epidemic obesity, cardiovascular disease, and nephropathy are linked to T2D. Traditional medicinal plants with α-G inhibitory potential are commonly used to treat T2D due to the adverse effects of currently used α-G inhibitors miglitol, acarbose, and voglibose. Various bioactive compounds derived from natural sources, including lupenone, Wilforlide A, Baicalein, Betulinic acid, Ursolic acid, Oleanolic acid, Katononic acid, Carnosol, Hypericin, Astilbin, lupeol, betulonic acid, Fagomine, Lactucaxanthin, Erythritol, GP90-1B, Procyanidins, Galangin, and vomifoliol retain α-G inhibitory potential for regulating hyperglycaemia.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2023-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41177977","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}
引用次数: 0
Dapagliflozin attenuates high glucose-and hypoxia/reoxygenation-induced injury via activating AMPK/mTOR-OPA1-mediated mitochondrial autophagy in H9c2 cardiomyocytes. 达格列净通过激活AMPK/ mtor - opa1介导的H9c2心肌细胞线粒体自噬,减轻高糖和缺氧/再氧诱导的损伤。
IF 3 4区 医学
Archives of Physiology and Biochemistry Pub Date : 2023-09-01 DOI: 10.1080/13813455.2023.2252200
Weiling Tu, Liang Li, Ming Yi, Junyu Chen, Xiaoqing Wang, Yan Sun
{"title":"Dapagliflozin attenuates high glucose-and hypoxia/reoxygenation-induced injury via activating AMPK/mTOR-OPA1-mediated mitochondrial autophagy in H9c2 cardiomyocytes.","authors":"Weiling Tu,&nbsp;Liang Li,&nbsp;Ming Yi,&nbsp;Junyu Chen,&nbsp;Xiaoqing Wang,&nbsp;Yan Sun","doi":"10.1080/13813455.2023.2252200","DOIUrl":"https://doi.org/10.1080/13813455.2023.2252200","url":null,"abstract":"<p><p>This study investigated the protective effect of dapagliflozin on H9c2 cardiomyocyte function under high glucose and hypoxia/reoxygenation (HG-H/R) conditions and identified the underlying molecular mechanisms. Dapagliflozin reduced the level of lactate dehydrogenase and reactive oxygen species in cardiomyocytes under HG-H/R conditions and was accompanied by a decrease in caspase-3/9 activity. In addition, Dapagliflozin significantly reduced mitochondrial permeability transition pore opening and increased ATP content, accompanied by upregulation of OPA1 with autophagy-related protein molecules and activation of the AMPK/mTOR signalling pathway in HG-H/R treated cardiomyocytes. OPA1 knockdown or compound C treatment attenuated the protective effects of dapagliflozin on the cardiomyocytes under HG-H/R conditions. Downregulation of OPA1 expression increased mitochondrial intolerance in cardiomyocytes during HG-H/R injury and the AMPK-mTOR-autophagy signalling is a key mechanism for protecting mitochondrial function and reducing cardiomyocyte apoptosis. Collectively, dapagliflozin exerted protective effects on the cardiomyocytes under HG-H/R conditions. Dapagliflozin attenuated myocardial HG-H/R injury by activating AMPK/mTOR-OPA1-mediated mitochondrial autophagy.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10127097","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}
引用次数: 0
Development of pancreatic islet cells in the extrahepatic bile ducts of rats with experimentally-induced metabolic syndrome. 实验性代谢综合征大鼠肝外胆管胰岛细胞的发育。
IF 3 4区 医学
Archives of Physiology and Biochemistry Pub Date : 2023-08-31 DOI: 10.1080/13813455.2023.2252205
Maya Gulubova, Anna Tolekova, Dimitar Berbatov, Nurettin Aydogdu
{"title":"Development of pancreatic islet cells in the extrahepatic bile ducts of rats with experimentally-induced metabolic syndrome.","authors":"Maya Gulubova,&nbsp;Anna Tolekova,&nbsp;Dimitar Berbatov,&nbsp;Nurettin Aydogdu","doi":"10.1080/13813455.2023.2252205","DOIUrl":"https://doi.org/10.1080/13813455.2023.2252205","url":null,"abstract":"<p><strong>Context: </strong>There is data about the existence of some endocrine cells in the epithelial layer of the bile duct in humans and rats.</p><p><strong>Objective: </strong>We evaluated Ghrelin-, Insulin-, Glucagon- and Somatostatin-positive cells in peribiliary glands, mast cells, and nerve fibres.</p><p><strong>Materials and methods: </strong>Wistar rats were used for dietary manipulation with a 15% fructose solution for 12 weeks. Tissue samples were elaborated with immunohistochemistry for Insulin, Glucagon, Ghrelin, and Somatostatin. Glucose and lipid parameters were studied.</p><p><strong>Results: </strong>In treated animals, Ghrelin<sup>+</sup> and Insulin<sup>+</sup> cells in perybiliary glands (PBGs) were significantly increased. In the male fructose group there was a significant increase of the homeostasis model assessment insulin resistance (HOMA-IR).</p><p><strong>Conclusions: </strong>Stem/progenitor cells in extrahepatic bile tree (EHBT) could be a source of Insulin-producing cells in metabolic syndrome. Fructose treatment induces the increase of Ghrelin<sup>+</sup> and Insulin<sup>+</sup> cells in PBGs and the elevation of Insulin and Ghrelin plasma concentration.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2023-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10128034","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}
引用次数: 0
A review of the last decade: pancreatic cancer and type 2 diabetes. 回顾过去十年:胰腺癌和2型糖尿病。
IF 3 4区 医学
Archives of Physiology and Biochemistry Pub Date : 2023-08-30 DOI: 10.1080/13813455.2023.2252204
Jiaqi Wu, Liang Tang, Feng Zheng, Xun Chen, Lei Li
{"title":"A review of the last decade: pancreatic cancer and type 2 diabetes.","authors":"Jiaqi Wu,&nbsp;Liang Tang,&nbsp;Feng Zheng,&nbsp;Xun Chen,&nbsp;Lei Li","doi":"10.1080/13813455.2023.2252204","DOIUrl":"https://doi.org/10.1080/13813455.2023.2252204","url":null,"abstract":"<p><p>Pancreatic cancer (PC) is a prevalent gastrointestinal tumour known for its high degree of malignancy, resulting in a mere 10% five-year survival rate for most patients. Over the past decade, a growing body of research has shed light on the intricate bidirectional association between PC and Type 2 diabetes (T2DM). The collection of PC- and T2DM-related articles is derived from two comprehensive databases, namely WOS (Web of Science Core Collection) and CNKI (China National Knowledge Infrastructure). This article discusses the last 10 years of research trends in PC and T2DM and explores their potential regulatory relationship as well as related medications.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2023-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10486862","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}
引用次数: 0
Celastrol attenuates HFD-induced obesity and improves metabolic function independent of adiponectin signaling. Celastrol减轻hfd诱导的肥胖并改善独立于脂联素信号的代谢功能。
IF 3 4区 医学
Archives of Physiology and Biochemistry Pub Date : 2023-08-29 DOI: 10.1080/13813455.2023.2250929
Ling Ye, Yan Gao, Xuecheng Li, Xiaoshuang Liang, Yi Yang, Rufeng Zhang
{"title":"Celastrol attenuates HFD-induced obesity and improves metabolic function independent of adiponectin signaling.","authors":"Ling Ye,&nbsp;Yan Gao,&nbsp;Xuecheng Li,&nbsp;Xiaoshuang Liang,&nbsp;Yi Yang,&nbsp;Rufeng Zhang","doi":"10.1080/13813455.2023.2250929","DOIUrl":"https://doi.org/10.1080/13813455.2023.2250929","url":null,"abstract":"<p><p><b>Backgound:</b> Celastrol, a leptin sensitiser, has been shown to inhibit food intake and reduce body weight in diet-induced obese mice, making it a potential treatment for obesity and metabolic diseases. Adiponectin signalling has been reported to play an important role in the treatment of obesity, inflammation, and non-alcoholic fatty liver disease.<b>Materials and methods:</b> Wild-type (WT) and AdipoR1 knockout (AdipoR1<sup>-/-</sup>) mice were placed on a chow diet or a high-fat diet (HFD) and several metabolic parameters were measured. Celastrol was then administered to the HFD-induced mice and the response of WT and AdipoR1<sup>-/-</sup> mice to celastrol in terms of body weight, blood glucose, and food intake was also recorded.<b>Results:</b> AdipoR1 knockout caused elevated blood glucose and lipids, impaired glucose tolerance and insulin resistance in mice, as well as increased susceptibility to HFD-induced obesity. After 14 days of treatment, WT and AdipoR1<sup>-/-</sup> mice showed significant reductions in body weight and blood glucose and improvements in glucose tolerance.<b>Conclusion:</b> The present study demonstrated that AdipoR1 plays a critical role in metabolic regulation and that the improvement of weight and metabolic function by celastrol is independent of the AdipoR1-mediated signalling pathway.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2023-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10103207","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}
引用次数: 0
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