Archives of Physiology and Biochemistry最新文献

{"title":"Cardiovascular protective effects of cinnamic acid as a natural phenolic acid: a review.","authors":"Leila Safaeian, Mansooreh Asghari-Varzaneh, Seyed-Sadegh Alavi, Mahnaz Halvaei-Varnousfaderani, Ismail Laher","doi":"10.1080/13813455.2024.2387694","DOIUrl":"https://doi.org/10.1080/13813455.2024.2387694","url":null,"abstract":"<p><p>Phenolic acids derived from plants have beneficial effects on cardiovascular diseases (CVD). Cinnamic acid (CA) is a crucial phenolic acid that can form numerous hydroxycinnamic derivate found in many food groups. We review current data on the cardiovascular pharmacology of CA with a focus on CVD and their risk factors including hyperlipidaemia, obesity, hyperglycaemia, cardiomyopathy and myocardial ischaemia, vascular dysfunction, oxidative stress and inflammation. Both <i>in vivo</i> and <i>in vitro</i> laboratory studies demonstrate the lipid-lowering, anti-obesity, anti-hyperglycemic, cardio-protective and vasorelaxant activities of CA. The protective impacts of CA against CVD occur by inhibiting inflammatory, oxidative, and apoptotic pathways, regulating the genes and enzymes involved in glucose and lipid metabolisms, and promoting vasodilation. This review showed that the most studied and prominent effects of CA are anti-hyperlipidemic and anti-diabetic properties. In conclusion, intake of plant foods rich in CA may reduce CVD risk especially through regulating blood glucose and lipids levels.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141888320","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":"Protective effect of Galectin-3 inhibitor against cardiac remodelling in an isoprenaline-induced myocardial infarction in type 2 diabetes.","authors":"Manal Moustafa Mahmoud, Mai Mohammed Hassan, Hany El-Sebaee Elsayed, Amal E Fares, Mona M Saber, Laila Ahmed Rashed, Omaima Mohammed Abdelwahed","doi":"10.1080/13813455.2024.2387710","DOIUrl":"https://doi.org/10.1080/13813455.2024.2387710","url":null,"abstract":"<p><p>Type 2 Diabetes mellitus (T2DM) has the potential to impair cardiac function and cause heart failure. We aimed to study the cardioprotective influence of Galactin-3 (Gal-3) inhibitor; modified citrus pectin (MCP) in isoprenaline induced myocardial infarction (MI) in T2DM rats. Forty rats were allocated into 4 groups; groups I and II served as control. T2DM was provoked in groups III and IV by serving them high fat diet followed by a single low dose of Streptozotocin (STZ), then group IV were administered MCP in drinking water for 6 weeks. Groups III and IV were then subcutaneously injected isoprenaline hydrochloride once daily on the last 2 successive days to induce MI. MCP restored echocardiographic parameters with significant decline in Gal-3 area % in cardiac tissue alongside protection against cardiac remodelling. our data showed that there is a protective potential for Gal-3 inhibitor (MCP) against cardiac injury in isoprenaline induced MI in T2DM.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141888322","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":"Asprosin-induced alterations in female rat puberty and reproductive hormonal profiles.","authors":"Emine Kacar, Zeynep Dila Oz, Ihsan Serhatlioglu, Nalan Kaya Tektemur, Mehmet Ridvan Ozdede, Tugce Yalcin, Gulendam Ozbeg, Aslisah Ozgen, Fatih Tan, Seval Ulku Orhan, Ozge Zorlu, Aysun Ucer, Abdullah Yasar, Bayram Yilmaz, Haluk Kelestimur","doi":"10.1080/13813455.2024.2386279","DOIUrl":"https://doi.org/10.1080/13813455.2024.2386279","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the comprehensive effects of daily chronic asprosin administration on various pubertal and reproductive parameters in female rats. This study aims to elucidate the role of asprosin in regulating the onset of puberty and its influence on hormonal profiles and ovarian histology.</p><p><strong>Methods: </strong>Asprosin was administered intraperitoneally (i.p.) at a dose of 500 ng/kg daily for eight weeks. Hormonal assays and histological analyses were performed to evaluate the effects of asprosin on the onset of puberty and reproductive function.</p><p><strong>Results: </strong>Daily chronic administration of asprosin accelerated the onset of the first oestrus. Hormonal assays revealed significant elevations in serum levels of Follicle-Stimulating Hormone (FSH) and Oestradiol (E2), while Inhibin B levels decreased. Histological evaluations demonstrated an increased number of primary and secondary follicles in ovarian tissue, without affecting primordial follicle counts or reproductive organ weights.</p><p><strong>Conclusions: </strong>Role of adipokines in regulating puberty and reproductive function has increasingly gained recognition. This study aimed to provide the first comprehensive examination of the effects of daily chronic asprosin administration on pubertal and reproductive parameters in female rats. Utilising hormonal assays and histological analyses, asprosin was administered intraperitoneally (i.p.) at a dose of 500 ng/kg, daily, for eight weeks. Our findings revealed that daily chronic administration of asprosin accelerated the onset of the first oestrus. Hormonal assays showed significant elevations in serum levels of Follicle-Stimulating Hormone (FSH) and Oestradiol (E2), while Inhibin B levels decreased. Histological evaluations demonstrated an increased number of primary and secondary follicles in ovarian tissue, without affecting primordial follicle counts or reproductive organ weights. These results provide new insights into asprosin's role in advancing the age of first oestrus and modulating hormonal profiles, thereby offering potential benefits to the female reproductive system.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141874052","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":"Sweat gland morphology and physiology in diabetes, neuropathy, and nephropathy: a review.","authors":"Sudha Singaram, Kalpana Ramakrishnan, Jayashree Selvam, Mallika Senthil, Vigneswaran Narayanamurthy","doi":"10.1080/13813455.2022.2114499","DOIUrl":"10.1080/13813455.2022.2114499","url":null,"abstract":"<p><p><b>Context:</b> Sweat glands (SGs) play a vital role in thermal regulation. The function and structure are altered during the different pathological conditions.<b>Objective:</b> These alterations are studied through three techniques: biopsy, sweat analytes and electrical activity of SG.<b>Methods:</b> The morphological study of SG through biopsy and various techniques involved in quantifying sweat analytes is focussed on here. Electrical activities of SG in diabetes, neuropathy and nephropathy cases are also discussed, highlighting their limitations and future scope.<b>Results and Conclusion:</b> The result of this review identified three areas of the knowledge gap. The first is wearable sensors to correlate pathological conditions. Secondly, there is no device to look for its structure and quantify its associated function. Finally, therapeutic applications of SG are explored, especially for renal failure. With these aspects, this paper provides information collection and correlates SG with pathologies related to diabetes. Hence this could help researchers develop suitable technologies for the gaps identified.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40350598","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":"Silymarin inhibits the lipogenic pathway and reduces worsening of non-alcoholic fatty liver disease (NAFLD) in mice.","authors":"Luana Cristina Faria Carvalho, Flávia Monteiro Ferreira, Bruna Vidal Dias, Daniela Couto de Azevedo, Gustavo Henrique Bianco de Souza, Matheus Marque Milagre, Marta de Lana, Paula Melo de Abreu Vieira, Cláudia Martins Carneiro, Sílvia de Paula-Gomes, Silvia Dantas Cangussu, Daniela Caldeira Costa","doi":"10.1080/13813455.2022.2138445","DOIUrl":"10.1080/13813455.2022.2138445","url":null,"abstract":"<p><strong>Context: </strong>The role of silymarin in hepatic lipid dysfunction and its possible mechanisms of action were investigated.</p><p><strong>Objective: </strong>To evaluate the effects of silymarin on hepatic and metabolic profiles in mice fed with 30% fructose for 8 weeks.</p><p><strong>Methods: </strong>We evaluated the antioxidant profile of silymarin; mice consumed 30% fructose and were treated with silymarin (120<b> </b>mg/kg/day or 240 mg/kg/day). We performed biochemical, redox status, and histopathological assays. RT-qPCR was performed to detect ACC-1, ACC-2, FAS, and CS expression, and western blotting to detect PGC-1α levels.</p><p><strong>Results: </strong>Silymarin contains high levels of phenolic compounds and flavonoids and exhibited significant antioxidant capacity <i>in vitro. In vivo</i>, the fructose-fed groups showed increased levels of AST, ALT, SOD/CAT, TBARS, hepatic TG, and cholesterol, as well as hypertriglyceridaemia, hypercholesterolaemia, and increased ACC-1 and FAS. Silymarin treatment reduced these parameters and increased mRNA levels and activity of hepatic citrate synthase.</p><p><strong>Conclusions: </strong>These results suggest that silymarin reduces worsening of NAFLD.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40664444","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":"HECTD3 promotes NLRP3 inflammasome and pyroptosis to exacerbate diabetes-related cognitive impairment by stabilising MALT1 to regulate JNK pathway.","authors":"Zhongfan Ruan, Yan Li, Yanfang Chen","doi":"10.1080/13813455.2022.2093377","DOIUrl":"10.1080/13813455.2022.2093377","url":null,"abstract":"<p><strong>Background: </strong>HECTD3 (HECT domain E3 ubiquitin protein ligase 3) exerts biological activities in neuroinflammation of distinct diseases, such as autoimmune encephalomyelitis and donations after heart death. However, the effect of HECTD3 on diabetes-associated cognitive decline (DACD) remains unclear.</p><p><strong>Methods: </strong>Wild-type or HECTD3-knockout rats were administered with streptozotocin to establish diabetic model. Pathological changes in the hippocampus were assessed by NISSL and haematoxylin and eosin staining. Morris water maze test was used to assess cognitive function. Neuronal survival and inflammation were investigated by immunofluorescence staining and ELISA assay. NLRP3 inflammasome and pyroptosis were assessed by western blot, immunofluorescence and flow cytometry assays.</p><p><strong>Results: </strong>HECTD3 was up-regulated in hippocampus of streptozotocin-induced diabetic rats and high glucose-induced PC12 cells. Knockout of HECTD3 increased the number of neurons and improved the learning and memory function. Moreover, knockout of HECTD3 promoted <i>in vivo</i> neuronal survival, and reduced levels of IL-1β, TNF-α, and IL-6 in the hippocampus. Silencing of HECTD3 increased cell viability, and reduced IL-1β, TNF-α, and IL-6 in high glucose-induced PC12 cells. Fluorescence intensities of NLRP3, GSDMD-N and caspase-1 were reduced in HECTD3-knockout diabetic rats, and knockdown of HECTD3 down-regulated protein expression of NLRP3, GSDMD-N, caspase-1, IL-1β, and IL-18 in high glucose-induced PC12 cells to suppress the pyroptosis. HECTD3 promoted the stability of mucosa-associated lymphoid tissue 1 (MALT1) through up-regulation of c-JUN and phospho (p)-JNK in high glucose-induced PC12 cells. Over-expression of MALT1 attenuated neuroprotective effects of HECTD3 silencing on high glucose-induced PC12 cells.</p><p><strong>Conclusion: </strong>HECTD3 silencing exerted neuroprotective effect against DACD through MALT1-mediated JNK signalling.HighlightsHECTD3 was up-regulated in hippocampus of streptozotocin-induced diabetic rats and high glucose-induced PC12.Knockout of HECTD3 promoted <i>in vivo</i> neuronal survival, reduced inflammation and pyroptosis, and improved the learning and memory function in diabetic rats.Knockout of HECTD3 suppressed the activation of NLRP3 inflammasome in diabetic rats.Silencing of HECTD3 exerted neuroprotective effects through MALT1-mediated JNK signalling.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40684060","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":"Apolipoprotein A-IV restrains fat accumulation in skeletal and myocardial muscles by inhibiting lipogenesis and activating PI3K-AKT signalling.","authors":"Wenqian Zhang, Xiao-Huan Liu, Jin-Ting Zhou, Cheng Cheng, Jing Xu, Jun Yu, Xiaoming Li","doi":"10.1080/13813455.2022.2163261","DOIUrl":"10.1080/13813455.2022.2163261","url":null,"abstract":"<p><strong>Background: </strong>One of the pathological characteristics of obesity is fat accumulation of skeletal muscles (SKM) and the myocardium, involving mechanisms of insulin resistance and abnormal lipid metabolism. Apolipoprotein A-IV (ApoA-IV) is an essential gene in both glucose and lipid metabolisms.</p><p><strong>Materials and methods: </strong>Using high-fat diet (HFD) induced obese <i>apoA-IV</i>-knockout mice and subsequent introduction of exogenous recombinant-ApoA-IV protein and adeno-associated virus (AAV)-transformed <i>apoA-IV</i>, we examined lipid metabolism indicators of SKM and the myocardium, which include triglyceride (TG) content, RT-PCR for lipogenic indicators and western blotting for AKT phosphorylation. Similarly, we used high-glucose-fed or palmitate (Pal)-induced C2C12 cells co-cultured with ApoA-IV protein to evaluate glucose uptake, the phosphoinositide 3-kinase (PI3K)-AKT pathway, and lipid metabolisms.</p><p><strong>Results: </strong>In stable obese animal models, we find ApoA-IV-knockout mice show elevated TG content, enhanced expression of lipogenic enzymes and diminished phosphorylated AKT in SKM and the myocardium, but both stable hepatic expression of AAV-<i>apoA-IV</i> and brief ApoA-IV protein administration suppress lipogenesis and promote AKT phosphorylation. In a myoblast cell line C2C12, ApoA-IV protein suppresses Pal-induced lipid accumulation and lipogenesis but enhances AKT activation and glucose uptake, and the effect is abolished by a PI3K inhibitor.</p><p><strong>Conclusion: </strong>We find that ApoA-IV reduces fat accumulation by suppressing lipogenesis and improves glucose uptake in SKM and the myocardium by regulating the PI3K-AKT pathway.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10468663","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":"Cyproheptadine, a SET7/9 inhibitor, reduces hyperglycaemia-induced ER stress alleviating inflammation and fibrosis in renal tubular epithelial cells.","authors":"Himanshu Sankrityayan, Ajinath Kale, Vishwadeep Shelke, Anil Bhanudas Gaikwad","doi":"10.1080/13813455.2022.2105365","DOIUrl":"10.1080/13813455.2022.2105365","url":null,"abstract":"<p><strong>Context: </strong>Persistent hyperglycaemia increases SET7/9 expression and endoplasmic reticulum (ER) stress which causes inflammation, apoptosis, and fibrosis in renal tubular epithelial cells leading to diabetic kidney disease (DKD).</p><p><strong>Objective: </strong>Current study explores the renoprotective potential of a novel SET7/9 inhibitor, Cyproheptadine, and the underlying molecular mechanisms in hyperglycaemia-induced renal tubular epithelial cell injury.</p><p><strong>Methods: </strong>Change in expression of SET7/9, histone H3 lysine (K4) monomethylation (H3K4Me1), inflammatory, fibrotic, and ER stress proteins were evaluated <i>in-vivo</i> and <i>in-vitro</i>. NRK-52E cells were used to study the preventive effect of Cyproheptadine against hyperglycaemia-induced ER stress and subsequent inflammation and fibrosis.</p><p><strong>Results: </strong>SET7/9 and H3K4Me1 expression significantly increased with ER stress, inflammation, apoptosis, and fibrosis, <i>in-vivo</i> and <i>in-vitro</i> under hyperglycaemia. However, the cells treated with Cyproheptadine showed significant suppression of H3K4Me1 and reduction in ER stress, inflammation, apoptosis, and fibrosis.</p><p><strong>Conclusion: </strong>Cyproheptadine prevented hyperglycaemia-induced renal fibrosis and inflammation by reducing H3K4Me1 expression and ER stress.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40684062","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":"Activation of SIRT1 by silibinin improved mitochondrial health and alleviated the oxidative damage in experimental diabetic neuropathy and high glucose-mediated neurotoxicity.","authors":"Islauddin Khan, Kumari Preeti, Rahul Kumar, Dharmendra Kumar Khatri, Shashi Bala Singh","doi":"10.1080/13813455.2022.2108454","DOIUrl":"10.1080/13813455.2022.2108454","url":null,"abstract":"<p><strong>Background: </strong>Silibinin (SBN), a sirtuin 1 (SIRT1) activator, has been evaluated for its anti-inflammatory activity in many inflammatory diseases. However, its role in diabetes-induced peripheral neuropathy (DPN) remains unknown. The SIRT1 activation convalesces nerve functions by improving mitochondrial biogenesis and mitophagy.</p><p><strong>Methods: </strong>DPN was induced by streptozotocin (STZ) at a dose of 55 mg/kg, i.p. in the male SD rats whereas neurotoxicity was induced in Neuro2A cells by 30 mM (high glucose) glucose. Neurobehavioural (nerve conduction velocity and nerve blood flow) western blot, immunohistochemistry, and immunocytochemistry were performed to evaluate the protein expression and their cellular localisation.</p><p><strong>Results: </strong>Two-week SBN treatment improved neurobehavioural symptoms, SIRT1, PGC-1α, and TFAM expression in the sciatic nerve and HG insulted N2A cells. It has also maintained the mitophagy by up-regulating PARL, PINK1, PGAM5, LC3 level and provided antioxidant defence by upregulating Nrf2.</p><p><strong>Conclusion: </strong>SBN has shown neuroprotective potential in DPN through SIRT1 activation and antioxidant mechanism.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40681219","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":"Betulinic acid improves TNF-<i>α</i>-induced insulin resistance by inhibiting negative regulator of insulin signalling and inflammation-activated protein kinase in 3T3-L1 adipocytes.","authors":"Hyun-Ah Lee, Jung-Kyung Lee, Ji-Sook Han","doi":"10.1080/13813455.2022.2120503","DOIUrl":"10.1080/13813455.2022.2120503","url":null,"abstract":"<p><strong>Context: </strong>Obesity is related to insulin resistance, and adipose tissue-secreted TNF-<i>α</i> may play a role in inducing obesity. TNF-<i>α</i> activates inflammatory protein kinase and impairs insulin signalling.</p><p><strong>Objectives: </strong>We investigated the effect of betulinic acid on insulin resistance caused by TNF-<i>α</i> treatment in 3T3-L1 adipocytes.</p><p><strong>Material and methods: </strong>3T3-L1 was exposed to TNF-<i>α</i> in the presence and absence of betulinic acid. Various parameters such as glucose uptake assay, cell viability, expression of proteins involved in insulin resistance were studied.</p><p><strong>Results: </strong>Betulinic acid increased glucose uptake in TNF-<i>α</i> pre-treated cells and inhibited the activation of PTP1B and JNK and reduced IκB<i>α</i> degradation. Tyrosine phosphorylation was increased, and serine phosphorylation was decreased in IRS-1.</p><p><strong>Discussion: </strong>Betulinic acid restored TNF-<i>α</i> impaired insulin signalling and increased PI3K activation and phosphorylation of Akt and increased plasma membrane expression of GLUT 4, which stimulated glucose uptake concentration-dependently.</p><p><strong>Conclusion: </strong>These results suggest that betulinic acid is effective at improving TNF-<i>α</i>-induced insulin resistance in adipocytes via inhibiting the activation of negative regulator of insulin signalling and inflammation-activated protein kinase and may potentially improve insulin resistance.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40356348","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}