Metabolism open最新文献

{"title":"Effects of Ficus exasperata on neurotransmission and expression of BDNF, tau, ACHE and BACE in diabetic rats","authors":"Olorunsola Israel Adeyomoye ,&nbsp;Juliana Bunmi Adetunji ,&nbsp;Olugbemi Temitope Olaniyan ,&nbsp;Charles Oluwaseun Adetunji ,&nbsp;Ogunmiluyi Oluwafunmbi Ebenezer","doi":"10.1016/j.metop.2024.100333","DOIUrl":"10.1016/j.metop.2024.100333","url":null,"abstract":"<div><div>Diabetes mellitus, a chronic metabolic disorder, has significant global health implications, particularly due to its neurological complications, such as diabetic neuropathy. This condition increases the risk of neurodegenerative diseases by affecting peripheral nerves and cognition. <em>Ficus exasperata</em>, known for its neuroprotective properties, shows promise as a therapeutic option for addressing these complications. This study evaluates the effects of methanol extract of <em>Ficus exasperata</em> (MEFE) on neurotransmission and the expression of Tau, brain-derived neurotrophic factor (BDNF), acetylcholinesterase (ACHE), and Beta-Site Amyloid Precursor Protein Cleaving Enzyme (BACE) in alloxan-induced diabetic Wistar rats. The controlled experimental design involved 20 Wistar rats divided into four groups (n = 5): control, diabetic untreated, diabetes + MEFE (200 mg/kg), and diabetes + insulin (0.3 IU). The methanol extract was prepared using cold maceration, and an aliquot was subjected to gas chromatography-mass spectrometry. Constituents of MEFE were docked with neurologic receptors. Blood glucose levels were measured using the glucose oxidase method, and neurotransmitter levels, antioxidants, oxidative stress markers, and the expression of Tau, BDNF, ACHE, and BACE were assessed using standard procedures and qRT-PCR. Data were analyzed using one-way ANOVA at P &lt; 0.05. Results indicated that MEFE significantly reduced fasting blood glucose levels compared to untreated diabetic rats. <em>In silico</em> docking identified kaur-16-ene, a constituent of MEFE, as having the highest binding affinity for NMDA, TrkB, mAchR and nAchR receptors, indicating its neuroprotective potential. MEFE also enhanced antioxidant enzyme levels (SOD, GPx, catalase) while reducing oxidative stress markers (MDA, 8-OHdG). Gene expression analysis revealed that MEFE modulates the expression of Tau, BDNF, ACHE, and BACE, suggesting its potential to influence neurodegenerative pathways associated with diabetic neuropathy. <em>Ficus exasperata</em> demonstrates significant therapeutic potential in managing diabetic neuropathy and related cognitive impairments by modulating neurotransmission, protein expression, and antioxidant defenses.</div></div>","PeriodicalId":94141,"journal":{"name":"Metabolism open","volume":"24 ","pages":"Article 100333"},"PeriodicalIF":0.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142746222","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fish oil attenuates the expression of the CCL2 chemokine and histone-modifying enzymes in LPS-stimulated human preadipocytes.","authors":"Jussara de Jesus Simão, Andressa França de Sousa Bispo, Victor Tadeu Gonçalves Plata, Ana Beatriz Marques Abel, Monica Marques Telles, Lucia Maria Armelin-Correa, Maria Isabel Cardoso Alonso-Vale","doi":"10.1016/j.metop.2024.100336","DOIUrl":"10.1016/j.metop.2024.100336","url":null,"abstract":"<p><p>In obesity, C-C chemokine ligand 2 (CCL2) plays a critical role in recruiting macrophages to white adipose tissue (WAT), contributing to chronic inflammation. In this study, we sought to explore the effects of fish oil (FO) on CCL2 expression and histone (H3K27)-modifying enzymes in both human model of preadipocytes and primary adipose-derived stem cells (ASCs). Present findings in preadipocytes lineage evidenced that lipopolysaccharide (LPS) increased <i>TNF-alpha</i> (∼5.8-fold) and <i>CCL2</i> (∼3.8-fold) expression, modulating H3K27 modifying enzymes expression, including KDM6B and EP300. FO, in turn, significantly attenuated LPS-induced <i>CCL2</i> expression and secretion and downregulated <i>KDM6B</i> and <i>EP300</i>, elucidating an important mechanism of action involved in the anti-inflammatory role of FO. We next isolated mature hypertrophied adipocytes from patient with overweight and exposed to LPS, resulting in increased <i>CCL2/MCP-1</i> (∼3.8-fold) and <i>TNF-alpha</i> (∼4.5-fold) expression, effects significantly attenuated by FO. We also generated adipocyte-conditioned medium (ACM) and exposed ASCs to LPS or ACM for up to 72 h to assess CCL2/MCP-1 secretion. ACM from hypertrophied adipocytes stimulated increased <i>CCL2/MCP-1</i> expression, which was partially reduced by FO. LPS treatment of primary ASCs led to a marked increase in CCL2 secretion, which was completely abolished by FO after 6 h, highlighting its potent anti-inflammatory effect. After 72 h, FO consistently maintained lower levels of CCL2, even during sustained inflammatory stimulation, underscoring its ability to modulate chronic inflammation. Additionally, the inhibition of NF-κB with JSH-23 mimicked the effects of FO on <i>CCL2</i> expression, further suggesting that the anti-inflammatory actions of FO may involve NF-κB signaling. In conclusion, FO attenuates CCL2 expression and secretion in both preadipocytes and ASCs, providing evidence of its potential in modulating inflammation in WAT progenitor cells by modulating histone-modifying enzymes and inflammatory pathways.</p>","PeriodicalId":94141,"journal":{"name":"Metabolism open","volume":"24 ","pages":"100336"},"PeriodicalIF":0.0,"publicationDate":"2024-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11665696/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142883968","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Higher levels of plasmatic saturated fatty acid were significantly associated with liver fibrosis in HIV mono-infection: A case-control study.","authors":"Cristiane Fonseca de Almeida, Wilza Arantes Ferreira Peres, Paula Simplício da Silva, Claudia Santos de Aguiar Cardoso, Michelle Morata de Andrade, Julio Castro-Alves, Marcel de Souza Borges Quintana, Marina Campos Araujo, Karla Yasmin Dias Fraga, Julliana Antunes Cormack, Ronaldo Ismerio Moreira, Sandra W Cardoso, Valdilea G Veloso, Beatriz Grinsztejn, Patricia Dias de Brito, Hugo Perazzo","doi":"10.1016/j.metop.2024.100334","DOIUrl":"10.1016/j.metop.2024.100334","url":null,"abstract":"<p><strong>Background: </strong>The relationship between plasmatic fatty acid (FA) composition and liver fibrosis remains scarce in people living with HIV/AIDS (PLWHA). We aimed to evaluate the association of plasmatic FAs and liver fibrosis in HIV mono-infected individuals.</p><p><strong>Methods: </strong>This case-control study included PLWHA with liver fibrosis (cases) and randomly selected subjects without fibrosis (controls) from the PROSPEC-HIV study (NCT02542020). Participants with viral hepatitis, abusive alcohol consumption and lipid supplements use were excluded. Liver fibrosis was defined using transient elastography (TE) by liver stiffness measurement (LSM) ≥ 7.1 kPa or ≥ 6.2 kPa with M or XL probe, respectively. All HIV mono-infected participants with liver fibrosis identified at the baseline PROSPEC-HIV visit were included. Controls (1:1) were randomly selected among those HIV mono-infected participants without liver fibrosis. Plasmatic FA profile, dietary lipid intake, anthropometric measures, and blood samples were assessed. Plasmatic fatty acid was analyzed using gas chromatography and intake of fats lipids were assessed by two 24-h dietary recall (24-HDR). Multivariate logistic regression models adjusted by age, sex at birth and duration of antiretroviral therapy (ART) were performed.</p><p><strong>Results: </strong>A total of 142 participants (71 cases and 71 controls) [62 % female, median age = 46 (IQR, 37-53) years, 14.8 % with diabetes, median CD4 count = 655 cells/mm3, 96.5 % under ART] were included. Higher percentages of plasmatic palmitc acid (16:0) and saturated fatty acids (SFA) were observed in participants with liver fibrosis (cases) compared to those without (controls). Presence of higher percentage of plasmatic palmitc acid (16:0) was associated with an increased odds for liver fibrosis [adjusted OR = 1.23 (95%CI 1.04-1.46); p = 0.02] in multivariate models.</p><p><strong>Conclusion: </strong>This study showed the potential role of the plasmatic FA composition in the pathogenesis of liver fibrosis in PLWHA.</p>","PeriodicalId":94141,"journal":{"name":"Metabolism open","volume":"24 ","pages":"100334"},"PeriodicalIF":0.0,"publicationDate":"2024-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11664064/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142883363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deciphering the mechanisms and effects of hyperglycemia on skeletal muscle atrophy","authors":"Khushboo Gaur ,&nbsp;Lucy Mohapatra ,&nbsp;Pranay Wal ,&nbsp;Amana Parveen ,&nbsp;Shivam Kumar ,&nbsp;Vaishali Gupta","doi":"10.1016/j.metop.2024.100332","DOIUrl":"10.1016/j.metop.2024.100332","url":null,"abstract":"<div><div>Hyperglycemia, a hallmark of diabetes mellitus, significantly contributes to skeletal muscle atrophy, characterized by progressive muscle mass and strength loss. This review summarizes the mechanisms of hyperglycemia-induced muscle atrophy, examines clinical evidence, and discusses preventive and therapeutic strategies. A systematic search of electronic databases, including PubMed, Scopus, and Web of Science, was conducted to identify relevant papers on hyperglycemic skeletal muscle atrophy. Key mechanisms include insulin resistance, chronic inflammation, oxidative stress, and mitochondrial dysfunction. Crucial molecular pathways involved are Phosphoinositide 3-kinase/Protein kinase B signaling, Forkhead box O transcription factors, the ubiquitin-proteasome system, and myostatin-mediated degradation. Hyperglycemia disrupts normal glucose and lipid metabolism, exacerbating muscle protein degradation and impairing synthesis. Clinical studies support the association between hyperglycemia and muscle atrophy, emphasizing the need for early diagnosis and intervention. Biomarkers, imaging techniques, and functional tests are vital for detecting and monitoring muscle atrophy in hyperglycemic patients. Management strategies focus on glycemic control, pharmacological interventions targeting specific molecular pathways, nutritional support, and tailored exercise regimens. Despite these advances, research gaps remain in understanding the long-term impact of hyperglycemia on muscle health and identifying novel therapeutic targets. The review aims to provide a comprehensive understanding of the mechanisms, clinical implications, and potential therapeutic strategies for addressing hyperglycemia-induced skeletal muscle atrophy.</div></div>","PeriodicalId":94141,"journal":{"name":"Metabolism open","volume":"24 ","pages":"Article 100332"},"PeriodicalIF":0.0,"publicationDate":"2024-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142699472","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Outdoor environment and obesity: A review of current evidence","authors":"Evangelia A. Polyzou ,&nbsp;Stergios A. Polyzos","doi":"10.1016/j.metop.2024.100331","DOIUrl":"10.1016/j.metop.2024.100331","url":null,"abstract":"<div><div>Obesity is a global epidemic whose management needs long-term, preventive measures. Since the outdoor environment has been linked with obesity, this review aims to summarize data on this association, which may potentially bear clinical implication in the future, i.e., to affect obesity trends by changing the outdoor environment. In this regard, there are increasing data linking obesity with green and open spaces, walkable and bikeable areas, and accessibility to affordable healthy foods and fresh drinking water. Most studies have shown an inverse association of obesity with the availability of safe outdoor green and open spaces, which favor physical activity. Physical activity also seems to be favored by the greater availability of a variety of portable play equipment and the presence of certain fixed playground equipment. The presence of pedestrian walks and aids was also associated with lower rates of obesity, whereas higher proportion of streets was associated with less outdoor activity and higher rates of obesity. Furthermore, higher accessibility and new infrastructure for walking and cycling was associated with greater physical activity and lower rates of obesity. It seems that longer walkable and cyclable areas favor safe walk or ride a bike to work, play or shop, thus lowering the rates of obesity. Moreover, the accessibility to affordable healthy foods and fresh drinking water, and lower consumption of sugar-sweetened beverages have been linked to lower rates of obesity. In this regard, the restriction in public advertisements of unhealthy food and sugar-sweetened beverages may play a certain role towards this direction.</div></div>","PeriodicalId":94141,"journal":{"name":"Metabolism open","volume":"24 ","pages":"Article 100331"},"PeriodicalIF":0.0,"publicationDate":"2024-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142661918","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Understanding the impact of diabetes on bone health: A clinical review","authors":"Preeti Sharma ,&nbsp;Rahul Kumar Sharma ,&nbsp;Khushboo Gaur","doi":"10.1016/j.metop.2024.100330","DOIUrl":"10.1016/j.metop.2024.100330","url":null,"abstract":"<div><div>Diabetic bone disease, a form of secondary osteoporosis, is characterized by weakened bones and an increased risk of fractures, especially in patients with type 2 diabetes (T2D). This review explores the key mechanisms driving this condition, including hyperglycemia, insulin resistance, advanced glycation end products (AGEs), and proinflammatory cytokines, all of which disturb normal bone turnover by disrupting the functions of osteoblasts and osteoclasts. We examine the roles of bone turnover and mineralization, as well as how microvascular complications affect bone microarchitecture. Additionally, the influence of gut hormones, such as GLP-1 and GIP, and gut microbiota, particularly species like <em>Akkermansia muciniphila</em>, on the gut-bone axis is discussed, as these factors play a role in regulating bone density and structure. While T2D patients may show normal or even elevated bone mineral density (BMD), the underlying quality of bone is often compromised, leading to increased fragility. This review integrates current knowledge on the molecular, hormonal, and microbial interactions contributing to diabetic bone disease. By highlighting these pathways, we aim to offer insights into potential therapeutic strategies and inform future research aimed at improving the diagnosis, treatment, and overall management of this condition.</div></div>","PeriodicalId":94141,"journal":{"name":"Metabolism open","volume":"24 ","pages":"Article 100330"},"PeriodicalIF":0.0,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142661919","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of allulose on blood glucose in type 2 diabetes: A meta-analysis of clinical trials","authors":"Hazem Ayesh ,&nbsp;Sajida Suhail ,&nbsp;Suhail Ayesh","doi":"10.1016/j.metop.2024.100329","DOIUrl":"10.1016/j.metop.2024.100329","url":null,"abstract":"<div><h3>Objective</h3><div>This meta-analysis aims to evaluate the impact of allulose on blood glucose levels in patients with type 2 diabetes mellitus (T2DM). Primary outcomes include postprandial blood glucose, while secondary outcomes are time in range (TIR), time above range (TAR), fasting plasma glucose (FPG), and insulin area under the curve (AUC).</div></div><div><h3>Methods</h3><div>A systematic search was conducted across PubMed/MEDLINE, Web of Science, Scopus, and Cochrane Library until May 20, 2024. Randomized controlled trials assessing the effect of allulose on glycemic parameters in T2DM patients were included. Data were synthesized using a random-effects meta-analysis model, and the quality of studies was assessed using the Cochrane Risk of Bias tool.</div></div><div><h3>Results</h3><div>Six studies involving 126 participants were included. Allulose significantly reduced glucose AUC (SMD: −0.6662, 95 % CI [-1.1360, −0.1964], p = 0.0054) with moderate heterogeneity (I² = 58.3 %). Insulin AUC showed a non-significant reduction (SMD: −0.3648, 95 % CI [-0.7783, 0.0488], p = 0.0839). FPG demonstrated a non-significant reduction (MD: −5.8925, 95 % CI [-20.4892, 8.7043], p = 0.4288), while TAR significantly decreased (MD: −8.8204, 95 % CI [-14.4101, −3.2307], p = 0.0020). No significant changes were observed in TIR (MD: 7.1211, 95 % CI [-1.6028, 15.8450], p = 0.1096).</div></div><div><h3>Conclusion</h3><div>Allulose demonstrated a significant reduction in postprandial glucose levels and TAR, supporting its role as a dietary intervention for glycemic control in T2DM patients. The findings are robust, though further research is needed to confirm its long-term effects on insulin sensitivity and metabolic health.</div></div>","PeriodicalId":94141,"journal":{"name":"Metabolism open","volume":"24 ","pages":"Article 100329"},"PeriodicalIF":0.0,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142661917","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of novel inflammation-associated biomarkers in diabetic peripheral neuropathy","authors":"Theodoros Panou,&nbsp;Evanthia Gouveri,&nbsp;Dimitrios Papazoglou,&nbsp;Nikolaos Papanas","doi":"10.1016/j.metop.2024.100328","DOIUrl":"10.1016/j.metop.2024.100328","url":null,"abstract":"<div><div>Diabetic neuropathy is one of the commonest complications of diabetes mellitus. Its most frequent form is diabetic peripheral neuropathy (DPN). Currently, there is no established and widely used biomarker for diagnosis and clinical staging of DPN. There is accumulating evidence that low-grade systemic inflammation is a key element in its pathogenesis. In this context, several clinical studies have so far identified potential biomarkers of DPN. These studies have enrolled both subjects with type 1 diabetes mellitus (T1DM) and subjects with type 2 diabetes mellitus (T2DM), including children with T1DM and elderly T2DM subjects. They have also evaluated participants with prediabetes. Potential biomarkers include a wide spectrum of cytokines, chemokines and immune receptors, notably interleukins (IL), mostly IL-1, IL-6 or IL-10, as well as mediators of the tumour necrosis factor-α (TNF-α) related pathway. Cell-ratios, such as neurtrophil-to-lymphocyte ratio (NLR), have yielded promising results as well. Other works have focused on adipokines and identified several signalling molecules (adiponectin, neuregulin 4, isthmin-1 and omentin) as promising biomarkers of DPN. Finally, epigenetic biomarkers have been investigated. Further experience is being gathered with the use of biomarkers in specific age groups and in the discrimination between painless and painful DPN. Prospective studies appear promising in monitoring of DPN progression, but experience is rather limited. Finally, certain cut-off values have been proposed for DPN screening, but these need confirmation. Future large-scale studies are now required to validate biomarkers and to investigate their potential clinical utility.</div></div>","PeriodicalId":94141,"journal":{"name":"Metabolism open","volume":"24 ","pages":"Article 100328"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142587278","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Growth hormone attenuates obesity and reshapes gut microbiota in high-fat diet-fed mice","authors":"Yu Wang ,&nbsp;Liyuan Ran ,&nbsp;Fang Zhang ,&nbsp;Haolin Li ,&nbsp;Qianqian Cha ,&nbsp;Kun Yang ,&nbsp;Haoan Wang ,&nbsp;Yingjie Wu ,&nbsp;Zichao Yu","doi":"10.1016/j.metop.2024.100326","DOIUrl":"10.1016/j.metop.2024.100326","url":null,"abstract":"<div><div>Growth hormone (GH) and gut microbiota are key regulators of metabolism and have been linked to the development and treatment of obesity. Although variations in GH levels are associated with changes in gut microbiota composition, the specific effects of GH on gut microbiota and its role in obesity remain unclear. This study explored the effects of various GH doses (0.25, 0.75 and 1.5 IU/kg) on adipose tissue mass and gut microbiota in high-fat diet-induced obese mice. Notably, high-dose GH (1.5 IU/kg) significantly reduced the adipose tissue mass. This dose also reversed high-fat diet-induced gut microbiota dysbiosis, restoring microbial diversity and increasing the abundance of beneficial genera such as <em>Ruminococcaceae</em> and <em>Muribaculaceae</em>. Additionally, high-dose GH normalized several obesity-related gut microbiota pathways, including starch and sucrose metabolism, galactose metabolism, and secondary bile acid biosynthesis. GH therapy also improved intestinal barrier function, a key determinant of gut microbial homeostasis. These findings underscore the therapeutic potential of GH in obesity management through its effects on gut microbiota, providing new avenues for obesity interventions.</div></div>","PeriodicalId":94141,"journal":{"name":"Metabolism open","volume":"24 ","pages":"Article 100326"},"PeriodicalIF":0.0,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142530250","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the epidemiology and awareness of metabolic dysfunction-associated steatotic liver disease (MASLD) among health sciences students in an academic health care institute in India","authors":"Umasankari S.,&nbsp;S. Aishwarya,&nbsp;S.K. Aishwarya,&nbsp;Shivangi Bhardwaj,&nbsp;R.B. Pavithra,&nbsp;Soumili Ray,&nbsp;V.M. Vinodhini","doi":"10.1016/j.metop.2024.100325","DOIUrl":"10.1016/j.metop.2024.100325","url":null,"abstract":"<div><h3>Background</h3><div>Metabolic dysfunction-associated steatotic liver disease (MASLD) affects over 25 % of the global population, presenting a significant health challenge. It is often asymptomatic but linked to severe conditions like cirrhosis and liver cancer. Previous research indicates that people often underestimate MASLD risks. This study examines MASLD prevalence and awareness among medical students in an academic health care institute in India.</div></div><div><h3>Material and methods</h3><div>This cross-sectional study at SRM Medical College Hospital, Chennai, involved 80 medical and paramedical students aged 18–25. Exclusion criteria included history of alcohol use, neurological disorders, thyroid issues, diabetes, and hypertension. After obtaining informed consent, anthropometric data and blood samples were collected. Biochemical parameters including fasting plasma glucose, triglycerides, HDL-C, and GGT were measured. The Fatty Liver Index (FLI) was used to assess liver steatosis, with an FLI ≥60 indicating NAFLD. Data were analysed using SPSS Version 22.0, with statistical significance set at p &lt; 0.05.</div></div><div><h3>Results</h3><div>Among 80 participants, the mean age and BMI were 20.2 ± 1.03 years and 23.16 ± 4.55 kg/m². The mean Fatty Liver Index (FLI) score was 15.11 ± 19.68. MASLD prevalence was 7.5 % (n = 6). Significant positive correlations were found between FLI and BMI, waist circumference, fasting plasma glucose, triglycerides, and GGT, while HDL-C showed a non-significant negative correlation. Most participants were aware of MASLD and its risk factors but showed varied adherence to preventive measures.</div></div><div><h3>Conclusion</h3><div>Health Sciences undergraduates had a 7.5 % MASLD prevalence, highlighting a gap in understanding and testing. Addressing this requires better guidelines, awareness, and healthcare system enhancements.</div></div>","PeriodicalId":94141,"journal":{"name":"Metabolism open","volume":"24 ","pages":"Article 100325"},"PeriodicalIF":0.0,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142530251","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}