Pub Date : 2024-11-09DOI: 10.1016/j.metop.2024.100331
Evangelia A. Polyzou , Stergios A. Polyzos
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.
{"title":"Outdoor environment and obesity: A review of current evidence","authors":"Evangelia A. Polyzou , 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}
Pub Date : 2024-11-08DOI: 10.1016/j.metop.2024.100330
Preeti Sharma , Rahul Kumar Sharma , Khushboo Gaur
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 Akkermansia muciniphila, 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.
{"title":"Understanding the impact of diabetes on bone health: A clinical review","authors":"Preeti Sharma , Rahul Kumar Sharma , 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}
Pub Date : 2024-11-07DOI: 10.1016/j.metop.2024.100329
Hazem Ayesh , Sajida Suhail , Suhail Ayesh
Objective
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).
Methods
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.
Results
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).
Conclusion
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.
本荟萃分析旨在评估阿洛糖对 2 型糖尿病 (T2DM) 患者血糖水平的影响。主要结果包括餐后血糖，次要结果包括在量程内的时间（TIR）、超过量程的时间（TAR）、空腹血浆葡萄糖（FPG）和胰岛素曲线下面积（AUC）。方法截至 2024 年 5 月 20 日，在 PubMed/MEDLINE、Web of Science、Scopus 和 Cochrane Library 上进行了系统检索。纳入了评估阿洛糖对 T2DM 患者血糖参数影响的随机对照试验。采用随机效应荟萃分析模型对数据进行了综合分析，并使用 Cochrane 偏倚风险工具对研究质量进行了评估。阿洛糖能明显降低血糖 AUC（SMD：-0.6662，95 % CI [-1.1360，-0.1964]，p = 0.0054），异质性适中（I2 = 58.3 %）。胰岛素 AUC 下降不显著（SMD：-0.3648，95 % CI [-0.7783，0.0488]，p = 0.0839）。FPG 下降不明显（MD：-5.8925，95 % CI [-20.4892，8.7043]，p = 0.4288），而 TAR 显著下降（MD：-8.8204，95 % CI [-14.4101，-3.2307]，p = 0.0020）。结论 阿洛糖能显著降低餐后血糖水平和 TAR，支持其作为 T2DM 患者血糖控制的饮食干预措施。研究结果是可靠的，但还需要进一步的研究来证实其对胰岛素敏感性和代谢健康的长期影响。
{"title":"Impact of allulose on blood glucose in type 2 diabetes: A meta-analysis of clinical trials","authors":"Hazem Ayesh , Sajida Suhail , 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 (I<sup>2</sup> = 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}
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.
{"title":"The role of novel inflammation-associated biomarkers in diabetic peripheral neuropathy","authors":"Theodoros Panou, Evanthia Gouveri, Dimitrios Papazoglou, 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}
Pub Date : 2024-10-22DOI: 10.1016/j.metop.2024.100326
Yu Wang , Liyuan Ran , Fang Zhang , Haolin Li , Qianqian Cha , Kun Yang , Haoan Wang , Yingjie Wu , Zichao Yu
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 Ruminococcaceae and Muribaculaceae. 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.
{"title":"Growth hormone attenuates obesity and reshapes gut microbiota in high-fat diet-fed mice","authors":"Yu Wang , Liyuan Ran , Fang Zhang , Haolin Li , Qianqian Cha , Kun Yang , Haoan Wang , Yingjie Wu , 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}
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.
Material and methods
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 < 0.05.
Results
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.
Conclusion
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.
{"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., S. Aishwarya, S.K. Aishwarya, Shivangi Bhardwaj, R.B. Pavithra, Soumili Ray, 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 < 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/m<sup>2</sup>. 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}
Breast cancer development and progression are driven by intricate networks involving receptor tyrosine kinases (RTKs) and steroid hormone receptors specifically estrogen receptor (ER) and progesterone receptor (PR). This review examined roles of each receptor under normal physiology and in breast cancer, and explored their multifaceted interactions via signaling pathways, focusing on their contributions to breast cancer progression. Since defining the mechanism by which these two-receptor mediated signaling pathways cooperate is essential for understanding breast cancer progression, we discussed the mechanisms of cross-talk between RTKs and ER and PR and their potential therapeutic implications as well. The crosstalk between RTKs and steroid hormone receptors (ER and PR) in breast cancer can influence the disease's progression and treatment outcomes. Therefore, understanding the functions of the aforementioned receptors and their interactions is crucial for developing effective therapies.
{"title":"Receptor tyrosine kinases and steroid hormone receptors in breast cancer: Review of recent evidences","authors":"Awgichew Behaile Teklemariam , Zelalem Tilahun Muche , Melaku Mekonnen Agidew , Anemut Tilahun Mulu , Edgeit Abebe Zewde , Nega Dagnew Baye , Dagnew Getnet Adugna , Lemlemu Maru , Teklie Mengie Ayele","doi":"10.1016/j.metop.2024.100324","DOIUrl":"10.1016/j.metop.2024.100324","url":null,"abstract":"<div><div>Breast cancer development and progression are driven by intricate networks involving receptor tyrosine kinases (RTKs) and steroid hormone receptors specifically estrogen receptor (ER) and progesterone receptor (PR). This review examined roles of each receptor under normal physiology and in breast cancer, and explored their multifaceted interactions via signaling pathways, focusing on their contributions to breast cancer progression. Since defining the mechanism by which these two-receptor mediated signaling pathways cooperate is essential for understanding breast cancer progression, we discussed the mechanisms of cross-talk between RTKs and ER and PR and their potential therapeutic implications as well. The crosstalk between RTKs and steroid hormone receptors (ER and PR) in breast cancer can influence the disease's progression and treatment outcomes. Therefore, understanding the functions of the aforementioned receptors and their interactions is crucial for developing effective therapies.</div></div>","PeriodicalId":94141,"journal":{"name":"Metabolism open","volume":"24 ","pages":"Article 100324"},"PeriodicalIF":0.0,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142441562","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}
Pub Date : 2024-10-10DOI: 10.1016/j.metop.2024.100323
Stephan Mayntz, Rose Peronard
{"title":"Missed opportunities in statin therapy: A critical appraisal of prescription practices in sub-Saharan Africa","authors":"Stephan Mayntz, Rose Peronard","doi":"10.1016/j.metop.2024.100323","DOIUrl":"10.1016/j.metop.2024.100323","url":null,"abstract":"","PeriodicalId":94141,"journal":{"name":"Metabolism open","volume":"24 ","pages":"Article 100323"},"PeriodicalIF":0.0,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142433041","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}
Pub Date : 2024-09-24DOI: 10.1016/j.metop.2024.100322
Cuncun Lu , Lixin Ke , Alexios-Fotios A. Mentis , Qiang Zhang , Ziyi Wang , Zhifei Wang
Background
Non-alcoholic fatty liver disease (NAFLD) is a major global health problem due to its great disease and economic burdens. Tea is a popular beverage consumed by billions of people.
globally owing to its health benefits. However, the evidence regarding the association between tea intake and NAFLD risk is inconsistent.
Objective
To examine the genetically predicted causal association between tea intake and NAFLD risk using the two-sample Mendelian randomization (MR) method.
Methods
Single‐nucleotide polymorphisms (SNPs) strongly associated with tea intake were obtained from a large dataset (N = 447,485) in the UK biobank, and summary‐level genetic data for NAFLD (2,275 cases and 375,002 controls) were collected from the FinnGen consortium. The two-sample MR method was used to investigate the causal association between tea intake and NAFLD risk. The random‐effects inverse‐variance weighted (IVW) was used as the primary approach for estimating the causal effect, and MR Egger, weighted median, simple mode, and weighted mode were used to verify the robustness of the primary results.
Results
Twenty-four valid SNPs were selected as the instrumental variables for tea intake. The IVW results indicated that tea intake was not causally associated with NAFLD risk (Odds ratio: 1.48; 95 % confidence interval: 0.64, 3.43; p = 0.364); moreover, the results from other methods were consistent with this finding. A leave-one-out analysis further demonstrated the robustness of our results. No evidence of heterogeneity, outliers, or horizontal pleiotropy was found.
Conclusion
Our results do not support tea intake being causally associated with a decreased risk of NAFLD.
{"title":"Tea intake and non-alcoholic fatty liver disease risk: A two-sample Mendelian randomization study","authors":"Cuncun Lu , Lixin Ke , Alexios-Fotios A. Mentis , Qiang Zhang , Ziyi Wang , Zhifei Wang","doi":"10.1016/j.metop.2024.100322","DOIUrl":"10.1016/j.metop.2024.100322","url":null,"abstract":"<div><h3>Background</h3><div>Non-alcoholic fatty liver disease (NAFLD) is a major global health problem due to its great disease and economic burdens. Tea is a popular beverage consumed by billions of people.</div><div>globally owing to its health benefits. However, the evidence regarding the association between tea intake and NAFLD risk is inconsistent.</div></div><div><h3>Objective</h3><div>To examine the genetically predicted causal association between tea intake and NAFLD risk using the two-sample Mendelian randomization (MR) method.</div></div><div><h3>Methods</h3><div>Single‐nucleotide polymorphisms (SNPs) strongly associated with tea intake were obtained from a large dataset (N = 447,485) in the UK biobank, and summary‐level genetic data for NAFLD (2,275 cases and 375,002 controls) were collected from the FinnGen consortium. The two-sample MR method was used to investigate the causal association between tea intake and NAFLD risk. The random‐effects inverse‐variance weighted (IVW) was used as the primary approach for estimating the causal effect, and MR Egger, weighted median, simple mode, and weighted mode were used to verify the robustness of the primary results.</div></div><div><h3>Results</h3><div>Twenty-four valid SNPs were selected as the instrumental variables for tea intake. The IVW results indicated that tea intake was not causally associated with NAFLD risk (Odds ratio: 1.48; 95 % confidence interval: 0.64, 3.43; <em>p</em> = 0.364); moreover, the results from other methods were consistent with this finding. A leave-one-out analysis further demonstrated the robustness of our results. No evidence of heterogeneity, outliers, or horizontal pleiotropy was found.</div></div><div><h3>Conclusion</h3><div>Our results do not support tea intake being causally associated with a decreased risk of NAFLD.</div></div>","PeriodicalId":94141,"journal":{"name":"Metabolism open","volume":"24 ","pages":"Article 100322"},"PeriodicalIF":0.0,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142327334","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}
Pub Date : 2024-09-15DOI: 10.1016/j.metop.2024.100320
Katia Mangano , Aristidis Diamantopoulos , Natalia G. Vallianou , Theodora Stratigou , Fotis Panagopoulos , Dimitris Kounatidis , Maria Dalamaga , Paolo Fagone , Ferdinando Nicoletti
Background
Macrophage migration inhibitory factor (MIF) is a highly conserved cytokine with pleiotropic properties, mainly pro-inflammatory. MIF seems to exert its pro-inflammatory features by binding to its transmembrane cellular receptor CD74. MIF also has CXCR4, which acts as a co-receptor in this inflammatory process. Apart from MIF, D-dopachrome tautomerase (DDT) or MIF2, which belongs to the MIF superfamily, also binds to receptor CD74. Therefore, these molecules, MIF, CD74, DDT and CXCR4 are suggested to work together orchestrating an inflammatory process. Diabetes mellitus is characterised by chronic low-grade inflammation. Therefore, the aim of the present study was to evaluate serum and urinary levels of the aforementioned molecules among patients with type 1 diabetes mellitus (T1DM), type 2 diabetes mellitus (T2DM) and among healthy controls.
Methods
We enrolled 13 patients with T1DM, 74 patients with T2DM and 25 healthy individuals as controls. Levels of CD74, CXCR4, DDT, and MIF were measured using ELISA Kits according to the manufacturer's instructions.
Results
We documented increased serum MIF levels together with higher urinary CD74 levels among patients with T1DM, when compared to patients with T2DM and healthy adults. In particular, patients with T1DM showed significantly increased levels of MIF compared to T2DM (p = 0.011) and healthy controls (p = 0.0093). CD74 in urine were significantly higher in patients with T1DM compared to those affected with T2DM (p = 0.0302) and healthy group (p = 0.0099). On the contrary, serum CD74 were similar among the three groups. No statistical differences were identified in CXCR4 levels both in serum and in urine of all groups. Patients with T2DM and overweight/obesity had increased urinary levels of CD74, when compared to lean patients with T2DM.
Conclusion
The increased serum MIF levels and urinary CD74 levels among patients with T1DM may be attributed to the autoimmune milieu, which characterises patients with T1DM, when compared to patients with T2DM. These two findings merit further attention as they could pave the way for further research regarding the potential beneficial effects of inhibitors of MIF among patients with T1DM, especially in the early stages of T1DM. Finally, the role of inhibitors of MIF could be further explored in the context of obesity among patients with T2DM.
{"title":"Serum and urinary levels of MIF, CD74, DDT and CXCR4 among patients with type 1 diabetes mellitus, type 2 diabetes and healthy individuals: Implications for further research","authors":"Katia Mangano , Aristidis Diamantopoulos , Natalia G. Vallianou , Theodora Stratigou , Fotis Panagopoulos , Dimitris Kounatidis , Maria Dalamaga , Paolo Fagone , Ferdinando Nicoletti","doi":"10.1016/j.metop.2024.100320","DOIUrl":"10.1016/j.metop.2024.100320","url":null,"abstract":"<div><h3>Background</h3><p>Macrophage migration inhibitory factor (MIF) is a highly conserved cytokine with pleiotropic properties, mainly pro-inflammatory. MIF seems to exert its pro-inflammatory features by binding to its transmembrane cellular receptor CD74. MIF also has CXCR4, which acts as a co-receptor in this inflammatory process. Apart from MIF, D-dopachrome tautomerase (DDT) or MIF2, which belongs to the MIF superfamily, also binds to receptor CD74. Therefore, these molecules, MIF, CD74, DDT and CXCR4 are suggested to work together orchestrating an inflammatory process. Diabetes mellitus is characterised by chronic low-grade inflammation. Therefore, the aim of the present study was to evaluate serum and urinary levels of the aforementioned molecules among patients with type 1 diabetes mellitus (T1DM), type 2 diabetes mellitus (T2DM) and among healthy controls.</p></div><div><h3>Methods</h3><p>We enrolled 13 patients with T1DM, 74 patients with T2DM and 25 healthy individuals as controls. Levels of CD74, CXCR4, DDT, and MIF were measured using ELISA Kits according to the manufacturer's instructions.</p></div><div><h3>Results</h3><p>We documented increased serum MIF levels together with higher urinary CD74 levels among patients with T1DM, when compared to patients with T2DM and healthy adults. In particular, patients with T1DM showed significantly increased levels of MIF compared to T2DM (p = 0.011) and healthy controls (p = 0.0093). CD74 in urine were significantly higher in patients with T1DM compared to those affected with T2DM (p = 0.0302) and healthy group (p = 0.0099). On the contrary, serum CD74 were similar among the three groups. No statistical differences were identified in CXCR4 levels both in serum and in urine of all groups. Patients with T2DM and overweight/obesity had increased urinary levels of CD74, when compared to lean patients with T2DM.</p></div><div><h3>Conclusion</h3><p>The increased serum MIF levels and urinary CD74 levels among patients with T1DM may be attributed to the autoimmune milieu, which characterises patients with T1DM, when compared to patients with T2DM. These two findings merit further attention as they could pave the way for further research regarding the potential beneficial effects of inhibitors of MIF among patients with T1DM, especially in the early stages of T1DM. Finally, the role of inhibitors of MIF could be further explored in the context of obesity among patients with T2DM.</p></div>","PeriodicalId":94141,"journal":{"name":"Metabolism open","volume":"24 ","pages":"Article 100320"},"PeriodicalIF":0.0,"publicationDate":"2024-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2589936824000525/pdfft?md5=6cabb9a4c9b9616d76285a67013c8432&pid=1-s2.0-S2589936824000525-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142239008","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}
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