Tony Alfiere, M. Alexander, Yanmin Wang, Jonathan RT Lakey
{"title":"Transient coating of intestine in type 2 diabetic patients: Pilot trial outcome of Glucolate","authors":"Tony Alfiere, M. Alexander, Yanmin Wang, Jonathan RT Lakey","doi":"10.15761/tdm.1000124","DOIUrl":"https://doi.org/10.15761/tdm.1000124","url":null,"abstract":"","PeriodicalId":92596,"journal":{"name":"Trends in diabetes and metabolism","volume":"108 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84862964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The evidence behind early aggressive multi-drug treatment in type 2 diabetes","authors":"E. Cersosimo, Carolina Solis-Herrera, C. Triplitt","doi":"10.15761/tdm.1000121","DOIUrl":"https://doi.org/10.15761/tdm.1000121","url":null,"abstract":"","PeriodicalId":92596,"journal":{"name":"Trends in diabetes and metabolism","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88341837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The basis of metabolic homeostasis: Demand regulated energy metabolism","authors":"D. F. Wilson, Franz M. Matschinsky","doi":"10.15761/tdm.1000122","DOIUrl":"https://doi.org/10.15761/tdm.1000122","url":null,"abstract":"","PeriodicalId":92596,"journal":{"name":"Trends in diabetes and metabolism","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78809169","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Metabolism, molecular hypometabolism and inflammation: Complications of proliferative physiology include metabolic acidosis, pulmonary hypertension, T reg cell deficiency, insulin resistance and neuronal injury","authors":"Ritchi C Shoemaker","doi":"10.15761/tdm.1000118","DOIUrl":"https://doi.org/10.15761/tdm.1000118","url":null,"abstract":"","PeriodicalId":92596,"journal":{"name":"Trends in diabetes and metabolism","volume":"12 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84548176","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Trends Med, 2017 Volume 3: 1-2 Glucose-6-phosphate dehydrogenase (G6PD) is an enzyme that catalyzes the initial and the rate-limiting reaction step in the pentose phosphate pathway (HMP) which converts NADP into NADPH. NADPH is required for the generation of reduced glutathione an important antioxidant used to protects red blood cells from oxidative damage.Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common enzymopathy worldwide, affecting an estimated 400 million people and exists in concentrated regions in Africa, the Middle East, and Southeast Asia, and about one in 10 African-American males are affected in the United States [1-3]. G6PD-deficient patients may develop acute hemolytic anemia after exposure to oxidative stress because the HMP shunt is their only source of NADPH. Oxidative stress constitutes a failure of anti-oxidation defence systems to keep reactive oxygen and nitrogen species under control due to decrease of reduced glutathione synthesis in G6PD-deficient patients [4]. Hemolytic anemia may be life-threatening in some individuals due to three main triggers for hemolytic anemia in G6PD-deficient patients these are bacterial or viral infections, certain foods, and certain drugs [5]. These factors can increase the levels of reactive oxygen species, causing red blood cells to be destroyed faster than the body can replace them. Investigators found that G6PD-deficient cells were more susceptible to infection and death by human coronavirus, HCoV229E, a common pathogen for respiratory tract infection [6].In previous study we noticed a concurrent decrease in the concentration of reduced glutathione when the G6PD activity decreased [7]. Furthermore, we presented evidence that maintaining glutathione levels may help in easing the symptoms of certain diseases and supplementation of bilingual glutathione as a therapeutic strategy [8]. Since the onset of the COVID-19 pandemic and in light of the notion that some people become severely ill while others are asymptomatic, researchers started to believe that people who have a G6PD deficiency may be significantly affected by COVID-19 pandemic like the human coronavirus, HCoV229E and raised the question: Is there any scientific evidences to support a correlation/ association between G6PD deficiency and COVID-19 infection, susceptibility, severity or mortality [9]. Recent retrospective studies strongly suggesting that G6PD-deficient COVID-19 patients may suffer highest chloroquine induced toxicity a drug along with hydroxychloroquine are commonly prescribed widely used worldwide in the treatment of COVID-19 pandemic [10,11]. Moreover, a brief overview of the protective action of GSH against the exacerbated inflammation triggered by COVID-19 upon ACE/ACE2 imbalance was reported [12]. Additional evidence continued to suggest G6PD deficiency may not only play a role in COVID-19 susceptibility, but also severity of infection, therefore in order to answer this question, it would be Cli
{"title":"Clinical perspective on the impact of coronavirus (COVID-19) pandemic on individuals with glucose -6- phosphate dehydrogenase deficiency (G6PD)","authors":"Abdelrahim A Hunaiti","doi":"10.15761/tdm.1000120","DOIUrl":"https://doi.org/10.15761/tdm.1000120","url":null,"abstract":"Trends Med, 2017 Volume 3: 1-2 Glucose-6-phosphate dehydrogenase (G6PD) is an enzyme that catalyzes the initial and the rate-limiting reaction step in the pentose phosphate pathway (HMP) which converts NADP into NADPH. NADPH is required for the generation of reduced glutathione an important antioxidant used to protects red blood cells from oxidative damage.Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common enzymopathy worldwide, affecting an estimated 400 million people and exists in concentrated regions in Africa, the Middle East, and Southeast Asia, and about one in 10 African-American males are affected in the United States [1-3]. G6PD-deficient patients may develop acute hemolytic anemia after exposure to oxidative stress because the HMP shunt is their only source of NADPH. Oxidative stress constitutes a failure of anti-oxidation defence systems to keep reactive oxygen and nitrogen species under control due to decrease of reduced glutathione synthesis in G6PD-deficient patients [4]. Hemolytic anemia may be life-threatening in some individuals due to three main triggers for hemolytic anemia in G6PD-deficient patients these are bacterial or viral infections, certain foods, and certain drugs [5]. These factors can increase the levels of reactive oxygen species, causing red blood cells to be destroyed faster than the body can replace them. Investigators found that G6PD-deficient cells were more susceptible to infection and death by human coronavirus, HCoV229E, a common pathogen for respiratory tract infection [6].In previous study we noticed a concurrent decrease in the concentration of reduced glutathione when the G6PD activity decreased [7]. Furthermore, we presented evidence that maintaining glutathione levels may help in easing the symptoms of certain diseases and supplementation of bilingual glutathione as a therapeutic strategy [8]. Since the onset of the COVID-19 pandemic and in light of the notion that some people become severely ill while others are asymptomatic, researchers started to believe that people who have a G6PD deficiency may be significantly affected by COVID-19 pandemic like the human coronavirus, HCoV229E and raised the question: Is there any scientific evidences to support a correlation/ association between G6PD deficiency and COVID-19 infection, susceptibility, severity or mortality [9]. Recent retrospective studies strongly suggesting that G6PD-deficient COVID-19 patients may suffer highest chloroquine induced toxicity a drug along with hydroxychloroquine are commonly prescribed widely used worldwide in the treatment of COVID-19 pandemic [10,11]. Moreover, a brief overview of the protective action of GSH against the exacerbated inflammation triggered by COVID-19 upon ACE/ACE2 imbalance was reported [12]. Additional evidence continued to suggest G6PD deficiency may not only play a role in COVID-19 susceptibility, but also severity of infection, therefore in order to answer this question, it would be Cli","PeriodicalId":92596,"journal":{"name":"Trends in diabetes and metabolism","volume":"151 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76856940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
G. Manjarrez‐Gutierrez, Rocío Herrera-Márquez, Guillermina Lara-Pérez, Yesenia Serrano-Hernández, José A Mondragón-Herrera, J. Hernández-Rodríguez
Objective: To determine if brain serotonergic activity increase induced by the treatment with fluoxetine plus metformin can decrease insulin resistance (IR) in adolescents with metabolic syndrome (MetS). Methods: A quasi-experimental study was conducted in 40 adolescents with MetS and IR. IR was determined through homeostatic model assessment (HOMA). After IR was determined in MetS patients, treatment with fluoxetine and metformin was started and continued for 20 weeks. At the beginning and at the end of treatment, all patients had L-tryptophan free fraction (FFT), glucose and insulin plasma levels determined, as well as HOMA, lipid profile and intensity-dependent auditory-evoked potentials (IDAEPs) in order to measure brain 5-HT activity. Results: At baseline, the adolescents had obesity, hyperglycemia, hyperinsulinemia, IR, dyslipidemia and decreased FFT, as well as a steeper AFS slope of the N1/ P2 component of IDAEPs. The treatment with Fluoxetine and metformin reduced body weight, glucose, insulin, triglycerides and LDL-cholesterol and caused an increase in plasma FFT and decrease in the slope of the N1/P2 component of IDAEPs. Interestingly, the treatment also decreased IR at 20 weeks. Conclusion: This work shows that the combined treatment with fluoxetine and metformin decreases insulin resistance concurrently with an increase in brain serotonergic metabolic and functional activity, expressed by an increase in plasma FFT and a decrease in the N1/P2 ASF slope of the IDAEPs in patients with MetS.
{"title":"Fluoxetine and metformin combined treatment decreases insulin resistance in patients with metabolic syndrome","authors":"G. Manjarrez‐Gutierrez, Rocío Herrera-Márquez, Guillermina Lara-Pérez, Yesenia Serrano-Hernández, José A Mondragón-Herrera, J. Hernández-Rodríguez","doi":"10.15761/tdm.1000117","DOIUrl":"https://doi.org/10.15761/tdm.1000117","url":null,"abstract":"Objective: To determine if brain serotonergic activity increase induced by the treatment with fluoxetine plus metformin can decrease insulin resistance (IR) in adolescents with metabolic syndrome (MetS). Methods: A quasi-experimental study was conducted in 40 adolescents with MetS and IR. IR was determined through homeostatic model assessment (HOMA). After IR was determined in MetS patients, treatment with fluoxetine and metformin was started and continued for 20 weeks. At the beginning and at the end of treatment, all patients had L-tryptophan free fraction (FFT), glucose and insulin plasma levels determined, as well as HOMA, lipid profile and intensity-dependent auditory-evoked potentials (IDAEPs) in order to measure brain 5-HT activity. Results: At baseline, the adolescents had obesity, hyperglycemia, hyperinsulinemia, IR, dyslipidemia and decreased FFT, as well as a steeper AFS slope of the N1/ P2 component of IDAEPs. The treatment with Fluoxetine and metformin reduced body weight, glucose, insulin, triglycerides and LDL-cholesterol and caused an increase in plasma FFT and decrease in the slope of the N1/P2 component of IDAEPs. Interestingly, the treatment also decreased IR at 20 weeks. Conclusion: This work shows that the combined treatment with fluoxetine and metformin decreases insulin resistance concurrently with an increase in brain serotonergic metabolic and functional activity, expressed by an increase in plasma FFT and a decrease in the N1/P2 ASF slope of the IDAEPs in patients with MetS.","PeriodicalId":92596,"journal":{"name":"Trends in diabetes and metabolism","volume":"11 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80220189","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
David R Luke, Edith MY Cheng, Karen Ka Yan Lee, Carl W Rausch, Erin S. Stokes, Ronald W Harris
Background/objectives: Current practice is to treat diabetics with oral hypoglycemics, insulin, or a combination of both; these systemic interventions are not without risk. The reduction in glucose excursion is a new therapeutic paradigm with non-systemic interventions which has been suggested to delay diabetic-associated complications. BTI320, derived from galactomannan, is a non-systemic drug to attenuate postprandial glucose excursion by blocking carbohydrate hydrolyzing enzymes within the gastrointestinal tract. Earlier studies of BTI320 have shown decreased glucose excursions with relatively few adverse effects. Subjects/methods: This double-blind, placebo-controlled, 3-period crossover, outpatient study evaluated two different doses of BTI320, 4 g and 8 g three times daily before meals, for 7 days in 23 adults with Type 2 diabetes (mean age 54 years, BMI 31.4 kg/m2). The primary endpoint of the response of postprandial glucose excursion was measured by the area under the curve from 0 to 4 hours (PPG-AUC0-4) following a high carbohydrate meal on the final day of dosing in each crossover arm. Results: The mean (± SD) PPG-AUC0-4 after 7 days of dosing placebo, 4 g, and 8 g BTI320 were 179.09 ± 157.271, 146.61 ± 98.604, and 179.09 ± 157.27 mmol/L*min, respectively, in the intent-to-treat population, demonstrating appreciable effects of 4 g BTI-320 compared with placebo. Similar trends were found in the PPG peak glucose levels and time to peak glucose concentrations. Consistent with other studies, the mean glucose serum concentrations at 2 hours following 4 g BTI320 (7.57 ± 1.519 mmol/L) were markedly lower than those following placebo and 8 g BTI320 (7.63 ± 1.826 and 7.68 ± 1.711 mg/dL, respectively). Conclusion: Data from this proof of concept study comparing two doses (4 and 8 g) of BTI320 demonstrated evidence of 4 g BTI320 in reducing glucose excursions compared with the 8 g BTI320 and placebo arms per subject. Whereas these data support other published studies of BTI320 limiting the magnitude of glucose excursion, variables such as rate of glucose absorption, age of the patient, and amount of carbohydrates in each meal, amongst others, require an expanded population in a Phase 3 trial to confirm these findings. *Correspondence to: David R Luke, Senior Medical Consultant, Clinical Development, DRL Pharmaceutical Consulting, LLC, 43 Chriswood Trace, Ledyard, CT 06339 USA, Tel: (860) 608-5296, E-mail: DLuke4@Comcast.net
背景/目的:目前的做法是口服降糖药、胰岛素或两者联合治疗糖尿病;这些系统性干预并非没有风险。减少葡萄糖漂移是一种新的治疗模式，非系统性干预已被建议延迟糖尿病相关并发症。BTI320来源于半乳甘露聚糖，是一种非全身性药物，通过阻断胃肠道内的碳水化合物水解酶来减轻餐后葡萄糖漂移。早期的研究表明，BTI320降低了葡萄糖漂移，副作用相对较少。受试者/方法:这项双盲、安慰剂对照、3期交叉、门诊研究评估了23名2型糖尿病成年人(平均年龄54岁，体重指数31.4 kg/m2)每天饭前三次服用4 g和8 g两种不同剂量的BTI320，持续7天。餐后葡萄糖漂移反应的主要终点是通过在给药的最后一天高碳水化合物餐后0至4小时的曲线下面积(PPG-AUC0-4)来测量的。结果:意向治疗人群在给予安慰剂、4 g和8 g BTI-320 7天后PPG-AUC0-4的平均值(±SD)分别为179.09±157.271、146.61±98.604和179.09±157.27 mmol/L*min，与安慰剂相比，4 g BTI-320的效果明显。在PPG峰值葡萄糖水平和达到峰值葡萄糖浓度的时间上也发现了类似的趋势。与其他研究一致，服用4 g BTI320后2小时的平均血清葡萄糖浓度(7.57±1.519 mmol/L)明显低于服用安慰剂和服用8 g BTI320的患者(分别为7.63±1.826和7.68±1.711 mg/dL)。结论:这项概念验证研究的数据比较了两种剂量(4和8 g)的BTI320，结果表明，与8 g BTI320组和安慰剂组相比，4 g BTI320组在降低葡萄糖偏离方面有明显效果。尽管这些数据支持其他已发表的BTI320限制葡萄糖偏移幅度的研究，但诸如葡萄糖吸收率、患者年龄和每餐碳水化合物量等变量需要在3期试验中扩大人群以证实这些发现。*通讯:David R Luke，临床开发高级医学顾问，DRL Pharmaceutical Consulting, LLC, 43 Chriswood Trace, Ledyard, CT 06339 USA，电话:(860)608-5296,E-mail: DLuke4@Comcast.net
{"title":"Dose-ranging study of BTI320 in type 2 diabetic patients","authors":"David R Luke, Edith MY Cheng, Karen Ka Yan Lee, Carl W Rausch, Erin S. Stokes, Ronald W Harris","doi":"10.15761/tdm.1000116","DOIUrl":"https://doi.org/10.15761/tdm.1000116","url":null,"abstract":"Background/objectives: Current practice is to treat diabetics with oral hypoglycemics, insulin, or a combination of both; these systemic interventions are not without risk. The reduction in glucose excursion is a new therapeutic paradigm with non-systemic interventions which has been suggested to delay diabetic-associated complications. BTI320, derived from galactomannan, is a non-systemic drug to attenuate postprandial glucose excursion by blocking carbohydrate hydrolyzing enzymes within the gastrointestinal tract. Earlier studies of BTI320 have shown decreased glucose excursions with relatively few adverse effects. Subjects/methods: This double-blind, placebo-controlled, 3-period crossover, outpatient study evaluated two different doses of BTI320, 4 g and 8 g three times daily before meals, for 7 days in 23 adults with Type 2 diabetes (mean age 54 years, BMI 31.4 kg/m2). The primary endpoint of the response of postprandial glucose excursion was measured by the area under the curve from 0 to 4 hours (PPG-AUC0-4) following a high carbohydrate meal on the final day of dosing in each crossover arm. Results: The mean (± SD) PPG-AUC0-4 after 7 days of dosing placebo, 4 g, and 8 g BTI320 were 179.09 ± 157.271, 146.61 ± 98.604, and 179.09 ± 157.27 mmol/L*min, respectively, in the intent-to-treat population, demonstrating appreciable effects of 4 g BTI-320 compared with placebo. Similar trends were found in the PPG peak glucose levels and time to peak glucose concentrations. Consistent with other studies, the mean glucose serum concentrations at 2 hours following 4 g BTI320 (7.57 ± 1.519 mmol/L) were markedly lower than those following placebo and 8 g BTI320 (7.63 ± 1.826 and 7.68 ± 1.711 mg/dL, respectively). Conclusion: Data from this proof of concept study comparing two doses (4 and 8 g) of BTI320 demonstrated evidence of 4 g BTI320 in reducing glucose excursions compared with the 8 g BTI320 and placebo arms per subject. Whereas these data support other published studies of BTI320 limiting the magnitude of glucose excursion, variables such as rate of glucose absorption, age of the patient, and amount of carbohydrates in each meal, amongst others, require an expanded population in a Phase 3 trial to confirm these findings. *Correspondence to: David R Luke, Senior Medical Consultant, Clinical Development, DRL Pharmaceutical Consulting, LLC, 43 Chriswood Trace, Ledyard, CT 06339 USA, Tel: (860) 608-5296, E-mail: DLuke4@Comcast.net","PeriodicalId":92596,"journal":{"name":"Trends in diabetes and metabolism","volume":"12 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82489078","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
ocular space and the kidney as two distinct organs with vastly different functions and locations
眼腔和肾是两个不同的器官，功能和位置有很大的不同
{"title":"The commonalities of kidney and eye disease","authors":"C. Schultz","doi":"10.15761/tdm.1000119","DOIUrl":"https://doi.org/10.15761/tdm.1000119","url":null,"abstract":"ocular space and the kidney as two distinct organs with vastly different functions and locations","PeriodicalId":92596,"journal":{"name":"Trends in diabetes and metabolism","volume":"38 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76921755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Objective : To review efficacy and safety of the first orally available glucagon-like peptide (GLP-1) receptor agonist semaglutide. Methods : PubMed search published in English, French and Spanish from January 2000 until September 4, 2019. Search terms included “oral semaglutide”, “semaglutide”, glucagon-like peptide-1 receptor, “clinical trials”, “absorption”, “metabolism”, “efficacy”, “safety, “cardiovascular” ‘kidney disease”. Randomized trials, review articles, expert opinions and editorials are included in the review. Results: Oral semaglutide is effectively absorbed in the stomach by absorption enhancer but has to be taken in the fasting state with water, and no food allowed for 30 min after intake. It is generally comparable in efficacy to the subcutaneous form of semaglutide. When compared to liraglutide, oral semaglutide is slightly superior in decreasing hemoglobin A1c (HbA1c) (-0.3% vs liraglutide) and weight (-1.3 kg vs liraglutide) but is associated with more frequent adverse effects (reported by 80% vs 74% of patients). Limited data suggest that oral semaglutide is safe and effective in patients with moderate degree of renal impairment. A large randomized trial of median follow-up of 15.9 months, showed that oral semaglutide was non-inferior to placebo in terms of cardiovascular events and mortality, and might have beneficial effects on reducing some of these events. Conclusions : Oral semaglutide has an efficacy and safety profile consistent with the class of GLP-1 receptor agonists. It represents a useful therapeutic option for patients with type 2 diabetes who are reluctant to take injections. Further studies are needed to establish its long-term efficacy and safety in a large population of
{"title":"Role of oral semaglutide in management of type 2 diabetes","authors":"N. Mikhail","doi":"10.15761/tdm.1000114","DOIUrl":"https://doi.org/10.15761/tdm.1000114","url":null,"abstract":"Objective : To review efficacy and safety of the first orally available glucagon-like peptide (GLP-1) receptor agonist semaglutide. Methods : PubMed search published in English, French and Spanish from January 2000 until September 4, 2019. Search terms included “oral semaglutide”, “semaglutide”, glucagon-like peptide-1 receptor, “clinical trials”, “absorption”, “metabolism”, “efficacy”, “safety, “cardiovascular” ‘kidney disease”. Randomized trials, review articles, expert opinions and editorials are included in the review. Results: Oral semaglutide is effectively absorbed in the stomach by absorption enhancer but has to be taken in the fasting state with water, and no food allowed for 30 min after intake. It is generally comparable in efficacy to the subcutaneous form of semaglutide. When compared to liraglutide, oral semaglutide is slightly superior in decreasing hemoglobin A1c (HbA1c) (-0.3% vs liraglutide) and weight (-1.3 kg vs liraglutide) but is associated with more frequent adverse effects (reported by 80% vs 74% of patients). Limited data suggest that oral semaglutide is safe and effective in patients with moderate degree of renal impairment. A large randomized trial of median follow-up of 15.9 months, showed that oral semaglutide was non-inferior to placebo in terms of cardiovascular events and mortality, and might have beneficial effects on reducing some of these events. Conclusions : Oral semaglutide has an efficacy and safety profile consistent with the class of GLP-1 receptor agonists. It represents a useful therapeutic option for patients with type 2 diabetes who are reluctant to take injections. Further studies are needed to establish its long-term efficacy and safety in a large population of","PeriodicalId":92596,"journal":{"name":"Trends in diabetes and metabolism","volume":"50 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90820702","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yin Yu, Zhiyao Bao, W. Gong, Keqiang Chen, Y. Le, Ji Ming Wang
Hyperglycemia is linked to many inflammatory, metabolic and malignant diseases. High glucose provides inflammatory and cancer cells with more abundant “fuel” that promotes the cell motility, proliferation and production of pro-inflammatory mediators. The “malicious behavior” of activated inflammatory cells and cancer cells is further exacerbated by over-expression of chemoattractant receptors, notably FPRs (mouse Fprs) and tyrosine kinase receptors (TKRs) that are traditionally discovered as mediators of cell migration in response to a number of pathogen and host-derived chemotactic molecular patterns (PMAPs and DAMPs) existing at the diseased sites. In addition, the M1 macrophage polarizing capacity of one of FPRs, Fpr2, acts as a double-edged sword that exacerbates the insulin resistance and obesity in high-fat diet-fed mice. Therefore, while controlling glucose to a physiological level is important, targeting cell surface FPRs and TKRs should also be critical to manage hyperglycemia-associated disease conditions. Müller glial cells, an FPR variant FPR2 (Mouse Fpr2) mediates increased cell chemotaxis, thus recruitment, and proliferation in the retina, in response to an endogenous Fpr2 agonist peptide CRAMP. This process exacerbates the inflammatory conditions and the progression of diabetic retinopacy. In human glioblastoma cells, HG increases the expression and function of the prototype formylpeptide receptor FPR1, which promotes tumor cell invasion, proliferation and production of the angiogenic factor vascular endothelial cell growth factor (VEGF), by interaction with an agonist Annexin 1 (Anx A1) released by necrotic tumor cells. HG also elevates the expression and function of EGFR on glioblastoma cells and bFGFR on Müller cells. Both TKRs cooperation with FPRs to promote cell chemotaxis and proliferation. of the function of chemoattractant receptor FPR1 and the growth factor receptor
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