DiabetologiaPub Date : 2024-10-18DOI: 10.1007/s00125-024-06287-1
Qian Wang, Megan P. Leask, Kate Lee, Jagdish Jaiswal, Prasanna Kallingappa, Waruni Dissanayake, Chris Puli’uvea, Conor O’Sullivan, Huti Watson, Phillip Wilcox, Rinki Murphy, Troy L. Merry, Peter R. Shepherd
{"title":"The population-specific Thr44Met OCT3 coding variant affects metformin pharmacokinetics with subsequent effects on insulin sensitivity in C57Bl/6J mice","authors":"Qian Wang, Megan P. Leask, Kate Lee, Jagdish Jaiswal, Prasanna Kallingappa, Waruni Dissanayake, Chris Puli’uvea, Conor O’Sullivan, Huti Watson, Phillip Wilcox, Rinki Murphy, Troy L. Merry, Peter R. Shepherd","doi":"10.1007/s00125-024-06287-1","DOIUrl":"https://doi.org/10.1007/s00125-024-06287-1","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Aims/hypothesis</h3><p>Metformin is an important first-line treatment for type 2 diabetes and acts by increasing the body’s ability to dispose of glucose. Metformin’s efficacy can be affected by genetic variants in the transporters that regulate its uptake into cells. The <i>SLC22A3</i> gene (also known as <i>EMT; EMTH; OCT3</i>) codes for organic cation transporter 3 (OCT3), which is a broad-specificity cation transporter that also transports metformin. Most <i>SLC22A3</i> variants reduce the rate of metformin transport but the rs8187715 variant (p.Thr44Met) is reported to increase uptake of metformin in vitro. However, the impact of this on in vivo metformin transport and efficacy is unknown. Very few carriers of this variant have been reported globally, but, notably, all were of Pacific Island descent. Therefore, this study aims to understand the prevalence of this variant in Polynesian peoples (Māori and Pacific peoples) and to understand its impact on metformin transport and efficacy in vivo.</p><h3 data-test=\"abstract-sub-heading\">Methods</h3><p>rs8187715 was genotyped in 310 individuals with Māori and Pacific ancestry recruited in Aotearoa New Zealand. To study this variant in a physiological context, an orthologous knockin mouse model with C57BL/6J background was used. Pharmacokinetic analysis compared uptake rate of metformin into tissues. Plasma growth/differentiation factor 15 (GDF-15) was also measured as a marker of metformin efficacy. Glucose and insulin tolerance was assessed after acute or sustained metformin treatment in knockin and wild-type control mice to examine the impact of the variant on metformin’s glycaemic control.</p><h3 data-test=\"abstract-sub-heading\">Results</h3><p>The minor allele frequency of this variant in the Māori and Pacific participants was 15.4%. There was no association of the variant with common metabolic parameters including diabetes status, BMI, blood pressure, lipids, or blood glucose and HbA<sub>1c</sub>. However, in the orthologous knockin mouse model, the rate of metformin uptake into the blood and tissues was increased. Acute metformin dosing increased insulin sensitivity in variant knockin mice but this effect was lost after longer-term metformin treatment. Metformin’s effects on GDF-15 levels were also lost in variant knockin mice with longer-term metformin treatment.</p><h3 data-test=\"abstract-sub-heading\">Conclusions/interpretation</h3><p>These data provide evidence that the <i>SLC22A3</i> rs8187715 variant accelerates metformin uptake rate in vivo. While this acutely improves insulin sensitivity, there was no increased effect of metformin with longer-term dosing. Thus, our finding of a high prevalence of this variant specifically in Māori and Pacific peoples identifies it as a potential population-specific pharmacogenetic marker with potential to guide metformin therapy in these peoples.</p><h3 data-test=\"abstract-sub-heading\">Graphical Abstract</h3>\u0000","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":"40 1","pages":""},"PeriodicalIF":8.2,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142448154","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
DiabetologiaPub Date : 2024-10-15DOI: 10.1007/s00125-024-06286-2
Miwon Ahn,Sangeeta Dhawan,Erika M McCown,Pablo A Garcia,Supriyo Bhattacharya,Roland Stein,Debbie C Thurmond
{"title":"Beta cell-specific PAK1 enrichment ameliorates diet-induced glucose intolerance in mice by promoting insulin biogenesis and minimising beta cell apoptosis.","authors":"Miwon Ahn,Sangeeta Dhawan,Erika M McCown,Pablo A Garcia,Supriyo Bhattacharya,Roland Stein,Debbie C Thurmond","doi":"10.1007/s00125-024-06286-2","DOIUrl":"https://doi.org/10.1007/s00125-024-06286-2","url":null,"abstract":"AIMS/HYPOTHESISp21 (CDC42/RAC1) activated kinase 1 (PAK1) is depleted in type 2 diabetic human islets compared with non-diabetic human islets, and acute PAK1 restoration in the islets can restore insulin secretory function ex vivo. We hypothesised that beta cell-specific PAK1 enrichment in vivo can mitigate high-fat-diet (HFD)-induced glucose intolerance by increasing the functional beta cell mass.METHODSHuman islets expressing exogenous PAK1 specifically in beta cells were used for bulk RNA-seq. Human EndoC-βH1 cells overexpressing myc-tagged PAK1 were used for chromatin immunoprecipitation (ChIP) and ChIP-sequencing (ChIP-seq). Novel doxycycline-inducible beta cell-specific PAK1-expressing (iβPAK1-Tg) mice were fed a 45% HFD pre-induction for 3 weeks and for a further 3 weeks with or without doxycycline induction. These HFD-fed mice were evaluated for GTT, ITT, 6 h fasting plasma insulin and blood glucose, body composition, islet insulin content and apoptosis.RESULTSBeta cell-specific PAK1 enrichment in type 2 diabetes human islets resulted in decreased beta cell apoptosis and increased insulin content. RNA-seq showed an upregulation of INS gene transcription by PAK1. Using clonal human beta cells, we found that PAK1 protein was localised in the cytoplasm and the nucleus. ChIP studies revealed that nuclear PAK1 enhanced pancreatic and duodenal homeobox1 (PDX1) and neuronal differentiation 1 (NEUROD1) binding to the INS promoter in a glucose-responsive manner. Importantly, the iβPAK1-Tg mice, when challenged with HFD and doxycycline induction displayed enhanced glucose tolerance, increased islet insulin content and reduced beta cell apoptosis when compared with iβPAK1-Tg mice without doxycycline induction.CONCLUSIONS/INTERPRETATIONPAK1 plays an unforeseen and beneficial role in beta cells by promoting insulin biogenesis via enhancing the expression of PDX1, NEUROD1 and INS, along with anti-apoptotic effects, that culminate in increased insulin content and beta cell mass in vivo and ameliorate diet-induced glucose intolerance.DATA AVAILABILITYThe raw and processed RNA-seq data and ChIP-seq data, which has been made publicly available at Gene Expression Omnibus (GEO) at https://www.ncbi.nlm.nih.gov/geo/ , can be accessed in GSE239382.","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":"95 1","pages":""},"PeriodicalIF":8.2,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142439662","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
DiabetologiaPub Date : 2024-10-15DOI: 10.1007/s00125-024-06275-5
Paola S Apaolaza,Yi-Chun Chen,Kavi Grewal,Yannik Lurz,Severin Boulassel,C Bruce Verchere,Teresa Rodriguez-Calvo
{"title":"Quantitative analysis of islet prohormone convertase 1/3 expression in human pancreas donors with diabetes.","authors":"Paola S Apaolaza,Yi-Chun Chen,Kavi Grewal,Yannik Lurz,Severin Boulassel,C Bruce Verchere,Teresa Rodriguez-Calvo","doi":"10.1007/s00125-024-06275-5","DOIUrl":"https://doi.org/10.1007/s00125-024-06275-5","url":null,"abstract":"AIMS/HYPOTHESISIslet prohormone-processing enzymes convert peptide hormone precursors to mature hormones. Defective beta cell prohormone processing and the release of incompletely processed peptide hormones are observed prior to the onset of diabetes, yet molecular mechanisms underlying impaired prohormone processing during the development of diabetes remains largely unknown. Previous studies have shown that prohormone convertase 1/3 (PC1/3) protein and mRNA expression levels are reduced in whole islets from donors with type 1 diabetes, although whether PC1/3-mediated prohormone processing in alpha and beta cells is disrupted in type 1 diabetes remained to be explored. Herein, we aimed to analyse the expression of PC1/3 in islets from non-diabetic donors, autoantibody-positive donors and donors diagnosed with type 1 diabetes or type 2 diabetes.METHODSImmunostaining and high-dimensional image analysis were performed on pancreatic sections from a cross-sectional cohort of 54 donors obtained from the Network for Pancreatic Organ Donors with Diabetes (nPOD) repository, to evaluate PC1/3 expression patterns in islet alpha, beta and delta cells at different stages of diabetes.RESULTSAlpha and beta cell morphology were altered in donors with type 1 diabetes, including decreased alpha and beta cell size. As expected, the insulin-positive and PC1/3-positive areas in the islets were both reduced, and this was accompanied by a reduced percentage of PC1/3-positive and insulin-positive/PC1/3-positive cells in islets. PC1/3 and insulin co-localisation was also reduced. The glucagon-positive area, as well as the percentage of glucagon-positive and glucagon-positive/PC1/3-positive cells in islets, was increased. PC1/3 and glucagon co-localisation was also increased in donors with type 1 diabetes. The somatostatin-positive cell area and somatostatin staining intensity were elevated in islets from donors with recent-onset type 1 diabetes.CONCLUSIONS/INTERPRETATIONOur high-resolution histomorphological analysis of human pancreatic islets from donors with and without diabetes has uncovered details of the cellular origin of islet prohormone peptide processing defects. Reduced beta cell PC1/3 and increased alpha cell PC1/3 in islets from donors with type 1 diabetes pinpointed the functional deterioration of beta cells and the concomitant potential increase in PC1/3 usage for prohormone processing in alpha cells during the pathogenesis of type 1 diabetes. Our finding of PC1/3 loss in beta cells may inform the discovery of new prohormone biomarkers as indicators of beta cell dysfunction, and the finding of elevated PC1/3 expression in alpha cells may encourage the design of therapeutic targets via leveraging alpha cell adaptation in diabetes.","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":"23 1","pages":""},"PeriodicalIF":8.2,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142439658","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
DiabetologiaPub Date : 2024-10-01Epub Date: 2024-08-02DOI: 10.1007/s00125-024-06220-6
Bibi U Nielsen, Inger H M Mathiesen, Rikke Krogh-Madsen, Terese L Katzenstein, Tacjana Pressler, James A M Shaw, Michael R Rickels, Thomas P Almdal, Daniel Faurholt-Jepsen, Darko Stefanovski
{"title":"Insulin sensitivity, disposition index and insulin clearance in cystic fibrosis: a cross-sectional study.","authors":"Bibi U Nielsen, Inger H M Mathiesen, Rikke Krogh-Madsen, Terese L Katzenstein, Tacjana Pressler, James A M Shaw, Michael R Rickels, Thomas P Almdal, Daniel Faurholt-Jepsen, Darko Stefanovski","doi":"10.1007/s00125-024-06220-6","DOIUrl":"10.1007/s00125-024-06220-6","url":null,"abstract":"<p><strong>Aims/hypothesis: </strong>The aim of this study was to investigate insulin secretion, insulin sensitivity, disposition index and insulin clearance by glucose tolerance status in individuals with cystic fibrosis (CF) and exocrine pancreatic insufficiency.</p><p><strong>Methods: </strong>In a cross-sectional study, we conducted an extended (ten samples) OGTT in individuals with pancreatic-insufficient CF (PI-CF). Participants were divided into normal glucose tolerance (NGT), early glucose intolerance (EGI), impaired glucose tolerance (IGT) and CF-related diabetes (CFRD) groups. We used three different oral minimal models to assess insulin secretion, insulin sensitivity and insulin clearance during the OGTT. We evaluated insulin secretion using total secretion (Φ total), first-phase secretion (Φ dynamic) and second-phase secretion (Φ static) from the model, and we estimated the disposition index by multiplying Φ total and insulin sensitivity.</p><p><strong>Results: </strong>Among 61 participants (NGT 21%, EGI 33%, IGT 16%, CFRD 30%), insulin secretion indices (Φ total, dynamic and static) were significantly lower in the CFRD group compared with the other groups. Insulin sensitivity declined with worsening in glucose tolerance (p value for trend <0.001) and the disposition index declined between NGT and EGI and between IGT and CFRD. Those with CFRD had elevated insulin clearance compared with NGT (p=0.019) and low insulin secretion (Φ total) was also associated with high insulin clearance (p<0.001).</p><p><strong>Conclusions/interpretation: </strong>In individuals with PI-CF, disposition index declined with incremental impairment in glucose tolerance due to a reduction in both insulin secretion and insulin sensitivity. Moreover in CF, reduced insulin secretion was associated with higher insulin clearance.</p>","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":" ","pages":"2188-2198"},"PeriodicalIF":8.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11447061/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141874454","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
DiabetologiaPub Date : 2024-10-01Epub Date: 2024-07-30DOI: 10.1007/s00125-024-06231-3
Agnete T Lundgaard, David Westergaard, Timo Röder, Kristoffer S Burgdorf, Margit H Larsen, Michael Schwinn, Lise W Thørner, Erik Sørensen, Kaspar R Nielsen, Henrik Hjalgrim, Christian Erikstrup, Bertram D Kjerulff, Lotte Hindhede, Thomas F Hansen, Mette Nyegaard, Ewan Birney, Hreinn Stefansson, Kári Stefánsson, Ole B V Pedersen, Sisse R Ostrowski, Peter Rossing, Henrik Ullum, Laust H Mortensen, Dorte Vistisen, Karina Banasik, Søren Brunak
{"title":"Longitudinal metabolite and protein trajectories prior to diabetes mellitus diagnosis in Danish blood donors: a nested case-control study.","authors":"Agnete T Lundgaard, David Westergaard, Timo Röder, Kristoffer S Burgdorf, Margit H Larsen, Michael Schwinn, Lise W Thørner, Erik Sørensen, Kaspar R Nielsen, Henrik Hjalgrim, Christian Erikstrup, Bertram D Kjerulff, Lotte Hindhede, Thomas F Hansen, Mette Nyegaard, Ewan Birney, Hreinn Stefansson, Kári Stefánsson, Ole B V Pedersen, Sisse R Ostrowski, Peter Rossing, Henrik Ullum, Laust H Mortensen, Dorte Vistisen, Karina Banasik, Søren Brunak","doi":"10.1007/s00125-024-06231-3","DOIUrl":"10.1007/s00125-024-06231-3","url":null,"abstract":"<p><strong>Aims/hypothesis: </strong>Metabolic risk factors and plasma biomarkers for diabetes have previously been shown to change prior to a clinical diabetes diagnosis. However, these markers only cover a small subset of molecular biomarkers linked to the disease. In this study, we aimed to profile a more comprehensive set of molecular biomarkers and explore their temporal association with incident diabetes.</p><p><strong>Methods: </strong>We performed a targeted analysis of 54 proteins and 171 metabolites and lipoprotein particles measured in three sequential samples spanning up to 11 years of follow-up in 324 individuals with incident diabetes and 359 individuals without diabetes in the Danish Blood Donor Study (DBDS) matched for sex and birth year distribution. We used linear mixed-effects models to identify temporal changes before a diabetes diagnosis, either for any incident diabetes diagnosis or for type 1 and type 2 diabetes mellitus diagnoses specifically. We further performed linear and non-linear feature selection, adding 28 polygenic risk scores to the biomarker pool. We tested the time-to-event prediction gain of the biomarkers with the highest variable importance, compared with selected clinical covariates and plasma glucose.</p><p><strong>Results: </strong>We identified two proteins and 16 metabolites and lipoprotein particles whose levels changed temporally before diabetes diagnosis and for which the estimated marginal means were significant after FDR adjustment. Sixteen of these have not previously been described. Additionally, 75 biomarkers were consistently higher or lower in the years before a diabetes diagnosis. We identified a single temporal biomarker for type 1 diabetes, IL-17A/F, a cytokine that is associated with multiple other autoimmune diseases. Inclusion of 12 biomarkers improved the 10-year prediction of a diabetes diagnosis (i.e. the area under the receiver operating curve increased from 0.79 to 0.84), compared with clinical information and plasma glucose alone.</p><p><strong>Conclusions/interpretation: </strong>Systemic molecular changes manifest in plasma several years before a diabetes diagnosis. A particular subset of biomarkers shows distinct, time-dependent patterns, offering potential as predictive markers for diabetes onset. Notably, these biomarkers show shared and distinct patterns between type 1 diabetes and type 2 diabetes. After independent replication, our findings may be used to develop new clinical prediction models.</p>","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":" ","pages":"2289-2303"},"PeriodicalIF":8.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11446992/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141792098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
DiabetologiaPub Date : 2024-10-01Epub Date: 2024-07-05DOI: 10.1007/s00125-024-06213-5
Douwe F de Wit, Coco M Fuhri Snethlage, Elena Rampanelli, Kim Maasen, Noortje Walpot, Daniël H van Raalte, Max Nieuwdorp, Maarten R Soeters, Nordin M J Hanssen
{"title":"Higher fibre and lower carbohydrate intake are associated with favourable CGM metrics in a cross-sectional cohort of 470 individuals with type 1 diabetes.","authors":"Douwe F de Wit, Coco M Fuhri Snethlage, Elena Rampanelli, Kim Maasen, Noortje Walpot, Daniël H van Raalte, Max Nieuwdorp, Maarten R Soeters, Nordin M J Hanssen","doi":"10.1007/s00125-024-06213-5","DOIUrl":"10.1007/s00125-024-06213-5","url":null,"abstract":"<p><strong>Aims/hypothesis: </strong>The aim of this work was to investigate the association between macronutrient intakes and continuous glucose monitoring (CGM) metrics in individuals with type 1 diabetes.</p><p><strong>Methods: </strong>In 470 individuals with type 1 diabetes of the GUTDM1 cohort (65% female, median age 40 [IQR 28-53] years, median diabetes duration 15 [IQR 6-29] years), we used logistic regression to establish associations between macronutrient intakes and the CGM metrics time in range (TIR, time spent between 3.9-10.0 mmol/l blood glucose, optimally set at ≥70%) and time below range (TBR, <3.9 mmol/l blood glucose, optimally set at <4%). ORs were expressed per 1 SD intake of nutrient and were adjusted for other macronutrient intakes, age, sex, socioeconomic status, BMI, duration of type 1 diabetes, pump use, insulin dose and alcohol intake.</p><p><strong>Results: </strong>The median (IQR) TIR was 67 (51-80)% and TBR was 2 (1-4)%; the mean ± SD energy intake was 6879±2001 kJ, fat intake 75±31 g, carbohydrate intake 162±63 g, fibre intake 20±9 g and protein intake 70±24 g. A higher fibre intake and a lower carbohydrate intake were associated with higher odds of having a TIR≥70% (OR [95% CI] 1.64 [1.22, 2.24] and 0.67 [0.51, 0.87], respectively), whereas solely a higher carbohydrate intake was associated with TBR<4% (OR 1.34 [95% CI 1.02, 1.78]).</p><p><strong>Conclusions/interpretation: </strong>A higher fibre intake is independently associated with a higher TIR. A higher carbohydrate intake is associated with less time spent in hypoglycaemia, a lower TIR and a higher time above range. These findings warrant confirmatory (interventional) investigations and may impact current nutritional guidelines for type 1 diabetes.</p>","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":" ","pages":"2199-2209"},"PeriodicalIF":8.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11446970/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141533951","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
DiabetologiaPub Date : 2024-10-01Epub Date: 2024-07-05DOI: 10.1007/s00125-024-06216-2
Anna McLean, Louise Maple-Brown, Helen R Murphy
{"title":"Technology advances in diabetes pregnancy: right technology, right person, right time.","authors":"Anna McLean, Louise Maple-Brown, Helen R Murphy","doi":"10.1007/s00125-024-06216-2","DOIUrl":"10.1007/s00125-024-06216-2","url":null,"abstract":"<p><p>This review outlines some of the extraordinary recent advances in diabetes technology, which are transforming the management of type 1 diabetes before, during and after pregnancy. It highlights recent improvements associated with use of continuous glucose monitoring (CGM) but acknowledges that neither CGM nor insulin pump therapy are adequate for achieving the pregnancy glucose targets. Furthermore, even hybrid closed-loop (HCL) systems that are clinically effective outside of pregnancy may not confer additional benefits throughout pregnancy. To date, there is only one HCL system, the CamAPS FX, with a strong evidence base for use during pregnancy, suggesting that the pregnancy benefits are HCL system specific. This is in stark contrast to HCL system use outside of pregnancy, where benefits are HCL category specific. The CamAPS FX HCL system has a rapidly adaptive algorithm and lower glucose targets with benefits across all maternal glucose categories, meaning that it is applicable for all women with type 1 diabetes, before and during pregnancy. For women of reproductive years living with type 2 diabetes, the relative merits of using non-insulin pharmacotherapies vs diabetes technology (dipeptidyl peptidase-4 inhibitors, glucagon-like peptide-1 receptor agonists and sodium-glucose cotransporter 2 inhibitors) are unknown. Despite the urgent unmet need and potential benefits, studies of pharmacotherapy and technology use are extremely limited in pregnant women with type 2 diabetes.</p>","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":" ","pages":"2103-2113"},"PeriodicalIF":8.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11447080/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141533953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
DiabetologiaPub Date : 2024-10-01Epub Date: 2024-08-15DOI: 10.1007/s00125-024-06195-4
Peter M Nilsson, Allan Vaag
{"title":"Reduced type 2 diabetes incidence reflecting end of post-World War II calorie restrictions in Germany.","authors":"Peter M Nilsson, Allan Vaag","doi":"10.1007/s00125-024-06195-4","DOIUrl":"10.1007/s00125-024-06195-4","url":null,"abstract":"","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":" ","pages":"2367-2368"},"PeriodicalIF":8.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141981973","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
DiabetologiaPub Date : 2024-10-01Epub Date: 2024-08-17DOI: 10.1007/s00125-024-06255-9
Carolin T Lehner, Gunther Schauberger, Stefanie J Klug
{"title":"Reduced type 2 diabetes incidence reflecting end of post‑World War II calorie restrictions in Germany. Reply to Nilsson PM, Vaag A [letter].","authors":"Carolin T Lehner, Gunther Schauberger, Stefanie J Klug","doi":"10.1007/s00125-024-06255-9","DOIUrl":"10.1007/s00125-024-06255-9","url":null,"abstract":"","PeriodicalId":11164,"journal":{"name":"Diabetologia","volume":" ","pages":"2369-2370"},"PeriodicalIF":8.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11446940/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141995482","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}