Jennifer L. Sherr, Lutz Heinemann, G. Alexander Fleming, Richard M. Bergenstal, Daniela Bruttomesso, Hélène Hanaire, Reinhard W. Holl, John R. Petrie, Anne L. Peters & Mark EvansÂ
doi : 10.1007/s00125-022-05744-z
A technological solution for the management of diabetes in people who require intensive insulin therapy has been sought for decades. The last 10 years have seen substantial growth in devices that can be integrated into clinical care.
Beatrice C. Lupsa, Richard G. Kibbey & Silvio E. InzucchiÂ
doi : 10.1007/s00125-022-05815-1
Sodium–glucose cotransporter 2 (SGLT2) inhibitors are a class of medications used by individuals with type 2 diabetes that reduce hyperglycaemia by targeting glucose transport in the kidney, preventing its reabsorption, thereby inducing glucosuria.
Gernot Desoye, Lene Ringholm, Peter Damm, Elisabeth R. Mathiesen & Mireille N. M. van PoppelÂ
doi : 10.1007/s00125-022-05820-4
Despite enormous progress in managing blood glucose levels, pregnancy in women with type 1 diabetes still carries risks for the growing fetus. While, previously, fetal undergrowth was not uncommon in these women, with improved maternal glycaemic control we now see an increased prevalence of fetal overgrowth.
Stamatina Iliodromiti, James McLaren, Nazim Ghouri, Melissa R. Miller, Olof Dahlqvist Leinhard, Jennifer Linge, Stuart Ballantyne, Jonathan Platt, John Foster, Scott Hanvey, Unjali P. Gujral, Alka Kanaya, Naveed Sattar, Mary Ann Lumsden & Jason M. R. GillÂ
doi : 10.1007/s00125-022-05803-5
South Asians have a two- to fivefold higher risk of developing type 2 diabetes than those of white European descent. Greater central adiposity and storage of fat in deeper or ectopic depots are potential contributing mechanisms.
Theresia Sarabhai, Lucia Mastrototaro, Sabine Kahl, Gidon J. Bönhof, Marc Jonuscheit, Pavel Bobrov, Hisayuki Katsuyama, Rainer Guthoff, Martin Wolkersdorfer, Christian Herder, Sven G. Meuth, Sven Dreyer & Michael RodenÂ
doi : 10.1007/s00125-022-05797-0
Hyperbaric oxygen (HBO) therapy may improve hyperglycaemia in humans with type 2 diabetes, but underlying mechanisms are unclear. Our objective was to examine the glucometabolic effects of HBO on whole-body glucose disposal in humans with type 2 diabetes.
Jessica Edstorp, Yuxia Wei, Emma Ahlqvist, Lars Alfredsson, Valdemar Grill, Leif Groop, Bahareh Rasouli, Elin P. Sørgjerd, Per M. Thorsby, Tiinamaija Tuomi, Bjørn O. Ã…svold & Sofia CarlssonÂ
doi : 10.1007/s00125-022-05763-w
Smoking and use of smokeless tobacco (snus) are associated with an increased risk of type 2 diabetes. We investigated whether smoking and snus use increase the risk of latent autoimmune diabetes in adults (LADA) and elucidated potential interaction with HLA high-risk genotypes.
Roger E. Henriksen, Roy M. Nilsen & Ragnhild B. StrandbergÂ
doi : 10.1007/s00125-022-05791-6
Type 2 diabetes is one of the leading causes of death globally and its incidence has increased dramatically over the last two decades. Recent research suggests that loneliness is a possible risk factor for type 2 diabetes.
Kenney Ng, Vibha Anand, Harry Stavropoulos, Riitta Veijola, Jorma Toppari, Marlena Maziarz, Markus Lundgren, Kathy Waugh, Brigitte I. Frohnert, Frank Martin, Olivia Lou, William Hagopian & Peter Achenbach for the T1DI Study Group
doi : 10.1007/s00125-022-05799-y
The aim of this study was to explore the utility of islet autoantibody (IAb) levels for the prediction of type 1 diabetes in autoantibody-positive children.
Brian T. Steffen, Weihong Tang, Pamela L. Lutsey, Ryan T. Demmer, Elizabeth Selvin, Kunihiro Matsushita, Alanna C. Morrison, Weihua Guan, Mary R. Rooney, Faye L. Norby, Nathan Pankratz, David Couper & James S. PankowÂ
doi : 10.1007/s00125-022-05801-7
Genetic predisposition to type 2 diabetes is well-established, and genetic risk scores (GRS) have been developed that capture heritable liabilities for type 2 diabetes phenotypes. However, the proteins through which these genetic variants influence risk have not been thoroughly investigated. This study aimed to identify proteins and pathways through which type 2 diabetes risk variants may influence pathophysiology.
Lauren A. Stalbow, Michael H. Preuss, Roelof A. J. Smit, Nathalie Chami, Lise Bjørkhaug, Ingvild Aukrust, Anna L. Gloyn & Ruth J. F. LoosÂ
doi : 10.1007/s00125-022-05806-2
We examined the contribution of rare HNF1A variants to type 2 diabetes risk and age of diagnosis, and the extent to which their impact is affected by overall genetic susceptibility, across three ancestry groups.
Maria J. Redondo, Sarah J. Richardson, Daniel Perry, Charles G. Minard, Alice L. J. Carr, Todd Brusko, Irina Kusmartseva, Alberto Pugliese & Mark A. AtkinsonÂ
doi : 10.1007/s00125-022-05818-y
TCF7L2 variants are the strongest genetic risk factor for type 2 diabetes. In individuals with type 1 diabetes, these variants are associated with a higher C-peptide AUC, a lower glucose AUC during an OGTT, single autoantibody positivity near diagnosis, particularly in individuals older than 12 years of age, and a lower frequency of type 1 diabetes-associated HLA genotypes.
Rocky Strollo, Chiara Vinci, Y. K. Stella Man, Sara Bruzzaniti, Erica Piemonte, Ghadeer Alhamar, Silvia Irina Briganti, Ilaria Malandrucco, Flavia Tramontana, Chiara Fanali, James Garnett, Roberto Buccafusca, Perrin Guyer, Mark Mamula, Eddie A. James, Paolo Pozzilli, Johnny Ludvigsson, Paul G. Winyard, Mario Galgani & Ahuva NissimÂ
doi : 10.1007/s00125-022-05812-4
Antibodies specific to oxidative post-translational modifications (oxPTM) of insulin (oxPTM-INS) are present in most individuals with type 1 diabetes, even before the clinical onset. However, the antigenic determinants of such response are still unknown. In this study, we investigated the antibody response to oxPTM-INS neoepitope peptides (oxPTM-INSPs) and evaluated their ability to stimulate humoral and T cell responses in type 1 diabetes.
Kyota Aoyagi, Shun-ichi Yamashita, Yoshihiro Akimoto, Chiyono Nishiwaki, Yoko Nakamichi, Haruhide Udagawa, Manabu Abe, Kenji Sakimura, Tomotake Kanki & Mica Ohara-ImaizumiÂ
doi : 10.1007/s00125-022-05800-8
Mitophagy, the selective autophagy of mitochondria, is essential for maintenance of mitochondrial function. Recent studies suggested that defective mitophagy in beta cells caused diabetes. However, because of technical difficulties, the development of a convenient and reliable method to evaluate mitophagy in beta cells in vivo is needed.
Bernhard J. Hering, Cassandra M. Ballou, Melena D. Bellin, Elizabeth H. Payne, Fouad Kandeel, Piotr Witkowski, Rodolfo Alejandro, Michael R. Rickels & Franca B. BartonÂ
doi : 10.1007/s00125-022-05804-4
Islet transplantation has been studied in small cohorts of recipients with type 1 diabetes complicated by severe hypoglycaemic events (SHEs). We determined factors associated with favourable outcomes in a large cohort of recipients reported to the Collaborative Islet Transplant Registry (CITR).
Amy E. Mendham, Lisa K. Micklesfield, Fredrik Karpe, Andre Pascal Kengne, Tinashe Chikowore, Clement N. Kufe, Maphoko Masemola, Nigel J. Crowther, Shane A. Norris, Tommy Olsson, Sölve ElmstÃ¥hl, Tove Fall, Lars Lind & Julia H. GoedeckeÂ
doi : 10.1007/s00125-022-05788-1
Using a targeted proteomics approach, we aimed to identify and validate circulating proteins associated with impaired glucose metabolism (IGM) and type 2 diabetes in a Black South African cohort. In addition, we assessed sex-specific associations between the validated proteins and pathophysiological pathways of type 2 diabetes.
Juyeon Ko, Ivana R. Sequeira, Loren Skudder-Hill, Jaelim Cho, Sally D. Poppitt & Maxim S. PetrovÂ
doi : 10.1007/s00125-022-05793-4
The clinical importance of fat deposition in the liver and pancreas is increasingly recognised. However, to what extent deposition of fat in these two depots is affected by intermediate variables is unknown.
Jacob D. Kohlenberg, Marcello C. Laurenti, Aoife M. Egan, Daniel Schembri Wismayer, Kent R. Bailey, Claudio Cobelli, Chiara Dalla Man & Adrian VellaÂ
doi : 10.1007/s00125-022-05794-3
People with isolated impaired fasting glucose (IFG) have normal beta cell function. We hypothesised that an increased glucose threshold for beta cell secretion explains IFG.
Pomme I. H. G. Simons, Olivier Valkenburg, Marjo P. H. van de Waarenburg, Marleen M. J. van Greevenbroek, M. Eline Kooi, Jacobus F. A. Jansen, Casper G. Schalkwijk, Coen D. A. Stehouwer & Martijn C. G. J. BrouwersÂ
doi : 10.1007/s00125-022-05790-7
Serum sex hormone-binding globulin (SHBG) has been proposed to act as a hepatokine that contributes to the extrahepatic complications observed in non-alcoholic fatty liver disease (NAFLD).
Xin-Ping Zhao, Shiao-Ying Chang, Yuchao Pang, Min-Chun Liao, Junzheng Peng, Julie R. Ingelfinger, John S. D. Chan & Shao-Ling ZhangÂ
doi : 10.1007/s00125-022-05810-6
Senescent renal tubular cells may be linked to diabetic kidney disease (DKD)-related tubulopathy. We studied mice with or without diabetes in which hedgehog interacting protein (HHIP) was present or specifically knocked out in renal tubules (HhipRT-KO), hypothesising that local deficiency of HHIP in the renal tubules would attenuate tubular cell senescence, thereby preventing DKD tubulopathy.
Vit Neuman, Stepanka Pruhova, Michal Kulich, Stanislava Kolouskova, Jan Vosahlo, Martina Romanova, Lenka Petruzelkova, Jaroslav Havlik, Anna Mascellani, Svatopluk Henke, Zdenek Sumnik & Ondrej CinekÂ
doi : 10.1007/s00125-022-05805-3
We previously detected indications that beta cell function is protected by gluten-free diet (GFD) introduced shortly after the onset of childhood type 1 diabetes. The present aim was to assess whether GFD was associated with changes in the gut bacteriome composition and in its functional capacity, and whether such changes mediated the observed effects of GFD on beta cell function.
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