Browsing by Author "Powers, Alvin C."

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    COVID-19 vaccine prioritisation for type 1 and type 2 diabetes
    (Elsevier, 2021) Powers, Alvin C.; Aronoff, David M.; Eckel, Robert H.; Medicine, School of Medicine
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    Integrated Physiology of the Exocrine and Endocrine Compartments in Pancreatic Diseases: Workshop Proceedings
    (Wolters Kluwer, 2022) Mastracci, Teresa L.; Apte, Minoti; Amundadottir, Laufey T.; Alvarsson, Alexandra; Artandi, Steven; Bellin, Melena D.; Bernal-Mizrachi, Ernesto; Caicedo, Alejandro; Campbell-Thompson, Martha; Cruz-Monserrate, Zobeida; El Ouaamari, Abdelfattah; Gaulton, Kyle J.; Geisz, Andrea; Goodarzi, Mark O.; Hara, Manami; Hull-Meichle, Rebecca L.; Kleger, Alexander; Klein, Alison P.; Kopp, Janel L.; Kulkarni, Rohit N.; Muzumdar, Mandar D.; Naren, Anjaparavanda P.; Oakes, Scott A.; Olesen, Søren S.; Phelps, Edward A.; Powers, Alvin C.; Stabler, Cherie L.; Tirkes, Temel; Whitcomb, David C.; Yadav, Dhiraj; Yong, Jing; Zaghloul, Norann A.; Sander, Maike; Pandol, Stephen J.; Biology, School of Science
    The Integrated Physiology of the Exocrine and Endocrine Compartments in Pancreatic Diseases Workshop was a 1.5-day scientific conference at the National Institutes of Health (Bethesda, MD) that engaged clinical and basic science investigators interested in diseases of the pancreas. This report summarizes the workshop proceedings. The goal of the workshop was to forge connections and identify gaps in knowledge that could guide future research directions. Presentations were segregated into six major themes, including: (a) Pancreas Anatomy and Physiology; (b) Diabetes in the Setting of Exocrine Disease; (c) Metabolic Influences on the Exocrine Pancreas; (d) Genetic Drivers of Pancreatic Diseases; (e) Tools for Integrated Pancreatic Analysis; and (f) Implications of Exocrine-Endocrine Crosstalk. For each theme, there were multiple presentations followed by panel discussions on specific topics relevant to each area of research; these are summarized herein. Significantly, the discussions resulted in the identification of research gaps and opportunities for the field to address. In general, it was concluded that as a pancreas research community, we must more thoughtfully integrate our current knowledge of the normal physiology as well as the disease mechanisms that underlie endocrine and exocrine disorders so that there is a better understanding of the interplay between these compartments.
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    The MafA transcription factor becomes essential to islet β-cells soon after birth
    (American Diabetes Association, 2014-06) Hang, Yan; Yamamoto, Tsunehiko; Benninger, Richard K. P.; Brissova, Marcela; Guo, Min; Bush, Will; Piston, David W.; Powers, Alvin C.; Magnuson, Mark; Thurmond, Debbie C.; Stein, Roland; Department of Pediatrics, IU School of Medicine
    The large Maf transcription factors, MafA and MafB, are expressed with distinct spatial-temporal patterns in rodent islet cells. Analysis of Mafa(-/-) and pancreas-specific Mafa(∆panc) deletion mutant mice demonstrated a primary role for MafA in adult β-cell activity, different from the embryonic importance of MafB. Our interests here were to precisely define when MafA became functionally significant to β-cells, to determine how this was affected by the brief period of postnatal MafB production, and to identify genes regulated by MafA during this period. We found that islet cell organization, β-cell mass, and β-cell function were influenced by 3 weeks of age in Mafa(Δpanc) mice and compromised earlier in Mafa(Δpanc);Mafb(+/-) mice. A combination of genome-wide microarray profiling, electron microscopy, and metabolic assays were used to reveal mechanisms of MafA control. For example, β-cell replication was produced by actions on cyclin D2 regulation, while effects on granule docking affected first-phase insulin secretion. Moreover, notable differences in the genes regulated by embryonic MafB and postnatal MafA gene expression were found. These results not only clearly define why MafA is an essential transcriptional regulator of islet β-cells, but also why cell maturation involves coordinated actions with MafB.
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    β-cell failure in type 2 diabetes: postulated mechanisms and prospects for prevention and treatment
    (Endocrine Society, 2014-06) Halban, Philippe A.; Polonsky, Kenneth S.; Bowden, Donald W.; Hawkins, Meredith A.; Ling, Charlotte; Mather, Kieren J.; Powers, Alvin C.; Rhodes, Christopher J.; Sussel, Lori; Weir, Gordon C.; Medicine, School of Medicine
    OBJECTIVE: This article examines the foundation of β-cell failure in type 2 diabetes (T2D) and suggests areas for future research on the underlying mechanisms that may lead to improved prevention and treatment. RESEARCH DESIGN AND METHODS: A group of experts participated in a conference on 14-16 October 2013 cosponsored by the Endocrine Society and the American Diabetes Association. A writing group prepared this summary and recommendations. RESULTS: The writing group based this article on conference presentations, discussion, and debate. Topics covered include genetic predisposition, foundations of β-cell failure, natural history of β-cell failure, and impact of therapeutic interventions. CONCLUSIONS: β-Cell failure is central to the development and progression of T2D. It antedates and predicts diabetes onset and progression, is in part genetically determined, and often can be identified with accuracy even though current tests are cumbersome and not well standardized. Multiple pathways underlie decreased β-cell function and mass, some of which may be shared and may also be a consequence of processes that initially caused dysfunction. Goals for future research include to 1) impact the natural history of β-cell failure; 2) identify and characterize genetic loci for T2D; 3) target β-cell signaling, metabolic, and genetic pathways to improve function/mass; 4) develop alternative sources of β-cells for cell-based therapy; 5) focus on metabolic environment to provide indirect benefit to β-cells; 6) improve understanding of the physiology of responses to bypass surgery; and 7) identify circulating factors and neuronal circuits underlying the axis of communication between the brain and β-cells.