Tag Archives: diabetes

We Know More Than We Can Tell About Diabetes and Vascular Disease: The 2016 Edwin Bierman Award Lecture

The Edwin Bierman Award Lecture is presented in honor of the memory of Edwin L. Bierman, MD, an exemplary scientist, mentor, and leader in the field of diabetes, obesity, hyperlipidemia, and atherosclerosis. The award and lecture recognizes a leading scientist in the field of macrovascular complications and contributing risk factors in diabetes. Clay F. Semenkovich, MD, the Irene E. and Michael M. Karl Professor and Chief of the Division of Endocrinology, Metabolism and Lipid Research at Washington University School of Medicine in St. Louis, St. Louis, MO, received the prestigious award at the American Diabetes Association’s 76th Scientific Sessions, 10–14 June 2016, in New Orleans, LA. He presented the Edwin Bierman Award Lecture, “We Know More Than We Can Tell About Diabetes and Vascular Disease,” on Sunday, 12 June 2016.

Diabetes is a disorder of abnormal lipid metabolism, a notion strongly supported by the work of Edwin Bierman, for whom this eponymous lecture is named. This abnormal lipid environment continues to be associated with devastating vascular complications in diabetes despite current therapies, suggesting that our understanding of the pathophysiology of blood vessel disease in diabetes is limited. In this review, potential new insights into the nature of diabetic vasculopathy will be discussed. Recent observations suggest that while the concept of distinct macrovascular and microvascular complications of diabetes has been useful, vascular diseases in diabetes may be more interrelated than previously appreciated. Moreover, the intermediary metabolic pathway of de novo lipogenesis, which synthesizes lipids from simple precursors, is robustly sensitive to insulin and may contribute to these complications. De novo lipogenesis requires fatty acid synthase, and recent studies of this enzyme suggest that endogenously produced lipids are channeled to specific intracellular sites to affect physiology. These findings raise the possibility that novel approaches to treating diabetes and its complications could be based on altering the intracellular lipid milieu.

Diabetes Journal current issue





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New Insulin Glargine 300 Units/mL Versus Glargine 100 Units/mL in People With Type 2 Diabetes Using Basal and Mealtime Insulin: Glucose Control and Hypoglycemia in a 6-Month Randomized Controlled Trial (EDITION 1)

Matthew C. Riddle
Oct 1, 2014; 37:2755-2762
Emerging Technologies and Therapeutics
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In This Issue of Diabetes

Diabetes Journal current issue





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In This Issue of Diabetes Care

May 1, 2017; 40:627-628
In This Issue
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Response to Comment on Chen et al. Risk of Developing Type 2 Diabetes in Adolescents and Young Adults With Autism Spectrum Disorder: A Nationwide Longitudinal Study. Diabetes Care 2016;39:788-793

Mu-Hong Chen
May 1, 2017; 40:e60-e60
e-Letters: Comments and Responses
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Genetic Screening for the Risk of Type 2 Diabetes: Worthless or valuable?

Valeriya Lyssenko
Aug 1, 2013; 36:S120-S126
Diabetes Pathophysiology
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Dietary Sugar and Body Weight: Have We Reached a Crisis in the Epidemic of Obesity and Diabetes?: Health Be Damned! Pour on the Sugar

George A. Bray
Apr 1, 2014; 37:950-956
Current Concepts of Type 2 Diabetes Prevention
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Diabetes: Leveraging the Tipping Point of the Diabetes Pandemic

Diabetes Journal current issue





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Comparative Pathogenesis of Autoimmune Diabetes in Humans, NOD Mice, and Canines: Has a Valuable Animal Model of Type 1 Diabetes Been Overlooked?

Despite decades of research in humans and mouse models of disease, substantial gaps remain in our understanding of pathogenic mechanisms underlying the development of type 1 diabetes. Furthermore, translation of therapies from preclinical efforts capable of delaying or halting β-cell destruction has been limited. Hence, a pressing need exists to identify alternative animal models that reflect human disease. Canine insulin deficiency diabetes is, in some cases, considered to follow autoimmune pathogenesis, similar to NOD mice and humans, characterized by hyperglycemia requiring lifelong exogenous insulin therapy. Also similar to human type 1 diabetes, the canonical canine disorder appears to be increasing in prevalence. Whereas islet architecture in rodents is distinctly different from humans, canine pancreatic endocrine cell distribution is more similar. Differences in breed susceptibility alongside associations with MHC and other canine immune response genes parallel that of different ethnic groups within the human population, a potential benefit over NOD mice. The impact of environment on disease development also favors canine over rodent models. Herein, we consider the potential for canine diabetes to provide valuable insights for human type 1 diabetes in terms of pancreatic histopathology, impairment of β-cell function and mass, islet inflammation (i.e., insulitis), and autoantibodies specific for β-cell antigens.

Diabetes Journal current issue





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Type 2 Diabetes: Demystifying the Global Epidemic

Type 2 diabetes (T2D) has attained the status of a global pandemic, spreading from affluent industrialized nations to the emerging economies of Asia, Latin America, and Africa. There is significant global variation in susceptibility to T2D, with Pacific Islanders, Asian Indians, and Native Americans being considerably more prone to develop the disorder. Although genetic factors may play a part, the rapidity with which diabetes prevalence has risen among these populations reflects the far-ranging and rapid socioeconomic changes to which they have been exposed over the past few decades. Traditionally, obesity and its correlate, insulin resistance, have been considered the major mediators of T2D risk; however, recent evidence shows that early loss of β-cell function plays an important role in the pathogenesis of T2D, especially in nonobese individuals such as South Asians. Knowledge of the modifiable risk factors of T2D is important, as it forms the basis for designing cost-effective preventive and therapeutic strategies to slow the epidemic in populations at increased risk. Lessons learned from randomized prevention trials need to be implemented with appropriate cultural adaptations, accompanied by empowerment of the community, if the diabetes epidemic is to be slowed or halted.

Diabetes Journal current issue





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