Research Topic

Unified Pathophysiologic Construct of Diabetes and its Complications in The Context of the B-cell–Classification of Diabetes

About this Research Topic

We have previously presented a proposal for a new, beta-cell centric classification of diabetes based on a consilience of genetic, metabolic, and clinical research that have accrued since the current classification was instituted . It recognizes that the beta-cell is THE core defect in all patients with diabetes. Differences in the genetics, insulin resistance, environment and inflammation/immune characteristics that damage the beta-cell in each individual will determine the phenotypic presentation of hyperglycemia and allow for a patient-centric, precision medicine therapeutic approach , part of which we have labeled ‘the Egregious Eleven’.

We now recognize the same pathophysiologic mechanisms that account for damage to the beta-cells govern the susceptibility of the cells involved in the complications of diabetes by the now well-defined abnormal metabolic environment that typifies beta-cell dysfunction. This abnormal metabolic environment is typified by oxidative stress which alters metabolic pathways a la Brownlee’s Hypothesis model, alterations in gene expression, epigenetics, and inflammation. This Unified Pathophysiologic Approach to The Complications of Diabetes in The Context of the B-cell–Classification of diabetes allows us to understand the varied risk of developing complications of diabetes with similar levels of glycemic control, how non-glycemic effects of some medications for diabetes result in marked complication risk modification and the value treating co-morbidities of diabetes in effecting complication risk.

Principles we outlined in using ‘the Egregious Eleven’ model- use agents that preserve beta-cell function, treat with least number of agents that treat most number of mechanisms of hyperglycemia without hypoglycemia- can be extended to use those agents, in combination, that also engender weight loss, and decrease CV outcomes. This approach allows for a more accurate assessment of each patient’s disease via markers for genomics, proteomics, and metabolomics and effecting true precision medicine.

We aim to publish a collection of articles -original research, perspective pieces, opinion pieces, reviews- discuss – positively as well as critically- these principles and their implications for refinement, future research , education , and most importantly, care for our patients with Diabetes Mellitus.


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

We have previously presented a proposal for a new, beta-cell centric classification of diabetes based on a consilience of genetic, metabolic, and clinical research that have accrued since the current classification was instituted . It recognizes that the beta-cell is THE core defect in all patients with diabetes. Differences in the genetics, insulin resistance, environment and inflammation/immune characteristics that damage the beta-cell in each individual will determine the phenotypic presentation of hyperglycemia and allow for a patient-centric, precision medicine therapeutic approach , part of which we have labeled ‘the Egregious Eleven’.

We now recognize the same pathophysiologic mechanisms that account for damage to the beta-cells govern the susceptibility of the cells involved in the complications of diabetes by the now well-defined abnormal metabolic environment that typifies beta-cell dysfunction. This abnormal metabolic environment is typified by oxidative stress which alters metabolic pathways a la Brownlee’s Hypothesis model, alterations in gene expression, epigenetics, and inflammation. This Unified Pathophysiologic Approach to The Complications of Diabetes in The Context of the B-cell–Classification of diabetes allows us to understand the varied risk of developing complications of diabetes with similar levels of glycemic control, how non-glycemic effects of some medications for diabetes result in marked complication risk modification and the value treating co-morbidities of diabetes in effecting complication risk.

Principles we outlined in using ‘the Egregious Eleven’ model- use agents that preserve beta-cell function, treat with least number of agents that treat most number of mechanisms of hyperglycemia without hypoglycemia- can be extended to use those agents, in combination, that also engender weight loss, and decrease CV outcomes. This approach allows for a more accurate assessment of each patient’s disease via markers for genomics, proteomics, and metabolomics and effecting true precision medicine.

We aim to publish a collection of articles -original research, perspective pieces, opinion pieces, reviews- discuss – positively as well as critically- these principles and their implications for refinement, future research , education , and most importantly, care for our patients with Diabetes Mellitus.


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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20 March 2018 Manuscript

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Manuscripts can be submitted to this Research Topic via the following journals:

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Topic Editors

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Submission Deadlines

20 March 2018 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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