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N o v e m b e r 0 5 - 0 6 , 2 0 1 8 | P h i l a d e l p h i a , U S A
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Obesity Summit 2018 & Diabetes Conference 2018 & Laser Photonics Conference 2018 Biomedical Research | ISSN: 0976-1683| Volume 29
3rd INTERNATIONAL OBESITY SUMMIT AND EXPO
&
&
DIABETES, NUTRITION, METABOLISM & MEDICARE
2nd International Conference on
Joint Event on
OF EXCELLENCE
IN INTERNATIONAL
MEETINGS
YEARS
LASER, OPTICS AND PHOTONICS
World Conference on
Stanley Schwartz, Biomed Res 2018, Volume 29 | DOI: 10.4066/biomedicalresearch-C7-018
A UNIFIED PATHOPHYSIOLOGIC
CONSTRUCT OF DIABETES AND
ITS COMPLICATIONS, INCLUDING
MALIGNANCIES, IN THE CONTEXT OF THE
β-CELL–CLASSIFICATION OF DIABETES
We have previously presented a proposal for a new, beta-cell centric classi-
fication of diabetes based on a consilience of genetic, metabolic, and clin-
ical 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 inflamma-
tion/immune characteristics of the damage to 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 la-
beled ‘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 to damage by the now well-defined abnormal meta-
bolic 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 construct of diabetes and its com-
plications, including malignancies, in the context of the β-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- can be extended to use those
agents, in combination, that also engender weight loss, and decrease CV out-
comes. This approach allows for a more accurate assessment and treatment
of each patient’s disease and effecting true precision medicine.
We also believe that the same pathophysiologic mechanisms that account for
damage to the beta-cells and govern the susceptibility of the cells involved in
the complications of diabetes are likely to explain the association of cancer
and cognitive deficiencies to diabetes and obesity, explaining why a diabetic
medication may affect cancer risk and therapy.
Biography
Stanley Schwartz is an affiliate of the main line
health system and an emeritus associate profes-
sor of medicine at the University of Pennsylvania,
currently in a private practice in Ardmore, Pennsyl-
vania. Stanley Schwartz received his MD in 1973
from the University of Chicago in Chicago, Illinois.
He then completed his residency at the University
of Pennsylvania, followed by a fellowship in endo-
crinology and metabolism at the University of Chi-
cago.
Stanley Schwartz
University of Pennsylvania, USA