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Diabetes, Cardio-Metabolic Newsletter
Beta-Cell Centric Classification of DM
11/30/2015
1/25/16
MY ARTICLE Published in Diabetes Care Feb issue- Reviewd by Diabetes in Control
The use of classification systems and unvarying diagnostic standards help form a mutual language among patients, physicians and other
healthcare professionals. As of now, the primary classification system identifies four types of diabetes mellitus: type 1, type 2, “other
specific types” (which include genetic defects of beta-cell function, genetic defects in insulin action, diseases of exocrine pancreas and
more) and gestational diabetes. Since the first distinction between presentations of the disease from back in January 1936, the
categorization of diabetes has been through numerous changes in order to keep up with new research and findings on the best way to help
patients combating the disease. However, the inherent setback with the currently established system lays in the fact that it is inadequate
with the present understanding of the phenotypes associated with diabetes. Alongside this and the limited research and information present
at the time of formulating the current system, the designations related with the different types of diabetes are vague and inaccurate. Due to
this fact and current evidence-based practice, there is a call to revise the current classification of diabetes mellitus and focus on a β-cell
centric classification schema, according to a new article published online in Diabetes Care Jan. 21, 2016.Based on new research performed
by Stanley Schwartz and affiliates, there is a new proposition for using a β-cell centered model for diabetes, which supports the notion that
all diabetes originates from an abnormal pancreatic β-cell. Type 1 diabetes has been thought of as an ailment of low insulin production,
while type 2 has usually been of insulin resistance. This discrepancy is not clear or helpful. Schwartz and colleagues suppose all diabetes is
a product of impairment to beta cells (which produce insulin) and according to this theory, insulin resistance just reveals the rudimentary
deficiency in insulin production. Only one-third of individuals with insulin resistance will go on to develop diabetes. The basis of the new
classification system is treatment of patients as individuals though currently most prescribers will initiate treatment based on a diagnosis
instead of the person. Schwartz believes that diabetes is rooted to β-cell and because of this, classification of diabetes types should be based
on causes of that damage so physicians will know how to go about treatment. This “β-cell centric” criterion recognizes that β-cell damage
can be caused by inflammation, immune actions, gut biome, high fatty acids, high glucose levels, genetics and other causes; categorization
founded on these sources can help cultivate an improved treatment strategy, as opposed to simply knocking down an individual’s glucose
level. Defining key markers and the processes of care in using them will allot appropriate patient-centric approaches with either currently
established medications or an up-and-coming drug.This proposed model acknowledges a total of 11 interconnecting pathways that
contribute to hyperglycemia, which are prompted by the transformation of genetic predispositions to insulin resistance. These pathways of
hyperglycemia contribute to β-cell dysfunction within the liver, adipose, brain, colon, immune dysregulation and muscle. The “damage
caused results in downstream hyperglycemia arising from increased glucagon secretion, as well as a reduction in insulin production,
incretin effect and amylin levels.” For any one patient, the routes for hyperglycemia vary and more than likely involve numerous pathways.
It is significant to note that these arbitrating pathways of hyperglycemia are common across prediabetes, type 1 diabetes, type 2 diabetes
and other outlined forms of the disease state. The most ideal management model presented was the impression that treatment should
comprise the use of the least amount of agents to help in targeting the greatest number of these particular mediating pathways of
hyperglycemia in any given patient. The research also noted that any treatment option that would potentially be detrimental to the longterm integrity of the β-cells–specifically including sulfonylureas and glinides–should be avoided because any potential benefits of the
medications are severely outweighed by the risks associated with their use.This proposed schema is a theoretical foundation that can help
enhance the management of patients with diabetes. The β-cell centered schema is a great step towards guiding research for the future of this
disease state with the hopes of influencing areas that focus on mechanisms that lead to β-cell damage, effects of reduced β-cell function and
overall pathology associated with these mechanisms.
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