August 14, 2018 : DCMS #410

DISASTERS AVERTED — Near Miss Case Studies

SGLT-2 Inhibitors: What You And Your Patient Should Know to Prevent DKA

EXCLUSIVE INTERVIEW — Candid Video Interviews with Top Practitioners

Stanley Schwartz on the Changing Classifications of Diabetes

HOMERUN SLIDES — Great Clinical Presentation Highlights

Pathophysiology of Type 1 Diabetes Part 4

CLINICAL GEMS — The Best from Diabetes Texts

International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #138: Pathogenesis of Type 2 Diabetes Mellitus Part 9

MOST POPULAR ARTICLES OF THE MONTH

#1 37-Year-Old Hypertensive Drug Improves Beta Cell Function and Insulin Production
#2 One More Benefit for SGLT-2 Inhibitors
#3 Vitamin D Supplementation for Diabetes Prevention

In my editor’s desk on Saturday I used the moniker “insulin dependent type 2 diabetes patients” describing an article our intern had done on adding an SGLT-2 Inhibitor to insulin use. I got some feedback from some of you as to my choice of words, and was this a new “type of diabetes.” I was surprised by the response that some of you were more concerned about the name than the information.

This week in our interview with Dr. Stanley Schwartz at the AACE meetings, he makes a good case as to how we really need to change the classifications of diabetes and standards of treatment to be based on the individual patient and not on what are common monikers or common step therapies. If you want to see what patient focused therapy is, and how he can hone in based on his own definitions, you need to watch this video.

Dave Joffe

Editor-in-chief

Teach patients what DKA is and how to prevent it. Include in your teaching that glucose can be normal or only slightly elevated and it can still happen. Teach that having an illness and/or dehydration increases this risk.

Stanley Schwartz, MD, FACP, FACE is an Affiliate of the Main Line Health System, and an Emeritus Associate Professor of Medicine at the University of Pennsylvania, currently in a private practice in Ardmore, Pa.  Dr. 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 endocrinology and metabolism at the University of Chicago.

In this week’s Homerun Slides, the conclusion of the pathophysiology of type 1 diabetes with the side effects of insulin and treating hypoglycemia.

In summary, postbinding defects in insulin action primarily are responsible for the insulin resistance in T2DM. Diminished insulin binding, when present, is modest and secondary to downregulation of the insulin receptor by chronic hyperinsulinemia. In type 2 diabetic patients with overt fasting hyperglycemia, a number of postbinding defects have been demonstrated, including reduced insulin receptor tyrosine kinase activity, insulin signal transduction abnormalities, decreased glucose transport, diminished glucose phosphorylation, and impaired glycogen synthase activity. The glycolytic/glucose oxidative pathway is largely intact and, when defects are observed, they appear to be acquired secondary to enhanced FFA/lipid oxidation. From the quantitative standpoint, impaired glycogen synthesis represents the major pathway responsible for the insulin resistance in T2DM, and is present long before the onset of overt diabetes, that is, in normal glucose-tolerant, insulin-resistant prediabetic subjects and in individuals with IGT. The impairment in glycogen synthase activation appears to result from a defect in the ability of insulin to phosphorylate IRS-1, causing a reduced association of the p85 subunit of PI-3 kinase with IRS-1 and decreased activation of the enzyme PI-3 kinase.

Researchers discover safe and effective therapy to reduce insulin requirements and hypoglycemic episodes in adult subjects with recent onset type 1.

Treatment method reduced the amount of liver fat more than standard treatment alone.

Vitamin D shows potential to lower HbA1c, FPG, insulin resistance, and 2-hour post-prandial glucose levels.