But temporary increase in type 2 diabetes risk does not attenuate benefits on total, CVD mortality

Gene variants do not modify the associations of 25(OH)D with lipids

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 …

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.

Transcript of our Exclusive Interview: Stanley Schwartz talks with Diabetes in Control Publisher Steve Free during the AACE 2018 convention in Boston about the changing classifications of diabetes, why we need to move beyond thinking in terms of type 1 and type 2, and the need for precision medicine in treating patients with all types of diabetes.

In this Exclusive Interview, Stanley Schwartz talks with Diabetes in Control Publisher Steve Free during the AACE 2018 convention in Boston about the changing classifications of diabetes and the need for precision medicine in treating patients with all types of diabetes.

In part 1 of this Exclusive Interview, Stanley Schwartz talks with Diabetes in Control Publisher Steve Freed during the AACE 2018 convention in Boston about the classification of diabetes and the learnings that have happened since first creating the various diabetes designators.