Monday , August 20 2018
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Production Assistant, Diabetes In Control

Diabetes Educators on the Front Lines of Care

Guest Post by David Kliff, Editor, Diabetic Investor
This weekend, the most dedicated people in diabetes will gather in Baltimore for the AADE conference. Year after year, these amazing people gather to see all the latest toys in the toy chest, learn about all the new drugs, and share insights into how they are impacting the lives of the patients they work with.

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Prescribing GLP-1

Would you be more open to prescribing a GLP-1 Inhibitor if there was an oral product rather than an injectable? Follow the link to share your opinion and see what your colleagues think.

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High-Temp Cooking

According to a recent study, frequently consuming meat, poultry, or fish cooked at high temperatures increases the risk for hypertension by how much?

A. 11%
B. 17%
C. 23%
D. 25%
E. 38%

Follow the link for the answer.

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

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.

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