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Production Assistant, Diabetes In Control

International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #136: Pathogenesis of Type 2 Diabetes Mellitus Part 7

Cellular mechanisms of insulin resistance: The cellular events via which insulin initiates its stimulatory effect on glucose metabolism start with binding of the hormone to specific receptors that are present on the cell surface of all insulin target tissues. After insulin has bound to and activated its receptor, “second messengers” are generated and these second messengers activate a cascade of phosphorylation-dephosphorylation reactions that result in stimulation of intracellular glucose metabolism. The first step in glucose utilization involves activation of the glucose transport system, leading to glucose influx into insulin target tissues, primarily muscle. The free glucose, which has entered the cell, subsequently is metabolized by a series of enzymatic steps that are under the control of insulin. Of these, the most important are glucose phosphorylation (catalyzed by hexokinase), glycogen synthase (which controls glycogen synthesis), and phosphofructokinase (PFK) and PDH (which regulate glycolysis and glucose oxidation, respectively).

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Is There a Future for BGM?

Guest Post by David Kliff, Editor, Diabetic Investor

With each passing day, it’s becoming more apparent that CGM will replace BGM as the standard for glucose measurement. CGM systems are becoming more patient-friendly, i.e. no calibrations, simple insertion, and cheaper too. The data provided by CGM is transformative, leading to improved outcomes. It is no longer a question of if this will happen but when this will happen.

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CGM for Type 2

Would you be open to using a CGM for your type 2 patients who are not on insulin? Follow the link to share your response.

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International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #135: Pathogenesis of Type 2 Diabetes Mellitus Part 6

In utero fetal malnutrition: Low birth weight is associated with the development of IGT and T2DM in a number of populations. Developmental studies in animals and humans have demonstrated that poor nutrition and impaired fetal growth (small babies at birth) are associated with impaired insulin secretion and/or reduced beta-cell mass. Fetal malnutrition can also lead to the development of insulin resistance later in life.

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