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What Can Happen When Patients Take Diabetes Holidays

Man, 36 years of age, type 2 diabetes, obesity class II, fatty liver, was taking metformin 1,000mg twice daily, and lower dose of SGLT-2. A1C was elevated 9% due to steroids; had been in the 6-7% range. Came in for 3-month follow up — A1C 9.9%, glucose 359, urine positive for glucose and for ketones, gained 19 pounds since last office visit, B/P 126/78-HR 78 and regular. The patient reports he took a "holiday" from everything during the holidays. He ate and drank anything and everything he wanted, including alcohol, and stopped his medications. He complained of  increased hunger and thirst. Very thirsty.

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Todd Hobbs Complete Interview

Todd Hobbs, MD, is Vice President and Diabetes Chief Medical Officer for Novo Nordisk in North America, where he leads the organization’s focus on the implications of diabetes for the patient, healthcare system and healthcare professionals. As the Diabetes Chief Medical Officer for Novo Nordisk in North America, he focuses on the implications of diabetes for the company and for patients, for healthcare professionals and for healthcare systems. He provides medical guidance and input to the clinical development and life cycle management strategies for diabetes and obesity-related projects, as well as input into the R&D pipeline and participate in consultant advisory boards. Prior to joining the Novo Nordisk team in 2004, he attended the University of Louisville School of Medicine and then serviced as a resident at the Anderson Area Medical Center in South Carolina.

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International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #160: Immunopathogenesis of Type 1 Diabetes in Western Society Part 3

Insulin itself is a prototypical TRA, its synthesis being virtually restricted to pancreatic beta cells. Thymic insulin production is critical for establishing self-tolerance to beta cells; simply abolishing insulin expression in the thymus leads to the rapid onset of autoimmune diabetes even in mice lacking a diabetogenic genetic background [26]. In humans, thymic insulin expression is modulated by allelic variation and epigenetic effects at the insulin gene locus; this effect is largely mediated by a polymorphic variable nucleotide tandem repeat (VNTR) sequence.

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