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A 30-year-old man with a 20-year history of well-controlled type 1 diabetes mellitus and no microvascular complications traveled from near sea level to an altitude of 3000 m within 6 hours. At altitude, his blood glucose levels began to rise, necessitating increased insulin delivery. Typical symptoms of acute mountain sickness (AMS) developed, and he became increasingly hyperglycemic and unwell. Upon presentation to an emergency clinic, diabetic ketoacidosis (DKA) was diagnosed and was managed with insulin, intravenous fluids with potassium, and acetazolamide orally. No other potential causes for diabetic ketoacidosis were identified. Hyperglycemia, ketosis, and acidosis resolved with treatment as expected, but an increased insulin requirement was noted for the next 48 hours, until returning to expected levels when acetazolamide was discontinued. This case describes an episode of mild diabetic ketoacidosis potentially precipitated by moderate to severe acute mountain sickness, and an apparent hyperglycemic effect of acetazolamide. Individuals with type 1 diabetes traveling to altitude and their physicians should be vigilant for this complication and should be aware of the effects of conventional first-line therapies for acute mountain sickness on insulin requirement, glycemic control, and preexisting microvascular diabetes complications.

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OBJECTIVE: Portable electronic devices play an important role in the management of type 1 diabetes mellitus. Electromagnetic interference from electronic devices has been shown to impair the function of an avalanche transceiver in search mode (but not in transmitting mode). This study investigates the influence of electromagnetic interference from diabetes devices on a searching avalanche beacon. METHODS: The greatest distance at which an avalanche transceiver (in search mode) could accurately indicate the location of a transmitting transceiver was assessed when portable electronic devices (including an insulin pump and commonly used real-time continuous subcutaneous glucose monitoring system [rtCGMS]) were held in close proximity to each transceiver. RESULTS: The searching transceiver could accurately locate a transmitted signal at a distance of 30 m when used alone. This distance was unchanged by the Dexcom G4 rtCGMS, but was reduced to 10 m when the Medtronic Guardian rtCGMS was held close (within 30 cm) to the receiving beacon. Interference from the Animas Vibe insulin pump reduced this distance to 5 m, impairing the searching transceiver in a manner identical to the effect of a cell phone. CONCLUSIONS: Electromagnetic interference produced by some diabetes devices when held within 30 cm of a searching avalanche transceiver can impair the ability to locate a signal. Such interference could significantly compromise the outcome of a companion rescue scenario. Further investigation using other pumps and rtCGMS devices is required to evaluate all available diabetes electronics. Meantime, all electronic diabetes devices including rtCGMS and insulin pumps should not be used within 30 cm of an avalanche transceiver.

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The regulated delivery of Glut4-containing vesicles to the plasma membrane is a specialised example of regulated membrane trafficking. Present models favour the transporter trafficking through two inter-related endosomal cycles. The first is the proto-typical endosomal system. This is a fast trafficking event that, in the absence of insulin, serves to internalise Glut4 from the plasma membrane. Once in this pathway, Glut4 is further sorted into a slowly recycling pathway that operates between recycling endosomes, the trans Golgi network, and a population of vesicles often referred to as Glut4-storage vesicles. Little is known about the molecules that regulate these distinct sorting steps. Here, we have studied the role of Stx16 in Glut4 trafficking. Using two independent strategies, we show that Stx16 plays a crucial role in Glut4 traffic in 3T3-L1 adipocytes. Over-expression of a mutant form of Stx16 devoid of a transmembrane anchor was found to significantly slow the reversal of insulin-stimulated glucose transport. Depletion of Stx16 using antisense approaches profoundly reduced insulin-stimulated glucose transport but was without effect on cell surface transferrin receptor levels, and also reduced the extent of Glut4 translocation to the plasma membrane in response to insulin. These data support a model in which Stx16 is crucial in the sorting of Glut4 from the fast cycling to the slow cycling intracellular trafficking pathways in adipocytes.

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