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SGLT2 inhibitors: updated advice on the risk of diabetic ketoacidosis
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<blockquote data-quote="Oldvatr" data-source="post: 1732017" data-attributes="member: 196898"><p>Sorry, [USER=196960]@ickihun[/USER] I am nor sure how your reply here relates to DKA. The classic Diabetic DKA is usually a result of there being insufficient insulin around to allow glucose to pass into the mitrochondia to be used, and the body burns fat instead to survive thus producing ketones in abundance. The classic DKA is associated with high (>20 mmol/l) bgl readings and severe ketobreathe (pear drops). Contrary to that SGLT-2 DKA differs in that it has been observed when bgl levels are in the 10 -15 mmol.l range, and so present a hazard in that ER staff may not realise the symptoms, and provide the wrong treatment.</p><p></p><p>So Classic DKA is due to loss of insulin (normally associated with Insulin dependants) or very high Insulin Resistance (e.g. T2D - rare event), but SGLT-2 DKA may only present ketobreath as a clue. I am not sure how a keto diet would lead to higher risk with SGLT-2 since it should not reduce insulin production or increase IR. Anyway, either of those events would show as high bgl levels and classic DKA symptoms, which is why I say there must be some other mechanism coming into play with SGLT-2 meds. </p><p></p><p>I suggested an interference with kidney function in that maybe the SGLT-2 med is causing them to stop filtering not just glucose as designed, but also other waste products that should normally be excreted in the urine. such as ketones. </p><p></p><p>For some reason DKA due to SGLT-2 is causing a backup of ketone byproducts in a big way leading to ketoacidosis (which is not the same as normal ketogenic waste due to diet restrictions or heavy exercise or fasting) An alternatice hypothesis is that SGLT-2 causes the kidneys to flush insulin instead, but I suspect that would lead to high bgl readings again, but then thinking about it on the fly, leaching insulin while having low bgl for keto may only cause a small rise in bgl i.e. to 10 -15 mmol/l as reported.</p></blockquote><p></p>
[QUOTE="Oldvatr, post: 1732017, member: 196898"] Sorry, [USER=196960]@ickihun[/USER] I am nor sure how your reply here relates to DKA. The classic Diabetic DKA is usually a result of there being insufficient insulin around to allow glucose to pass into the mitrochondia to be used, and the body burns fat instead to survive thus producing ketones in abundance. The classic DKA is associated with high (>20 mmol/l) bgl readings and severe ketobreathe (pear drops). Contrary to that SGLT-2 DKA differs in that it has been observed when bgl levels are in the 10 -15 mmol.l range, and so present a hazard in that ER staff may not realise the symptoms, and provide the wrong treatment. So Classic DKA is due to loss of insulin (normally associated with Insulin dependants) or very high Insulin Resistance (e.g. T2D - rare event), but SGLT-2 DKA may only present ketobreath as a clue. I am not sure how a keto diet would lead to higher risk with SGLT-2 since it should not reduce insulin production or increase IR. Anyway, either of those events would show as high bgl levels and classic DKA symptoms, which is why I say there must be some other mechanism coming into play with SGLT-2 meds. I suggested an interference with kidney function in that maybe the SGLT-2 med is causing them to stop filtering not just glucose as designed, but also other waste products that should normally be excreted in the urine. such as ketones. For some reason DKA due to SGLT-2 is causing a backup of ketone byproducts in a big way leading to ketoacidosis (which is not the same as normal ketogenic waste due to diet restrictions or heavy exercise or fasting) An alternatice hypothesis is that SGLT-2 causes the kidneys to flush insulin instead, but I suspect that would lead to high bgl readings again, but then thinking about it on the fly, leaching insulin while having low bgl for keto may only cause a small rise in bgl i.e. to 10 -15 mmol/l as reported. [/QUOTE]
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