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Euglycemic Dka Sglt2

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Susan Cornell, PharmD, CDE, FAPhA, FAADE, describes the risks for ketoacidosis and serious urinary tract infection associated with use of SGLT2 inhibitors. This video was recorded at APhA's 2016 Annual Meeting and Exposition in Baltimore, Maryland.

Sglt2 Inhibitors May Predispose To Ketoacidosis

SGLT2 Inhibitors May Predispose to Ketoacidosis Diabetes, Endocrinology, and Obesity Branch (S.I.T., J.E.B., K.I.R.), National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892; Division of Diabetes, Endocrinology, and Nutrition (S.I.T.), Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland 21201 Address all correspondence and requests for reprints to: Simeon I. Taylor, MD, PhD, Diabetes, Endocrinology, and Obesity Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Mail Stop 1453, 9000 Rockville Pike, Bethesda, MD 20892. Search for other works by this author on: Diabetes, Endocrinology, and Obesity Branch (S.I.T., J.E.B., K.I.R.), National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892; Search for other works by this author on: Diabetes, Endocrinology, and Obesity Branch (S.I.T., J.E.B., K.I.R.), National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892; Search for other works by this author on: The Journ Continue reading >>

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Popular Questions

  1. iwannalose50lbs

    On my 3rd month of Keto and having some success, but every so often I'm presented with an opportunity to "cheat" and sometimes it's rude if not impossible to pass up. Examples include but are not limited to:
    A friend buying a round of beers at the bar.
    A close friend or relative's child offering a piece of their birthday cake.
    A pancake social or a private dinner at a traditional Italian home.
    I tried searching but couldn't find anything discussing the SCIENCE of cheating while on Keto. For example:
    What are the variables that affect how quickly and how long you are kicked out of ketosis, and how long does it take to get back into ketosis in each scenario?
    How much different is the effect of eating a single Oreo cookie versus a whole plate of pasta?
    How strongly does exercise impact ketosis, and what types of exercises are best for getting back into ketosis if you get "kicked out" after a cheat day?
    How strongly does cheating impact actual weight loss? It seems to be common knowledge that cheating can actually help overcome plateaus, so what's the REAL difference between someone who practices Keto religiously versus someone who does Keto most of the time with the occasional treat thrown in every few days?
    To clarify, this is not a post advocating cheating. I am simply trying to open a discussion about the physical impact that cheating can have on your body while in ketosis. I have gone over a month without cheating, but I have also cheated multiple times in a week and I haven't really noticed much of a difference either way. This is more of a curiosity post than anything else. Looking forward to a good discussion.

  2. gogge

    What are the variables that affect how quickly and how long you are kicked out of ketosis, and how long does it take to get back into ketosis in each scenario?
    The carbs you take in will stop ketone production until they're used up, or stored away in muscle. Full liver glycogen (~100 grams of carbs) last roughly 12-16 hours, so you'll probably be able to clear around 6-9 grams of carbs per hour by just existing (and not all carbs you eat will get stored as liver glycogen, your muscles take up some).
    The major determinant of whether the liver will produce ketone bodies is the amount of liver glycogen present (8). The primary role of liver glycogen is to maintain normal blood glucose levels. When dietary carbohydrates are removed from the diet and blood glucose falls, glucagon signals the liver to break down its glycogen stores to glucose which is released into the bloodstream. After approximately 12-16 hours, depending on activity, liver glycogen is almost completely depleted. At this time, ketogenesis increases rapidly. In fact, after liver glycogen is depleted, the availability of FFA will determine the rate of ketone production. (12)
    "The Ketogenic Diet", by Lyle McDonald, page 30.
    It will also take a few hours to clear the ketones already produced (circulating in your blood) even if ketone production stops, here's a post on ketone clearance from blood.
    How much different is the effect of eating a single Oreo cookie versus a whole plate of pasta?
    Assuming one oreo has 21 grams of carbs and that a whole plate of pasta is something like 121 grams of carbs (three servings).
    You'll probably not get noticeably kicked out from the oreo as it'll probably be digested over 30 minutes and then you'll use up the carbs within an hour or two, it'll take longer than that for the ketones to clear your blood.
    The plate of pasta will probably be digested over several hours, a normal mixed meal takes 4-6 hours but your intestines can absorb around 60-100 grams of carbs per hour, so two or three hours to digest highly processed carbs sounds more likely. At 6-8 grams of carbs used per hour it'll take 15-20 hours to clear all the glucose if it was only burned, but some will probably get used by your digestive system and some will get picked up by other tissues of the body (stored in muscles). You have peripherial insulin resistance on keto, manifested as impaired glucose tolerance, which likely means that a large part of the glucose will end up as liver glycogen. So a full plate of pasta might kick you out of ketosis for at least 15-20 hours (assuming resuming ketone production takes about as long as ketone clearance), longer if your body uses less glucose.
    How strongly does exercise impact ketosis, and what types of exercises are best for getting back into ketosis if you get "kicked out" after a cheat day?
    High intensity exercise burns glucose, high intensity endurance close to the lactate threshold is probably the best way of depleting liver glycogen (muscle taking up blood glucose, forcing the liver to use stored glycogen to maintain blood glucose levels).
    Higher intensity cardiovascular exercise is a little bit harder to pinpoint in terms of carbohydrate requirements and can vary pretty significantly depending on the intensities and volumes. A sprinter running 60m repeats isn’t using a lot of glycogen, a trained endurance athlete working near their lactate threshold for extended periods can deplete glycogen fairly completely in 1-2 hours. Even at lower intensities, the 2-6 hour sessions done by endurance athletes can completely deplete both muscle and liver glycogen stores on a daily basis.
    Lyle McDonald, "How Many Carbohydrates Do You Need?".
    How strongly does cheating impact actual weight loss? It seems to be common knowledge that cheating can actually help overcome plateaus, so what's the REAL difference between someone who practices Keto religiously versus someone who does Keto most of the time with the occasional treat thrown in every few days?
    Actual short term fat gain (or lower loss) directly contributed to by the carbs is likely negligible, what matters for fat stored (or lower fat loss) directly affected by the cheat meal/day is total caloric intake.
    Short term weight gain might be because when carbs are stored as glycogen they bind 3-4 grams of water and the increased insulin levels can also lead to higher sodium retention (leading to water retention), which can help explain why some people gain large amounts of weight with cheat meals/days despite not eating a lot of calories (longer post on water loss on keto).
    Long term weight loss effects might be slightly different, a single cheat day might help you lower cortisol, raise leptin, and thyroid levels, which could help lessen water retention (and possibly increase metabolic rate, but not a lot of research on this that I know of). This might be why people break plateaus after cheat meals/days, Lyle talks some about it in "The LTDFLE".
    Eating a few carbs from time to time is unlikely to negatively influence your weight loss unless it adds significant calories.

  3. lovesfunnyposts

    Great helpful response!!

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SGLT2 inhibitors show no significant risk of DKA, study reports Follow this link: http://tinyurl.com/6irc9o5ia89 SGLT2 inhibitors show no significant risk of DKA, study reports click here full resolution --- for more information go to-http://tinyurl.com/pvwe7iu879/ Adults with type 2 diabetes who take SGLT2 inhibitors are less likely to experience diabetic ketoacidosis (DKA) than those on insulin treatment, a study suggests.These findings existed for those with type 2 diabetes either prescribed SGLT2 inhibitors as a single treatment or in combination with another drug.Scientists from the Steno Diabetes Center, Copenhagen, Denmark examined 415,670 people with type 2 diabetes during 1995-2017, all of whom were treated with medication, including insulin.They sought to evaluate the rates of DKA within patients to assess if any association could be made between DKA, a dangerous short-term complication, and SGLT2 inhibitors.SGLT2 inhibitors work by helping the kidneys to lower blood glucose levels, with excess blood glucose removed through urine. for more information go to-http://tinyurl.com/82d95inail/ type 2 diabetes, SGLT2 inhibitors, dka

Euglycemic Dka Secondary To Sglt2 Inhibitors

Authors: Priyanka Kailash (MS-4, Campbell University School of Osteopathic Medicine), Kevin Weaver, DO (Program Director, Lehigh Valley Health Network), and Krystle Shafer, MD (Attending Physician, York Hospital) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) and Brit Long, MD (@long_brit) A 35-year-old male with a past medical history of type 2 diabetes arrives at the Emergency Department (ED) with altered mental status, nausea, vomiting, and diffuse abdominal pain that started 10 hours ago. The patient was recently started on an SGLT2 inhibitor. On examination, the patient is tachycardic (HR 126) and tachypneic (RR 25), with normal blood pressure (110/90). He is further noted to have dry mucous membranes and poor skin turgor. Blood glucose is noted to be 140 mg/dl, serum ketones 6.2 mmol/L, and arterial pH of 6.9. The patient is diagnosed with euglycemic DKA and quickly admitted to ICU for treatment. Pathogenesis of Typical DKA Two major complications from type 1 diabetes mellitus and type 2 diabetes mellitus are diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS). DKA is typically Continue reading >>

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Popular Questions

  1. shykins

    well at 8g carbs per 100g they arent the lowest carb veg but as i am not that keen the most i would have is a slice with some salad and remember i am pretty much in maintenance now
    ketotis strips can be bought online if u cant get them at boots, remember to cut them in half so they last longer (very MSE!!!), i havent used them for ages tho i did when i first started atkins
    x

  2. elona

    Shykins
    Do you buy the ketosis strips from the Atkins site?
    Once DD has gone out and I have peace and quiet will cook a low carb breakfast for myself.
    I get so sick of the raised eyebrows when I eat "anything!"
    DH just cannot comprehend that when I cook his favourite pea soup or lentil soup that I should not be having any and if I were to cook something that fitted in for me no one else would like it!

  3. shykins

    i think ibought them from ebay... lowcarbmegastore do them too and as daisy said u can sometimes get them in boots, they arent really necessary tho so save yr money (even more MSE lol)
    x

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Prolonged Ketosis In A Patient With Euglycemic Diabetic Ketoacidosis Secondary To Dapagliflozin

Sodium-glucose cotransporter 2 inhibitors (SGLT2) are the newest class of oral agents to receive US Food and Drug Administration (FDA) approval for the treatment of type 2 diabetes (T2DM). SGLT2 inhibitors currently approved by the FDA include canagliflozin, dapagliflozin, and empagliflozin as well as various combination drugs (Table 1). The enthusiasm this class of drugs has been greeted with stems from the benefits associated with SGLT2 inhibitors. They include decrease in A1c by 0.5% to 1%, reduction in insulin doses, modest weight loss, and improved systolic and diastolic blood pressure.1 In addition, the EMPA-REG OUTCOME trial showed a reduction in all-cause and cardiovascular mortality with empagliflozin.2 Also, a post hoc analysis of a study on dapagliflozin in type 2 diabetics with moderate renal impairment showed improved albuminuria and delayed progression to severe renal failure.3 The popularity of SGLT2 inhibitors is understandable considering the paucity of oral diabetic drugs that promote both weight loss and reduction of insulin needs. Endocrinologists and internists alike have increasingly prescribed this class of drugs as to avoid initiation of insulin or escalatio Continue reading >>

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Popular Questions

  1. p-bromonitrobenzene

    Why isn't this molecule named 2-fluorocyclopent-1-one?

  2. Lighthart

    The 1-specification for the ketone function is superfluous, there is no information obscured by omitting the '1'. It is the most important functional group in molecule, and therefore establishes the 1-position.
    Also, cyclopentone is not a proper name. You are missing the 'ane' suffix to indicate saturation. It would be a cyclopentanone.
    Final name:
    2-fluorocyclopentanone.

  3. Loong

    According to the current version of Nomenclature of Organic Chemistry – IUPAC Recommendations and Preferred Names 2013 (Blue Book), names of cyclic ketones are formed substitutively by using the suffix ‘one’.
    The terminal letter ‘e’ in names of parent hydrides (here: cyclopentane) is systematically elided when followed by a suffix beginning with ‘a’, ‘e’, ‘i’, ‘o’, ‘u’, or ‘y’.
    Therefore, the name of the unsubstituted cyclic ketone given in the question is cyclopentanone.
    Note that the locant ‘1’ is omitted in monosubstituted homogeneous monocyclic rings.
    However, if any locants are essential for defining the structure, then all locants must be cited in preferred IUPAC names (PINs).
    Therefore, the omission of the locant ‘1’ in 2-fluorocyclopentanone, while permissible in general usage, is not allowed in PINs, thus the name 2-fluorocyclopentan-1-one is the PIN.

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