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Ketoacidosis When Fasting

Fasting And Lipolysis – Part 4

Fasting And Lipolysis – Part 4

Insulin is the main driver of both obesity and type 2 diabetes. The key to reversing both conditions is therefore not “How do we reduce calories?”, but instead “How do we reduce Insulin?” There are almost no drugs that will do this. There is actually two classes of medications that consistently reduces insulin – one by a lot, one by a little. Not by co-incidence, they are the only drugs that consistently reduces weight. But the problem is that they are both expensive and have side effects. Short of drugs, we need an efficient, effective way to lower insulin if we are to be successful in losing weight. A diet low in refined carbs and sugar will certainly do the trick for some, but for others it is not enough. The answer, if you haven’t guessed yet, is fasting. The classic descriptions of fasting physiology were written by Dr. George Cahill. We reviewed this in a previous post, but here’s a pictorial version. Essentially, fasting is the gradual shift of burning glucose to burning fat. In stage 1, most of the body is using exogenous glucose. By stage 2 and 3, glycogen (stored sugar) provides much of the glucose needed. Most tissues are still using sugar, but the liver, muscle and fat cells have started to burn fat. By stage 4 and 5, glycogen stores have run out. Hepatic and renal (liver and kidney) gluconeogenesis is now providing all the glucose, but only the brain, red blood cells and the renal medulla (the inner part of the kidney) uses glucose. Everything else has shifted over to burning fat. By stage 5, the brain has mostly shifted to burning fat in the form of ketone bodies. Only a small amount of glucose is needed for red blood cells. You can see that the origin of the blood glucose gradually switches from exogenous (dietary) to gluconeogenesis made fr Continue reading >>

Ketoacidosis: A Diabetes Complication

Ketoacidosis: A Diabetes Complication

Ketoacidosis can affect both type 1 diabetes and type 2 diabetes patients. It's a possible short-term complication of diabetes, one caused by hyperglycemia—and one that can be avoided. Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are two of the most serious complications of diabetes. These hyperglycemic emergencies continue to be important causes of mortality among persons with diabetes in spite of all of the advances in understanding diabetes. The annual incidence rate of DKA estimated from population-based studies ranges from 4.8 to 8 episodes per 1,000 patients with diabetes. Unfortunately, in the US, incidents of hospitalization due to DKA have increased. Currently, 4% to 9% of all hospital discharge summaries among patients with diabetes include DKA. The incidence of HHS is more difficult to determine because of lack of population studies but it is still high at around 15%. The prognosis of both conditions is substantially worsened at the extremes of age, and in the presence of coma and hypertension. Why and How Does Ketoacidosis Occur? The pathogenesis of DKA is more understood than HHS but both relate to the basic underlying reduction in the net effective action of circulating insulin coupled with a concomitant elevation of counter regulatory hormones such as glucagons, catecholamines, cortisol, and growth hormone. These hormonal alterations in both DKA and HHS lead to increased hepatic and renal glucose production and impaired use of glucose in peripheral tissues, which results in hyperglycemia and parallel changes in osmolality in extracellular space. This same combination also leads to release of free fatty acids into the circulation from adipose tissue and to unrestrained hepatic fatty acid oxidation to ketone bodies. Some drugs ca Continue reading >>

Short-term Fasting Is A Mechanism For The Development Of Euglycemic Ketoacidosis During Periods Of Insulin Deficiency.

Short-term Fasting Is A Mechanism For The Development Of Euglycemic Ketoacidosis During Periods Of Insulin Deficiency.

To determine the etiology of euglycemic ketoacidosis, the effect of a 32-h fast on the rate of metabolic deterioration was examined in a group of 10 healthy subjects with type I diabetes mellitus. Patients were studied during 5 h of insulin withdrawal after 8 h (postprandial) and 32 h (fasted) of food deprivation. Study parameters included substrate levels, electrolytes, counterregulatory hormone levels, and rates of glucose and glycerol turnover. In the fasted state, mean peak plasma glucose concentrations were significantly lower than those in the 8-h postprandial state (13.3 +/- 1.6 vs. 17.4 +/- 1.4 mmol/L, respectively; P < 0.05), and mean rates of glucose production were also significantly lower at all time points in the fasting state. The rate of development of ketosis was significantly more rapid during insulin deficiency after a fast (8.82 +/- 0.63 vs. 6.23 +/- 0.30 micro/L.min; P < 0.05), while plasma nonesterified fatty acids and glycerol turnover showed a biphasic response to insulin withdrawal, which was also more robust after a fast. Metabolic acidosis, as reflected in the rate of decrease in serum bicarbonate concentration, was more severe after 32 h of fasting than in the postprandial state (mean nadir, 15.4 +/- 0.9 vs. 18.6 +/- 0.5 mmol/L; P < 0.001). In contrast to values in the postprandial state, serum glucagon levels rose during insulin withdrawal in the fasting state, and plasma norepinephrine levels also correlated positively with the ongoing metabolic decompensation. Other counterregulatory hormones did not differ significantly in the fasted vs. postprandial states in these short term metabolic studies. We conclude that a fast of moderate duration, such as might be expected to occur during the development of diabetic ketoacidosis, predisposes pati Continue reading >>

Ketosis Vs. Ketoacidosis: What You Should Know

Ketosis Vs. Ketoacidosis: What You Should Know

Despite the similarity in name, ketosis and ketoacidosis are two different things. Ketoacidosis refers to diabetic ketoacidosis (DKA) and is a complication of type 1 diabetes mellitus. It’s a life-threatening condition resulting from dangerously high levels of ketones and blood sugar. This combination makes your blood too acidic, which can change the normal functioning of internal organs like your liver and kidneys. It’s critical that you get prompt treatment. DKA can occur very quickly. It may develop in less than 24 hours. It mostly occurs in people with type 1 diabetes whose bodies do not produce any insulin. Several things can lead to DKA, including illness, improper diet, or not taking an adequate dose of insulin. DKA can also occur in individuals with type 2 diabetes who have little or no insulin production. Ketosis is the presence of ketones. It’s not harmful. You can be in ketosis if you’re on a low-carbohydrate diet or fasting, or if you’ve consumed too much alcohol. If you have ketosis, you have a higher than usual level of ketones in your blood or urine, but not high enough to cause acidosis. Ketones are a chemical your body produces when it burns stored fat. Some people choose a low-carb diet to help with weight loss. While there is some controversy over their safety, low-carb diets are generally fine. Talk to your doctor before beginning any extreme diet plan. DKA is the leading cause of death in people under 24 years old who have diabetes. The overall death rate for ketoacidosis is 2 to 5 percent. People under the age of 30 make up 36 percent of DKA cases. Twenty-seven percent of people with DKA are between the ages of 30 and 50, 23 percent are between the ages of 51 and 70, and 14 percent are over the age of 70. Ketosis may cause bad breath. Ket Continue reading >>

Ketoacidosis During A Low-carbohydrate Diet

Ketoacidosis During A Low-carbohydrate Diet

To the Editor: It is believed that low-carbohydrate diets work best in reducing weight when producing ketosis.1 We report on a 51-year-old white woman who does not have diabetes but had ketoacidosis while consuming a “no-carbohydrate” diet. There was no family history of diabetes, and she was not currently taking any medications. While adhering to a regimen of carbohydrate restriction, she reached a stable weight of 59.1 kg, a decrease from 72.7 kg. After several months of stable weight, she was admitted to the hospital four times with vomiting but without abdominal pain. On each occasion, she reported no alcohol use. Her body-mass index (the weight in kilograms divided by the square of the height in meters) was 26.7 before the weight loss and 21.7 afterward. Laboratory evaluation showed anion-gap acidosis, ketonuria, and elevated plasma glucose concentrations on three of the four occasions (Table 1). She had normal concentrations of plasma lactate and glycosylated hemoglobin. Screening for drugs, including ethyl alcohol and ethylene glycol, was negative. Abdominal ultrasonography showed hepatic steatosis. On each occasion, the patient recovered after administration of intravenous fluids and insulin, was prescribed insulin injections on discharge, and gradually reduced the use of insulin and then discontinued it while remaining euglycemic for six months or more between episodes. Testing for antibodies against glutamic acid decarboxylase and antinuclear antibodies was negative. Values on lipid studies were as follows: serum triglycerides, 102 mg per deciliter; high-density lipoprotein (HDL) cholesterol, 50 mg per deciliter; and calculated low-density lipoprotein (LDL) cholesterol, 189 mg per deciliter. The patient strictly adhered to a low-carbohydrate diet for four Continue reading >>

Diabetic, Alcoholic And Starvation Ketoacidosis

Diabetic, Alcoholic And Starvation Ketoacidosis

Copious amounts of ketones which are generated in insulin-deficient or insulin-unresponsive patients will give rise to a high anion gap metabolic acidosis. Ketones are anions, and they form the high anion gap. Management of DKA and HONK is discussed elsewhere. Meet the ketones Chemically speaking, a ketone is anything with a carbonyl group between a bunch of other carbon atoms. The above are your three typical ketoacidosis-associated ketone bodies. The biochemistry nerds among us will hasten to add that the beta-hydroxybutyrate is in fact not a ketone but a carboxylic acid, but - because it is associated with ketoacidosis, we will continue to refer to it as a ketone for the remainder of this chapter, in the spirit of convention. In the same spirit, we can suspend our objections to acetone being included in a discussion of ketoacidosis, which (though a true ketone) is in fact not acidic or basic, as it does not ionise at physiological pH (its pKa is 20 or so). So really, the only serious ketone acid is acetoacetate, which has a pKa of 3.77. However, beta-hydroxybutyrate is the prevalent ketone in ketoacidosis; the normal ratio of beta-hydroxybutyrate and acetoacetate is 3:1, and it can rise to 10:1 in diabetic ketoacidosis. Acetone is the least abundant. The metabolic origin of ketones The generation of ketones is a normal response to fasting, which follows the depletion of hepatic glycogen stores. Let us discuss normal physiology for a change. You, a healthy adult without serious alcohol problems, are fasting from midnight for a routine elective hernia repair. You will go to be after dinner with a few nice lumps of undigested food in your intestine, as well as about 75g of hepatic glycogen. As you sleep, you gradually digest the food and dip into the glycogen store. At Continue reading >>

The Emedicinehealth Doctors Ask About Diabetic Ketoacidosis:

The Emedicinehealth Doctors Ask About Diabetic Ketoacidosis:

A A A Diabetic Ketoacidosis (cont.) A person developing diabetic ketoacidosis may have one or more of these symptoms: excessive thirst or drinking lots of fluid, frequent urination, general weakness, vomiting, loss of appetite, confusion, abdominal pain, shortness of breath, a generally ill appearance, increased heart rate, low blood pressure, increased rate of breathing, and a distinctive fruity odor on the breath. If you have any form of diabetes, contact your doctor when you have very high blood sugars (generally more than 350 mg) or moderate elevations that do not respond to home treatment. At initial diagnosis your doctor should have provided you with specific rules for dosing your medication(s) and for checking your urinary ketone level whenever you become ill. If not, ask your health care practitioner to provide such "sick day rules." If you have diabetes and start vomiting, seek immediate medical attention. If you have diabetes and develop a fever, contact your health care practitioner. If you feel sick, check your urinary ketone levels with home test strips. If your urinary ketones are moderate or higher, contact your health care practitioner. People with diabetes should be taken to a hospital's emergency department if they appear significantly ill, dehydrated, confused, or very weak. Other reasons to seek immediate medical treatment include shortness of breath, chest pain, severe abdominal pain with vomiting, or high fever (above 101 F or 38.3 C). Continue Reading A A A Diabetic Ketoacidosis (cont.) The diagnosis of diabetic ketoacidosis is typically made after the health care practitioner obtains a history, performs a physical examination, and reviews the laboratory tests. Blood tests will be ordered to document the levels of sugar, potassium, sodium, and oth Continue reading >>

In Defense Of Fasting: Common Misconceptions

In Defense Of Fasting: Common Misconceptions

Clearing misconceptions For those of you wondering, the tone of this article has been highly edited from my anger-rant earlier. I used my blog as catharsis, but now it’s back to business. I get a message across better being polite anyway. Fasting is a fairly unique diet technique. It’s at a crossroads (more like highway junction) of efficacy, health, social perception, eating disorders, and overall safety. It’s not bad given you avoid a few pitfalls and don’t blatantly starve yourself, but some people are still caught up in the midst of all this confusion, not knowing whether not eating for a single day will hurt them or help them. This article is subject to editing in the future. I am using this to keep tabs on the current science of fasting, both good and bad. It might be nice to keep it bookmarked and come back to it from time to time. I also suspect some time in the future it might become Tl;Dr, but a valuable tool nonetheless. This can be used in drug testing also and because of this some people have found a way to access synthetic urine. One of the most popular sites is Since fasting is put on ‘trail’ a lot, I figured I might bring up the common arguments like a court case. Just for kicks. Exhibit A: Ketosis and Ketoacidosis First, definitions: Ketosis is the state of an organism characterized by elevated serum levels of ketones Ketoacidosis is a metabolic state characterized by uncontrolled production of ketone bodies and decreased serum pH Ketosis is the presence of ketones, ketoacidosis is the presence of ketones combined with a drop in pH. The drop in pH is due in part to overproduction of ketones (which are acidic in nature) and a failure of the body/diet to buffer said acidity. So from this, we can preliminarily conclude that ketoacidosis will ki Continue reading >>

Fasting Ketosis And Alcoholic Ketoacidosis

Fasting Ketosis And Alcoholic Ketoacidosis

INTRODUCTION Ketoacidosis is the term used for metabolic acidoses associated with an accumulation of ketone bodies. The most common cause of ketoacidosis is diabetic ketoacidosis. Two other causes are fasting ketosis and alcoholic ketoacidosis. Fasting ketosis and alcoholic ketoacidosis will be reviewed here. Issues related to diabetic ketoacidosis are discussed in detail elsewhere. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Epidemiology and pathogenesis" and "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis" and "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment".) PHYSIOLOGY OF KETONE BODIES There are three major ketone bodies, with the interrelationships shown in the figure (figure 1): Acetoacetic acid is the only true ketoacid. The more dominant acid in patients with ketoacidosis is beta-hydroxybutyric acid, which results from the reduction of acetoacetic acid by NADH. Beta-hydroxybutyric acid is a hydroxyacid, not a true ketoacid. Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

The Facts Diabetic ketoacidosis (DKA) is a condition that may occur in people who have diabetes, most often in those who have type 1 (insulin-dependent) diabetes. It involves the buildup of toxic substances called ketones that make the blood too acidic. High ketone levels can be readily managed, but if they aren't detected and treated in time, a person can eventually slip into a fatal coma. DKA can occur in people who are newly diagnosed with type 1 diabetes and have had ketones building up in their blood prior to the start of treatment. It can also occur in people already diagnosed with type 1 diabetes that have missed an insulin dose, have an infection, or have suffered a traumatic event or injury. Although much less common, DKA can occasionally occur in people with type 2 diabetes under extreme physiologic stress. Causes With type 1 diabetes, the pancreas is unable to make the hormone insulin, which the body's cells need in order to take in glucose from the blood. In the case of type 2 diabetes, the pancreas is unable to make sufficient amounts of insulin in order to take in glucose from the blood. Glucose, a simple sugar we get from the foods we eat, is necessary for making the energy our cells need to function. People with diabetes can't get glucose into their cells, so their bodies look for alternative energy sources. Meanwhile, glucose builds up in the bloodstream, and by the time DKA occurs, blood glucose levels are often greater than 22 mmol/L (400 mg/dL) while insulin levels are very low. Since glucose isn't available for cells to use, fat from fat cells is broken down for energy instead, releasing ketones. Ketones accumulate in the blood, causing it to become more acidic. As a result, many of the enzymes that control the body's metabolic processes aren't able Continue reading >>

Incidence Of Diabetic Ketoacidosis During Ramadan Fasting In Benghazi, Libya

Incidence Of Diabetic Ketoacidosis During Ramadan Fasting In Benghazi, Libya

Background: Ramadan is the ninth month on the lunar calendar and for over a billion Muslims it is a holy month during which all healthy adults must observe absolute fasting from dawn to sunset. The risk of diabetic ketoacidosis is thought to be higher during Ramadan fasting due to hormonal disequilibrium. Aim and objectives: The aim of this study was to examine the hypothesis that diabetic ketoacidosis is more frequent during Ramadan fasting. Patients and methods: A retrospective analysis of the records of all patients admitted with DKA to all Benghazi hospitals during the lunar year 1428 Hijri (January 2007 to January 2008). Results: Fifteen episodes occurred during Ramadan (4.6 episode/10 000 diabetic) as compare to 19.45 episodes/month (6 episode/10 000 diabetic/month) during the other lunar months (P=0.000), there was no significant difference in the patients’ mean age (37.6±10 vs 38.3±19, P=0.8), or mortality rate (13.3 vs 14.4%, P=0.9) during Ramadan and other months. The commonest precipitating factor of diabetic ketoacidosis during Ramadan was infection (46.6%), followed by miss dosing (33.3%). Conclusion: There is no increase in the incidence and mortality from DKA during Ramadan which might indicate that Ramadan fasting is not a significant risk factor for diabetic ketoacidosis. ApoB plays a central role in lipoprotein metabolism through regulation of total cholesterol and LDL-cholesterol (LDL-C) concentrations in plasma. Two restriction fragment length polymorphisms (ECoRI and XbaI) represent single base alterations in the coding region of ApoB gene. ECoRI polymorphic region of ApoB gene is due to on an amino acid change (Glu→Lys). The XbaI polymorphic region of ApoB gene results from a substitution of (A→T) in the threonine codon and does not change Continue reading >>

Ketoacidosis Versus Ketosis

Ketoacidosis Versus Ketosis

Some medical professionals confuse ketoacidosis, an extremely abnormal form of ketosis, with the normal benign ketosis associated with ketogenic diets and fasting states in the body. They will then tell you that ketosis is dangerous. Testing Laboratory Microbiology - Air Quality - Mold Asbestos - Environmental - Lead emsl.com Ketosis is NOT Ketoacidosis The difference between the two conditions is a matter of volume and flow rate*: Benign nutritional ketosis is a controlled, insulin regulated process which results in a mild release of fatty acids and ketone body production in response to either a fast from food, or a reduction in carbohydrate intake. Ketoacidosis is driven by a lack of insulin in the body. Without insulin, blood sugar rises to high levels and stored fat streams from fat cells. This excess amount of fat metabolism results in the production of abnormal quantities of ketones. The combination of high blood sugar and high ketone levels can upset the normal acid/base balance in the blood and become dangerous. In order to reach a state of ketoacidosis, insulin levels must be so low that the regulation of blood sugar and fatty acid flow is impaired. *See this reference paper. Here's a table of the actual numbers to show the differences in magnitude: Body Condition Quantity of Ketones Being Produced After a meal: 0.1 mmol/L Overnight Fast: 0.3 mmol/L Ketogenic Diet (Nutritional ketosis): 1-8 mmol/L >20 Days Fasting: 10 mmol/L Uncontrolled Diabetes (Ketoacidosis): >20 mmol/L Here's a more detailed explanation: Fact 1: Every human body maintains the blood and cellular fluids within a very narrow range between being too acidic (low pH) and too basic (high pH). If the blood pH gets out of the normal range, either too low or too high, big problems happen. Fact 2: The Continue reading >>

Fasting Induces Ketoacidosis And Hypothermia In Pdhk2/pdhk4-double-knockout Mice

Fasting Induces Ketoacidosis And Hypothermia In Pdhk2/pdhk4-double-knockout Mice

Go to: Introduction The PDH complex (pyruvate dehydrogenase complex) plays a pivotal role in controlling the concentrations of glucose in the fed and fasted state [1]. In the well-fed state, the PDH complex is highly active, promoting glucose oxidation by generating acetyl-CoA, which can be oxidized by the citric acid cycle or used for fatty acid and cholesterol synthesis. In the fasted state, the PDH complex is inactivated by phosphorylation by PDHKs (pyruvate dehydrogenase kinases) to conserve three carbon compounds for the production of glucose [2]. The four PDHK isoenzymes responsible for phosphorylating the PDH complex are expressed in a tissue-specific manner [3–5]. Among the four, PDHK2 and PDHK4 are most abundantly expressed in the heart [5–7], skeletal muscle [5,8–10] and liver [5,11–14] of fasted mice. Of these two, PDHK2 is of interest because of its greater sensitivity to activation by acetyl-CoA and NADH and inhibition by pyruvate [15]. However, PDHK4 has received greater attention because its expression is increased in many tissues by fasting and diabetes [12] and transcription of its gene is regulated by insulin, glucocorticoids, thyroid hormone and fatty acids [16,17]. Inactivation of the PDH complex by phosphorylation helps to maintain euglycaemia during fasting, but contributes to hyperglycaemia in Type 2 diabetics. The increase in PDHK activity in diabetes raises the question of whether the PDHKs should be considered therapeutic targets for the treatment of diabetes [18]. Support for this possibility has been provided by the finding that mice lacking PDHK4 are euglycaemic in the fasted state and are more glucose tolerant than wild-type mice fed on a high-fat diet [19–21]. In the present study, PDHK2-KO (knockout) mice were produced to determ Continue reading >>

Starvation-induced True Diabetic Euglycemic Ketoacidosis In Severe Depression

Starvation-induced True Diabetic Euglycemic Ketoacidosis In Severe Depression

Go to: A 34-year-old man with a 19-year history of type 1 diabetes presented as an emergency with a 4-day history of nausea, vomiting, and flu-like symptoms. He was on a basal bolus insulin regime comprising 8 units of bolus insulin lispro injected at mealtimes and 12 units of basal isophane insulin at bedtime, but did not monitor capillary blood glucose levels. He did however empirically increase his insulin doses during times of illness and had increased his isophane insulin to 15 units during the 3 days prior to presentation. He had only one prior hospital admission, which occurred 6 years previously and was due to an episode of DKA precipitated by gastroenteritis. He was single, unemployed, did not drink alcohol, had no previous psychiatric history, no family history of diabetes or other medical conditions, and lived in a hostel. He had a record of poor clinic attendances and a history of long-term cannabis use. He denied any salicylate consumption, but admitted to some weight loss; however, he was unable to quantify this. His body mass index (BMI) was 19 kg/m2, and he looked unkempt. Physical examination revealed a temperature of 36.4°C (97.5°F), heart rate of 106 beats per minute, supine blood pressure of 131/85 mmHg, and sitting blood pressure of 122/80 mmHg. He had a respiratory rate of 30 breaths per minute, and his oxygen saturation using a pulsoximeter was 99% on room air. He appeared clinically dehydrated with dry oral mucosa, but cardiovascular, respiratory, abdominal, and neurological examinations were otherwise normal. Diabetic ketoacidosis (DKA) was suspected; metabolic acidosis was confirmed with a pH of 7.3, bicarbonate concentration of 10 mEq/l, and an elevated anion gap of 29 mEq/l [sodium = 134 mEq/l, potassium = 5.7 mEq/l, chloride = 101 mEq/l, b Continue reading >>

Ketoacidosis

Ketoacidosis

GENERAL ketoacidosis is a high anion gap metabolic acidosis due to an excessive blood concentration of ketone bodies (keto-anions). ketone bodies (acetoacetate, beta-hydroxybutyrate, acetone) are released into the blood from the liver when hepatic lipid metabolism has changed to a state of increased ketogenesis. a relative or absolute insulin deficiency is present in all cases. CAUSES The three major types of ketosis are: (i) Starvation ketosis (ii) Alcoholic ketoacidosis (iii) Diabetic ketoacidosis STARVATION KETOSIS when hepatic glycogen stores are exhausted (eg after 12-24 hours of total fasting), the liver produces ketones to provide an energy substrate for peripheral tissues. ketoacidosis can appear after an overnight fast but it typically requires 3 to 14 days of starvation to reach maximal severity. typical keto-anion levels are only 1 to 2 mmol/l and this will usually not alter the anion gap. the acidosis even with quite prolonged fasting is only ever of mild to moderate severity with keto-anion levels up to a maximum of 3 to 5 mmol/l and plasma pH down to 7.3. ketone bodies also stimulate some insulin release from the islets. patients are usually not diabetic. ALCOHOLIC KETOSIS Presentation a chronic alcoholic who has a binge, then stops drinking and has little or no oral food intake for a few days (ethanol and fasting) volume depletion is common and this can result in increased levels of counter regulatory hormones (eg glucagon) levels of free fatty acids (FFA) can be high (eg up to 3.5mM) providing plenty of substrate for the altered hepatic lipid metabolism to produce plenty of ketoanions GI symptoms are common (eg nausea, vomiting, abdominal pain, haematemesis, melaena) acidaemia may be severe (eg pH down to 7.0) plasma glucose may be depressed or normal or Continue reading >>

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