Fats and Cardiovascular Disease
Stephen T. Sinatra, Mark C. Houston in Nutritional and Integrative Strategies in Cardiovascular Medicine, 2015
Ketone bodies are formed when the glucose levels in the body become low. This can happen when the blood sugar becomes low due to low food intake, starvation, heavy exercise, or ingestion of a ketogenic diet (a diet with more fat than glucose). Ketosis, due to the ingestion of a ketogenic diet, is not to be confused with ketoacidosis, which is the result of uncontrolled diabetes and a dangerous medical emergency. Ketoacidosis is caused by excessive blood glucose and insufficient insulin to lower it, which tends to dehydrate the tissues. In the presence of low insulin, the adipose tissue can release FAs to the liver to form ketones for energy production. As ketone bodies accumulate, the pH of the blood drops and causes an acidic condition in the presence of ketones—ketoacidosis. The presence of high ketones and high blood sugar overwhelms the system and coma and often death occur. This is a medical emergency.
Athletes with Chronic Conditions
Flavia Meyer, Zbigniew Szygula, Boguslaw Wilk in Fluid Balance, Hydration, and Athletic Performance, 2016
Hyperglycemia can also affect kidney function with respect to maintaining electrolyte balance. Sodium reabsorption in both the proximal (Turner et al. 1997) and the distal tubule (Simkova et al. 2004) of the kidney can be elevated after as little as 90 min spent with blood glucose levels of 12 mmol/L or higher. With persistent hyper-glycemia, the activation of sodium/glucose cotransporters in the proximal tubule is elevated leading to sodium retention (Korner et al. 1994). While kidney function is affected by high blood glucose concentration, if hyperglycemia is short lived (<2 h) it might not have a large impact on plasma concentration of sodium, chloride, and calcium (Caduff et al. 2011). It might, however, lead to an increase in potassium concentration, potentially leading to muscle weakness and cardiac arrhythmia. High blood glucose levels can also increase urinary magnesium excretion (Djurhuus et al. 2000), which could eventually lead to muscle cramping. In extreme cases where hyperglycemia is severe and accompanied by ketoacidosis resulting in diarrhea and/or vomiting, hypokalemia may result (Arora et al. 2012). As ketoacidosis has several symptoms in common with heat stroke (nausea/vomiting, headache, confusion, and weakness), it is important for athletes with diabetes as well as their coaches/trainers to be able to differentiate between these two.
Diabetes mellitus
Judy Bothamley, Maureen Boyle in Medical Conditions Affecting Pregnancy and Childbirth, 2020
(Note: ketoacidosis should not be confused with ketosis, which is one of the body’s normal processes to metabolise body fat.) Ketoacidosis is a serious complication of diabetes and, although it is far more common in Type 1, it has been reported in Type 2 and even in women with gestational diabetes (Newton and Raskin, 2004). Development of ketoacidosis can be more rapid in pregnancy (Keely and Montoro, 2008). Uncontrolled hyperglycaemia occurs because of a lack of insulin exacerbated by the presence of catabolic counter-regulatory stress hormones, glucagons and catecholamines. An excess breakdown of fats releases free fatty acids into the circulation. In the liver these fatty acids are partially oxidised and contribute to keto acids and acetone. The latter gives a distinctive smell on the breath. Keto acids produce a metabolic acidosis disturbing the pH of the blood, which is harmful to cell metabolism (Yogev, et al., 2003). Acidosis stimulates the brain’s respiratory centre, which causes the deep sighing and rapid breathing known as Kussmaul’s respiration. Hyperglycaemia results in glycosuria and this triggers osmotic diuresis, dehydration and the loss of the important electrolytes potassium and sodium. SeeBox 1.2 for factors precipitating ketoacidosis in diabetic pregnancies.
Safety and efficacy of canagliflozin in elderly patients with type 2 diabetes mellitus: a 1-year post-marketing surveillance in Japan
Published in Current Medical Research and Opinion, 2018
Maki Goda, Tomoko Yamakura, Kazuyo Sasaki, Takumi Tajima, Makoto Ueno
Others: Renal impairment was reported in four patients (0.29%, four events), and the condition of one patient was serious. Two patients were recovering, and two did not recover by the end of the study. The serious case was complicated with diabetic retinopathy, diabetic nephropathy, hypertension, and hyperlipidemia, had high serum creatinine at baseline, and eGFR decreased from 34.3 mL/min/1.73 m2 to 16.6 mL/min/1.73 m2 at 3 month after the start of treatment. This patient did not recover by the end of the study. Hepatic function abnormalities were reported in three patients (0.22%, three events), and all patients recovered or were recovering at the end of the study. Body weight reduction (underweight and weight decreased in Table 3) occurred in three patients (0.22%, three events), and one patient experienced serious “underweight”. All patients recovered or were recovering at the end of the study. A case of “ketone body increased” was reported, but ketoacidosis was not observed.
The logistic organ dysfunction system score predicts the prognosis of patients with alcoholic ketoacidosis
Published in Renal Failure, 2018
Ha Nee Jang, Hee Jung Park, Hyun Seop Cho, Eunjin Bae, Tae Won Lee, Se-Ho Chang, Dong Jun Park
Alcoholic ketoacidosis (AKA) is usually characterized by metabolic acidosis, an increased anion gap, elevated serum ketone levels, and either a normal or low glucose concentration. A typical AKA patient has a history of chronic alcohol abuse, little or no food intake, and recent binge drinking followed by abrupt cessation of alcohol intake [1–6]. The physiological and mechanistic features of the condition are poorly known, but three factors may be in play. First, starvation may induce a decrease in insulin secretion and a rise in glucagon secretion. Second, the ratio of the level of the reduced form of nicotinamide adenine dinucleotide (NADH) to the oxidized form (nicotinamide adenine dinucleotide (NAD+)) may become elevated during alcohol metabolism. Finally, the extracellular fluid volume may be depleted by vomiting and low fluid intake [5–8]. The principal symptoms are nausea, vomiting, and/or abdominal pain [5,6]. Although the symptoms improve upon conservative management (infusion of large amounts of normal saline and glucose solution), AKA is occasionally associated with multiple complications [9,10].
Closed-loop insulin delivery: current status of diabetes technologies and future prospects
Published in Expert Review of Medical Devices, 2018
The goal of modern insulin therapy management is to mimic physiological pancreatic basal and bolus insulin release in response to a carbohydrate load as closely as possible (Figure 1) [4]. Insulin therapy is lifelong, as a sustainable cure for T1D has yet proved elusive. Insulin-delivery modality options include multiple daily injections (MDI) of insulin or continuous subcutaneous insulin infusion (CSII), also known as the ‘insulin pump’ [5]. Acute insulin deficiency leads to diabetic ketoacidosis; a potentially life threatening disorder arising from the body’s inability to utilize glucose as a source of fuel. Metabolic consequences include lipolysis which results in ketogenesis and ketoacidosis [6]. Long-term poorly controlled diabetes is associated with micro and macrovascular complications including retinopathy, nephropathy, neuropathy and cardiovascular disease, respectively [7].
Related Knowledge Centers
- Hyperglycemia
- Ketone Bodies
- Kussmaul Breathing
- Metabolic Acidosis
- Type 1 Diabetes
- Type 2 Diabetes
- Insulin
- Ketosis
- Acid–Base Homeostasis
- Diabetic Ketoacidosis