China
Africa
Explore chapters and articles related to this topic
Diabetes Mellitus, Obesity, Lipoprotein Disorders and other Metabolic Diseases
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Insulin inhibits glucose production in the liver and lipolysis in adipose tissue. In the absence of insulin, these processes are uninhibited, which results in hyperglycaemia and increased fatty acid release. The fatty acids released by adipose tissue are converted into ketone bodies in the liver (Figure 11.11). Ketone bodies are strong organic acids and dissociate at physiological pH to produce hydrogen ions (H+) and ketone anions. The resulting metabolic acidosis stimulates the brainstem vomiting and respiratory centres. Dehydration is produced by both the hyperglycaemic osmotic diuresis and vomiting.
Preparing the Malnourished Patient for Parenteral Nutrition (PN)
Published in Michael M. Rothkopf, Jennifer C. Johnson, Optimizing Metabolic Status for the Hospitalized Patient, 2023
Michael M. Rothkopf, Jennifer C. Johnson
Starvation ketosis is a state in which patients lose fluid due to the diuretic actions of the ketone bodies (acetone, acetoacetate and beta hydroxybutyrate). Along with the diuresis, major electrolytes will be depleted from the circulation. As the depletion continues, electrolyte shifts and losses will be present in the intracellular pools.
Improvement of Cognitive Function in Patients with Alzheimer’s Disease using Ketogenic Diets
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Ketone bodies are produced mainly in liver mitochondria. In addition to the liver, ketone bodies are also generated in astrocytes in brain. Fatty acids are broken down during β-oxidation to acetyl-coenzyme A (CoA) in mitochondria. Under normal conditions, acetyl-CoA is further oxidized in the citric acid cycle (TCA cycle). The hydrogen released from the TCA cycle generates ATP in the mitochondrial electron transport chain. When acetyl-CoA increases beyond the processing capability of the TCA cycle in liver mitochondria, part of acetyl-CoA is successively metabolized to acetoacetyl-CoA, β-hydroxy-β-methylglutaryl-CoA, and finally to ketone bodies, acetoacetic acid and β-hydroxybutyric acid. Exacerbation of β-oxidation and lower TCA cycle activity due to a shortage of oxalate (an intermediate of the TCA cycle) resulting from low glucose utilization increases the production of ketone bodies. Thus, ketone bodies increase after calorie restriction and fasting. Under normal conditions, ketone bodies are found in the blood at low concentrations, but their concentration increases up to 9 mM under fasting conditions. In addition to fasting, high-fat and low-carbohydrate diet also increases blood ketone bodies and is referred to as ketogenic diet (Cunnane et al. 2011; Theodore et al. 2003).
Evaluation of the point-of-care devices KetoSureTM and StatStrip Express® blood ketone tests using β-hydroxybutyrate spiked samples
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2022
Lise Nørkjær Bjerg, Henrik Holm Thomsen, Jeppe Buur Madsen, Birgitte Sandfeld-Paulsen
Diabetic ketoacidosis (DKA) is a serious acute complication to mainly type-1 diabetes that can be lethal if left untreated. DKA is characterized by insulinopenic hyperglycemia, metabolic acidosis and ketosis why precise and reliable monitoring of these parameters is key for optimal treatment of this condition [1,2]. Ketosis is characterized by elevated levels of the ketone bodies acetoacetate, acetone and β-hydroxybutyrate (BHB) in the blood [3]. Also, scientific interest in the application of exogenous ketoses as a therapeutic measure have gained traction in recent years underlining the importance of accurate quantification of BHB concentration [4]. Previously, ketosis was assessed by the nitroprusside test of acetoacetate in urine as a semiquantitative reflection of the average blood ketone concentration since last void. The collection of urine is cumbersome and, more importantly, only acetoacetate is estimated which substantially underestimates the degree of ketosis in DKA where ketosis is dominated by BHB over acetoacetate and the vaporizable acetone [3]. With the introduction of measuring BHB in the blood, the diagnostic certainty and quality of treatment improved owed to more timely and accurate measurements [5–10]. Hence, the use of BHB measured in the blood is now recommended as standard for DKA diagnosis and monitoring [11,12].
Food for thought: the emerging role of a ketogenic diet in Alzheimer’s disease management
Published in Expert Review of Neurotherapeutics, 2021
Another dietary pattern has attracted increasing interest in AD prevention and treatment is a ketogenic diet (KD). KD allows imitating effects of fasting and induces physiological ketosis, owing to the diet’s extremely low amount of carbohydrates (usually < 50 g/day), through which fats become the body’s main energy source. After two to three days following KD, the body’s glucose resources (e.g. glycogen in the liver) are depleted and become insufficient for the normal course of fat oxidation and meeting the needs of the central nervous system (CNS). Ketone bodies (KBs), which are produced from fatty acids (ketogenesis) in the matrix of hepatic cells, become a new source of energy. During ketogenesis, the concentration of KBs (mainly beta-hydroxybutyrate) in the blood gradually increases, and when it reaches over 4 mmol/L, KBs become a source of energy for the CNS. In physiological ketosis, the concentration of KBs does not exceed 8 mmol/L, blood pH is maintained at a normal level, and glycemia, although decreasing, remains at its physiological concentration [3].
Ketogenic diet: overview, types, and possible anti-seizure mechanisms
Published in Nutritional Neuroscience, 2021
Mohammad Barzegar, Mohammadreza Afghan, Vahid Tarmahi, Meysam Behtari, Soroor Rahimi Khamaneh, Sina Raeisi
During KD treatment, the metabolic efficiency of the tricarboxylic acid (TCA) cycle is reduced and body energy is generally derived from fatty acid oxidation in mitochondria that results in the generation of a large amount of acetyl-CoA. Acetyl-CoA accumulation leads to the synthesis of the two primary ketone bodies, β-hydroxybutyrate and acetoacetate, mainly in the liver that can then spill into the blood circulation. Acetone, the other major ketone, is a metabolite of acetoacetate. The ketone bodies can be used as an alternative source of energy instead of glucose in the brain. Fatty acids are not utilized due to their inability to pass through the blood–brain barrier (BBB) [12]. There are some specific monocarboxylate transporters in BBB and some mitochondrial enzymes in the brain which make the ketone bodies possible to be extracted and used by the brain [46]. It has been shown that KD by upregulating of these specific proteins can induce the using of ketone bodies by the brain [46]. After the entering to the brain, ketone bodies can be converted to acetyl-CoA and then enter the TCA cycle within brain mitochondria leading eventually to the production of adenosine triphosphate (ATP) [12]. Several hypotheses have been focused on the ketone bodies as the key mediators involved in the anticonvulsant effect of the KD. Based on the several studies [46–54], the potential mechanisms are generally center around the roles of brain energy metabolism, neurotransmitters, ion channels, and oxidative stress which are briefly discussed below.