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Pathophysiology of Diabetes
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
The liver can manufacture glucose, but glycogen synthesis is reduced. Without insulin, gluconeogenesis is uncontrolled. Therefore, blood glucose levels increase, and blood glucose remains in the body. The muscle and fat tissues are simultaneously starved for glucose. Glucagon secretion is not linked to blood glucose levels, yet insulin is important in the regulation of glucagon secretion. Gluconeogenesis, glycogenolysis, and lipolysis are processes in the body that become stimulated. Increased lipolysis causes elevation of free fatty acids in the blood. Fatty acid molecules are partly taken up by the liver, and incorporated into lipoproteins. This increases levels of very-low-density lipoprotein (VLDL) and low-density lipoprotein (LDL), risk factors for heart disease. Ketone bodies are produced by excessive lipolysis, unable to be inhibited without insulin. Dangerous ketoacidosis can develop if ketone levels are extremely elevated. Administration of insulin is required.
Diabetes
Published in Amy J. Litterini, Christopher M. Wilson, Physical Activity and Rehabilitation in Life-threatening Illness, 2021
Amy J. Litterini, Christopher M. Wilson
Symptoms of type I diabetes include polydipsia (excessive thirst), bedwetting, polyuria (excessive urination), lack of energy, fatigue, constant hunger, and/or sudden weight loss. Diabetic ketoacidosis, a serious complication of diabetes that occurs when the body produces high levels of blood acids called ketones, is seen in approximately one-third of individuals with type I diabetes. Symptoms of type II diabetes can have some similarities with those of type I diabetes; however, individuals with type II diabetes may also be completely asymptomatic.
The patient with acute endocrine problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Diabetes ketoacidosis is a life-threatening complication of diabetes and accounts for a significant amount of all diabetes emergency-related hospital admissions. Most cases of DKA occur in patients with type 1 diabetes, but occasionally occur in type 2 diabetes. It is due to an increased demand for insulin, inadequate adjustment of insulin injection to meet the required needs of the body, severe physical or psychological stress or physical trauma without compensatory insulin and increased resistance to insulin due to various factors such as pregnancy or infection (Brashers, Jones and Huether 2017). The resultant lack of adequate insulin required to drag glucose into the cells leads to the body burning fatty acids to provide energy and thereby producing ketone bodies.
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.