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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
Ketogenesis, or the production of ketone bodies, also occurs in type 1 diabetes. High blood levels of ketone bodies reduce the pH of blood, which is referred to as ketoacidosis. Excess ketone bodies are excreted in urine with potassium ions, which induces life-threatening hypokalemia (Theodore et al. 2003). Sever ketoacidosis occurs in untreated type 1 diabetes and from the consumption of a large quantity of alcohol without intake of enough carbohydrates. Ketogenic diets generally do not induce such severe ketoacidosis.
The patient with acute endocrine problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
The aim of insulin therapy is to suppress ketogenesis, reduce blood glucose level and correct electrolyte imbalance. Commence a fixed rate intravenous insulin infusion (FRII) based on 0.1 units/kg body weight and monitor blood ketones and capillary blood glucose level to determine whether adjustment is required. Avoid hypoglycaemia, and introduce dextrose regimen if blood glucose <14mmol (JBDS 2018).
Hormones of the Adrenal Gland
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
With respect to fat metabolism, epinephrine activates intracellular lipase via cAMP (β-adrenergic effect) and hence stimulates lipolysis. Free fatty acids are mobilized from fat tissues and form a substrate for ketogenesis in the liver.
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 induces autophagy to alleviate bleomycin-induced pulmonary fibrosis in murine models
Published in Experimental Lung Research, 2021
En Mu, Jinli Wang, Liang Chen, Shuirong Lin, Jieming Chen, Xiaoming Huang
Ketogenic diet (KD) is a dietary regimen characterized by high-fat, very low-carbohydrate and moderate-protein content. The special nutrition intake intends to increase the synthesis of ketone bodies (ketogenesis). KD has been widely utilized to treat children with epilepsy for many decades.14 In recent years, accumulating evidence has shown that KD had potential in treating multiple disorders, including polycystic ovary syndrome, diabetes, cancers, Alzheimer’s disease and cardiovascular disease.15–19 A previous study demonstrated that KD was able to inhibit the expression of phospho-AKT (p-AKT) and phospho-S6 ribosomal protein in the hippocampus and liver of normal Sprague-Dawley rats and the expression of phospho-S6 ribosomal protein in the hippocampus and neocortex of status epilepticus rats, indicating that KD was able to regulate mTOR signaling pathway.20 Furthermore, KD exerted neuroprotective effects on the hippocampus of seizure rats by promoting autophagy.21 Thus it was speculated that KD might alleviate PF through inhibiting mTOR activation and enhancing autophagy. To verify our hypothesis, the effect of KD on the survival of PF mice and the progression of PF, inflammation, fibrogenesis, autophagy and PI3K/AKT/mTOR signaling pathway in PF mice were investigated in the present study.
Associations between ketone bodies and fasting plasma glucose in individuals with post-pancreatitis prediabetes
Published in Archives of Physiology and Biochemistry, 2020
Sakina H. Bharmal, Sayali A. Pendharkar, Ruma G. Singh, David Cameron-Smith, Maxim S. Petrov
Ketone body metabolism is determined by two processes - ketogenesis and ketolysis (Fukao et al.2004). While ketolysis is controlled by acetoacetyl succinyl-CoA transferase (enzyme) activity, ketogenesis is regulated by the availability of acetyl-CoA substrate, enzymatic activity of lipase, acetyl-CoA carboxylase, and hydroxymethyl glutaryl (HMG)-CoA synthase (Laffel 1999). Glucoregulatory hormones (in particular insulin) are crucial to maintaining the balance between ketogenesis and ketolysis. Insulin, while demonstrating an inhibitory effect on ketogenesis, has been shown to enhance ketolysis by increasing the peripheral utilisation of ketones (Keller et al.1988). Evidence from studies conducted in individuals with prediabetes and obesity have shown ketone bodies levels to be below the normal threshold, which has been attributed to high insulin concentrations (Nosadini et al.1985, Soeters et al.2009, Vega et al.2009, Mahendran et al.2013). The present study showed that BHB contributed to 26.2% of variance in fasting glucose levels in individuals with PPP, as opposed to 0.1% in individuals with NAP. Further, BHB was inversely associated with plasma levels of insulin. For every unit change in insulin, BHB levels significantly decreased by 15% in PPP compared to a 3% non-significant decrease in NAP. Given that individuals with PPP had higher levels of circulating insulin, in comparison with NAP, findings from the present study could be explained by the following mechanisms.