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Fatty Acid and Ethanol oxidation Flashcards | Quizlet
All 3 events increase lipolysis and plasma free fatty acid levels, which are available as an alternative fuel and competitively inhibit glucose use. Increased plasma and urinary ketone levels indicate the use of fat as an energy source. Plasma free fatty acids also stimulate glucose production. Hypoglycemia occurs when 1 or more of these counterregulatory mechanisms fail because of the overuse of glucose (as in hyperinsulinism), the underproduction of glucose (as in the glycogen-storage diseases), or both (as in growth hormone or cortisol deficiency). (See Etiology.)
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Ethanol (including propranolol plus ethanol), haloperidol, pentamidine, quinine, salicylates, and sulfonamides ("sulfa drugs") have been associated with hypoglycemia. Other drugs that may be related to this condition include oral hypoglycemics, phenylbutazone, insulin, bishydroxycoumarin, p-aminobenzoic acid, propoxyphene, stanozolol, hypoglycin, carbamate insecticide, disopyramide, isoniazid, methanol, methotrexate, tricyclic antidepressants, cytotoxic agents, organophosphates, didanosine, chlorpromazine, fluoxetine, sertraline, fenfluramine, trimethoprim, 6-mercaptopurine, thiazide diuretics, thioglycolate, tremetol, ritodrine, disodium ethylenediaminetetraacetic acid (EDTA), clofibrate, angiotensin converting enzyme (ACE) inhibitors, and lithium.
Ethanol and the non-oxidative fatty acid/ethanol ..
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Antioxidant, antimicrobial, antiulcer and analgesic activities of nettle (Urtica dioica L.).
Ataturk University, Erzurum, Turkey.
J Ethnopharmacol. 2004.
In this study, water extract of (Urtica dioica L.) was studied for antioxidant, antimicrobial, antiulcer and analgesic properties. The antioxidant properties of stinging nettle were evaluated using different antioxidant tests, including reducing power, free radical scavenging, superoxide anion radical scavenging, hydrogen peroxide scavenging, and metal chelating activities. Stinging nettle had powerful antioxidant activity. The 50, 100 and 250 microg amounts of stinging nettle showed 39, 66 and 98% inhibition on peroxidation of linoleic acid emulsion, respectively, while 60 microg/ml of alpha-tocopherol, exhibited only 30% inhibition. Moreover, stinging nettle had effective reducing power, free radical scavenging, superoxide anion radical scavenging, hydrogen peroxide scavenging, and metal chelating activities at the same concentrations. In addition, total phenolic compounds in the stinging nettle were determined as pyrocatechol equivalent. Stinging nettle also showed antimicrobial activity against nine microorganisms, antiulcer activity against ethanol-induced ulcerogenesis and analgesic effect on acetic acid-induced stretching.
Inherited defects in fatty acid oxidation, including that resulting from systemic carnitine deficiency and inherited defects in ketogenesis (3-hydroxy-3-methylglutaryl-CoA lyase deficiency) cause fasting hypoglycemia by restricting the extent to which nonneural tissues can derive their energy from plasma free fatty acids (FFA) and ketones during fasting or exercise. This results in an abnormally high rate of glucose uptake by nonneural tissues under these conditions.
Role of Free Fatty Acids in Glucose Homeostasis
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As previously mentioned, in infants with one of several disorders (eg, ketotic hypoglycemia, glycogen-storage disorder, free fatty acid metabolism defect, mild hyperinsulinism), hypoglycemia can be prevented with frequent feedings using a specifically designed diet, but when feeding is inadequate because of GI problems or other illnesses, parenteral dextrose can be used to obtain a rapid response. Fructose must be avoided in children with fructose diphosphatase deficiency.
Oxidative stress plays an important role in ethanol-induced damage to the developing fetus (Cohen-Kerem and Koren 2003). Low levels of CYP2E1 are found in prenatal brain (Brezezinki et al. 1999), suggesting that CYP2E1-derived ROS could play a role in the development of alcohol-related birth defects, including fetal alcohol syndrome (FAS). Moreover, ROS produced during CYP2E1-mediated ethanol metabolism would likely be particularly harmful because the fetal brain shows only low levels of antioxidant enzyme activity compared with adult brain (Henderson et al. 1999). Researchers have studied whether administration of antioxidants, such as N-acetyl cysteine, SAMe, folic acid, and vitamin C, could improve cell survival during fetal ethanol exposure; however, these studies have yielded mixed results.
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All 3 events increase lipolysis and plasma free fatty acid ..
Today, much is known about ethanol metabolism, particularly its oxidation by ADH and ALDH in the liver. However, gaps remain in researchers’ understanding of certain aspects of ethanol metabolism. For instance, the relative contributions of ADH, catalase, and microsomal enzymes to ethanol metabolism in the brain have not yet been determined. Other questions include, How do oxidative pathways via catalase relate to fatty acid oxidation through mitochondrial pathways? Could ethanol metabolism affect satiety, insulin resistance, liver function, and fat formation by indirectly modulating the expression of certain genes, similar to the processes observed under conditions of caloric restriction? Can the fluctuations in cellular redox state resulting from ethanol metabolism directly influence ethanol-induced liver injury? What are the mechanisms responsible for the hypersensitivity of ethanol-exposed hepatocytes in TNF–α-induced injury? What is the role of changes in redox state on the expression of cytokines that promote or prevent inflammatory reactions? What are the interactions between ethanol metabolism, diabetes, and obesity? Answers to these and other questions will further elucidate the mechanisms underlying ethanol’s metabolism and their regulation, as well as the effects that alcohol metabolism and its byproducts have on all tissues and organs throughout the body. In addition, a deeper understanding of these processes will allow researchers to design intervention strategies that may ameliorate the harmful effects of alcohol and its metabolites.
Ethanol Metabolism - Biochemistry - Medbullets Step 1
Chronic alcohol consumption also is associated with disturbances in the metabolism of sulfur-containing amino acids, leading to increased levels of the amino acids glutamate, aspartate, and homocysteine in alcoholic patients. These increases may have serious adverse effects. For example, homocysteine increases and modulates certain nerve signaling processes, particularly during alcohol withdrawal, and increases in homocysteine levels may possibly contribute to the alcoholism-associated tissue shrinkage (i.e., atrophy) observed in brain tissue (Bleich et al. 2004).
Ethanol Metabolism - The Medical Biochemistry Page
Other metabolic derangements associated with ethanol metabolism result from the fact that ADH and ALDH metabolize not only ethanol but also other compounds. For example, ADH and ALDH oxidize retinol (i.e., vitamin A1) to retinal and, subsequently, retinoic acid, which plays an important role in growth and differentiation. In the presence of ethanol, ADH and ALDH may be occupied with ethanol metabolism and retinol metabolism may be inhibited. These interactions may have serious implications for fetal development, stem cell differentiation, maintenance of differentiated tissue function, and the normal structure and function of stellate cells in the liver (Crabb et al. 2001).
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