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The Metabolic Medicine Postoperative Bariatric Surgery Consultation
Published in Michael M. Rothkopf, Jennifer C. Johnson, Optimizing Metabolic Status for the Hospitalized Patient, 2023
Michael M. Rothkopf, Jennifer C. Johnson
The next major factor to consider in the postoperative bariatric patient is electrolyte balance. It is not uncommon to see underlying electrolyte disturbances in these patients, either because of medications (such as diuretics) or a history of fad dieting. As in the malnourished patient, hypokalemia, hypophosphatemia and hypomagnesemia need to be monitored carefully. The hospital recovery period should be used to correct these electrolyte disturbances if they are found. The levels should be normalized prior to the patient’s discharge. Remember that the patient will be on a very limited oral intake over the subsequent few weeks. Furthermore, they often enter nutritional ketosis that can further deplete electrolytes. Under these conditions, even a mild electrolyte deficiency can worsen quickly. Missing this step may end up requiring an ER visit or a readmission (Jammah 2015).
Bioenergetics
Published in Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan, Strength and Conditioning in Sports, 2023
Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan
Beginning with one molecule of glucose, the net production of glycolysis is two molecules of ATP. However, starting with glycogen, which is broken down into Glucose-6-phospohate (G-3-P) via the enzyme phosphorylase, then three ATP are produced (Figure 2.3a). The additional ATP is produced as a result of the phosphorylation step that uses an ATP (via hexokinase) is bypassed and one ATP is spared. In comparing fast versus slow glycolysis and the fate of the two sarcoplasmically produced NADH2, it can be argued that the net ATP production for slow glycolysis can be as much as eight ATP when the process starts with glucose. This occurs as a result of the NADH2 entering the mitochondria and producing an additional 6 ATP through oxidative phosphorylation. It should be noted that there can be differences in ATP production between cardiac and skeletal muscle. Evidence indicates that two different shuttle systems operate to transfer electrons into the mitochondria, one in heart muscle (malate-aspartate) and the other in skeletal muscle (glycerol-phosphate) (226). In the glycerol-phosphate system, FAD picks up the NADH+ and carries it to the electron transport system, thus reducing the number of ATP being produced. Some evidence indicates that the glycerol-phosphate system predominates in type II muscle fibers, while type I fibers can also use the malate-aspartate system (128, 226).
Cellular and Immunobiology
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Masood Moghul, Sarah McClelland, Prabhakar Rajan
TCA (Krebs) cycle takes place within the mitochondria.As acetyl CoA is oxidised, it de-oxidises (reduces) electron carriers NAD and FAD → NADH, FADH2.NAD and FAD pass their electrons into the electron transport chain—oxidative phosphorylation.As electrons pass along the chain, they lose energy, which is used to pump hydrogen ions into inter-membrane space of mitochondria, causing an electrochemical gradient.Hydrogen flows back down the electrochemical current and through membrane enzyme ATP synthase, producing ATP.This process is called chemiosmosis and yields the most ATP from glucose.
Photoperiod-induced alterations in biomarkers of oxidative stress and biochemical pathways in rats of different ages: Focus on individual physiological reactivity
Published in Chronobiology International, 2021
Natalia Kurhaluk, Halyna Tkachenko, Oleksandr Lukash
Thirdly, the Mel concentration in the blood of highly resistant rats was higher than in those with low resistance to hypoxia. Recently, the study of genetic and phenotypic mechanisms providing resistance of organs and tissues to hypoxia attract much attention. Rats with high and low resistance to hypoxia differ in the level of lipid peroxidation, antioxidant defenses, and mitochondrial functioning (Kurhaluk et al. 2019; Kurhalyuk and Tkachenko 2007). Our earlier data suggest that NADH- and FAD-generated electron transport in the mitochondrial respiratory chain determines the individual resistance to hypoxia processes and plays an important role in the impact of stressful agents (Kurhaluk et al. 2020; Tkachenko et al. 2007). A study conducted by Martin et al. (2000, 2002) regarding time-dependent increases in the activities of mitochondrial respiratory complexes I and IV and our data confirm the significant role of the NADH-generated substrates in the processes of mitochondrial respiration, i.e. alfa-ketoglutarate oxidation. Oxidation of FAD-generating substrates was found to result in a decrease in the efficiency of the phosphorylation process in both lipopolysaccharide- and ethanol-induced toxicity (Kurhaluk et al. 2020). The effects of Mel on the increased coupling of mitochondrial processes with oxygen are important for the functioning of the mitochondrial respiratory chain with increased oxidative stress and the production of free radicals due to the limitation of ATP synthesis (Acuña-Castroviejo et al. 2003).
Exploring the contribution of mitochondrial dynamics to multiple acyl-CoA dehydrogenase deficiency-related phenotype
Published in Archives of Physiology and Biochemistry, 2021
Sofia R. Brandão, Rita Ferreira, Hugo Rocha
During fasting conditions triacylglycerides are mobilized from adipose tissue, transported and distributed to various tissues through the bloodstream in lipoproteins (Houten and Wanders 2010). Once inside the cells, fatty acids are activated to their coenzyme A (CoASH) esters and transported into mitochondria for subsequent β-oxidation (Houten and Wanders 2010, Wanders et al.2010, Longo et al.2016). The main function of mitochondrial fatty acid β-oxidation (FAO) is to generate acetyl-coenzyme A (acetyl-CoA) and reducing equivalents such as flavin adenine dinucleotide (FADH2) and nicotinamide adenine dinucleotide (NADH) to be used at the Krebs cycle and oxidative phosphorylation (OXPHOS) system, leading to energy production in the form of adenosine triphosphate (ATP) (Houten and Wanders 2010, Wanders et al.2010). OXPHOS is the key metabolic pathway in mitochondrial energy production. It requires the action of five multi heteromeric complexes located in the inner mitochondrial membrane, designated complexes I to V (Smeitink et al.2001, Papa et al.2012). Electron transfer flavoprotein (ETF) and electron transfer flavoprotein dehydrogenase (ETFDH) are essential proteins for the activity of flavoproteins (Lund et al.2015), allowing the delivery of electrons to ubiquinone (CoQ). Indeed, crystallographic studies support the interplay of these two proteins during electron and hydrogen transfer (Toogood et al.2007). Therefore, they make the connection between the β-oxidation cycle and OXPHOS.
Non-alcoholic Wernicke’s encephalopathy: toxic ingestion or an honest mis-steak?
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Salahuddin Nasir, Moustafa Abou Areda, Elise L. Ma, Robert D. Chow, Avelino Verceles, Carol Chiung-Hui Peng
Thiamine is a water-soluble vitamin that is essential to energy metabolism. The body’s thiamine stores can be depleted without supplementation within 3 to 6 weeks. The average requirement per day is 1.0–2.0 mg of thiamine, which can be found through a variety of dietary sources, including vegetables and fruits[18]. It is becoming increasingly important to be aware of non-alcoholic WE as a potential consequence of fad-diets, which have been construed to yield a variety of benefits, including management of mood disorders, diabetes, arthritis, and weight loss. Fortunately, based on the published cases [4,7,10,15,17] as well as our case, early diagnosis and initiation of nutritional support are able to correct the nutritional imbalance and reverse the adverse neurological consequences[19].A thiamine serum measurement is not required to make this diagnosis as it is a clinical diagnosis made using the presenting symptomatology. A delay in diagnosis and treatment, however, can result in prolonged metabolic derangement, leading to irreversible brain damage with short-term memory loss, termed Korsakoff’s psychosis[2].