INTRODUCTION ............................................................. 198 CELLULAR LIPIDS ......................................................... 198 Extraction .................................................................. 198 Subcellular Distribution .................................................... 198 Cytoplasmic (plasma) membrane .......................................... 198 Intracytoplasmic elements ................................................. 199 Cell wall ................................................................. 199 LIPID COMPONENTS ....................................................... 199 Fatty Acids ................................................................. 199 Chemical nature .......................................................... 199 Mutant strains ............................................................ 201 Biosynthesis ............................................................. 201 Biological significance .................................................... 202 Taxonomy ................................................................ 202 Hydrocarbons and Sterols ................................................... 202 Hydrocarbons ............................................................ 202 Sterols (i) Chemical nature ................................................ 202 (ii) Mutant strains......................................................... 204 (iii) Biosynthesis ......................................................... 204 (iv) Biological significance ................................................ 206 Glycerophospholipids ....................................................... 207 Chemical nature .......................................................... 207 Biosynthesis ............................................................. 208 Cellular distribution ...................................................... 208 Biological significance .................................................... 208 Sphingolipids ............................................................... 209 Chemical nature .......................................................... 209 Biological significance .................................................... 209 Glycolipids ................................................................. 209 FACTORS INFLUENCING CELLULAR LIPID COMPOSITION ..... ......... 209 Growth Cycle ............................................................... 209 Sporulation ................................................................. 210 Carbon Source ............................................................. 210 Glucose .................................................................. 210 Hydrocarbons ............................................................ 211 Nutrients ................................................................... 213 Nitrogen ................................................................. 213 Phosphorus .............................................................. 213 Growth factors ........................................................... 213 (i) Inositol ................................................................ 213 (ii) Pantothenic acid ...................................................... 213 (iii) Vitamin B6 ........................................................... 213 (iv) Biotin ................................................................ 214 Miscellaneous Additives .................................................... 214 Sodium chloride .......................................................... 214 Choline and ethanolamine ................................................ 214 Benzo(a)pyrene and dibenzanthracene ..................................... 214 Propanediol .............................................................. 214 Oxygen ..................................................................... 214 Respiratory-deficient (Crabtree-positive) yeasts (i) Lipid composition ....... 214 (ii) Lipid supplementation of growth medium ....... ....................... 215 Respiratory-sufficient (Crabtree-negative) yeasts ...... .................... 216 Temperature ............................................................... 216 pH ..................................................................... 217 CONCLUDING COMMENTS ................................................. 217 LITERATURE CITED ....................................................... 219

https://mmbr.asm.org/content/mmbr/39/3/197.full.pdf

Lipids of yeasts.

Alcohol dependence is correlated with a wide spectrum of medical, psychological, behavioral, and social problems. Acute alcohol abuse causes damage to and functional impairment of several organs affecting protein, carbohydrate, and fat metabolism. Mitochondria participate with the conversion of acetaldehyde into acetate and the generation of increased amounts of NADH. Prenatal exposure to ethanol during fetal development induces a wide spectrum of adverse effects in offspring, such as neurologic abnormalities and pre- and post-natal growth retardation. Antioxidant effects have been described due to that alcoholic beverages contain different compounds, such as polyphenols as well as resveratrol. This review analyzes diverse topics on the alcohol consumption effects in several human organs and demonstrates the direct participation of mitochondria as potential target of compounds that can be used to prevent therapies for alcohol abusers.

Cellular and mitochondrial effects of alcohol consumption.

Exercise has a myriad of physiological benefits that derive in part from its ability to improve cardiometabolic health. The periodic metabolic stress imposed by regular exercise appears fundamental in driving cardiovascular tissue adaptation. However, different types, intensities, or durations of exercise elicit different levels of metabolic stress and may promote distinct types of tissue remodeling. In this review, we discuss how exercise affects cardiac structure and function and how exercise-induced changes in metabolism regulate cardiac adaptation. Current evidence suggests that exercise typically elicits an adaptive, beneficial form of cardiac remodeling that involves cardiomyocyte growth and proliferation; however, chronic levels of extreme exercise may increase the risk for pathological cardiac remodeling or sudden cardiac death. An emerging theme underpinning acute as well as chronic cardiac adaptations to exercise is metabolic periodicity, which appears important for regulating mitochondrial quality and function, for stimulating metabolism-mediated exercise gene programs and hypertrophic kinase activity, and for coordinating biosynthetic pathway activity. In addition, circulating metabolites liberated during exercise trigger physiological cardiac growth. Further understanding of how exercise-mediated changes in metabolism orchestrate cell signaling and gene expression could facilitate therapeutic strategies to maximize the benefits of exercise and improve cardiac health.

/pdf/metabolic-mechanisms-of-exercise-induced-cardiac-remodeling-3hc5bxghut.pdf

Metabolic Mechanisms of Exercise-Induced Cardiac Remodeling.

Dietary supplementation of a specific amino acid formula prevents both fat accumulation and mitochondrial dysfunction in hepatocytes of alcohol-consuming rats. These effects are accompanied also by...

/pdf/a-specific-amino-acid-formula-prevents-alcoholic-liver-39pmzbw50l.pdf

A specific amino acid formula prevents alcoholic liver disease in rodents.

To study the influence of a moderate dose of ethanol on the ultrastructure of myocardium in patients with heart disease, a 7·5% solution of ethanol was infused in six patients with myocardial and valvular disease, who underwent diagnostic cardiac catheterization. Before and after infusion of ethanol an endomyocardial biopsy was performed and the specimens were examined by electron microscopy. After ethanol all six patients revealed alterations in the mitochondrial structure and three of them also showed significant dilatation of the sarcoplasmic reticulum. Cardiac output increased in three of the patients, whereas in two patients a decrease of cardiac output was measured. The results suggest that the infusion of even small amounts of ethanol is able to provoke structural alterations of myocardial cell organelles and, therefore, possible impairment of myocardial function.

https://pmj.bmj.com/content/postgradmedj/51/595/325.full.pdf

Effect of ethanol infusion on the ultrastructure of human myocardium

The effect of prolonged adminstration of ehtanol on cardiac metabolism, contractility, and ultrastructure was investigated. Dogs received 400 ml of a 25 percent solution of ethanol during a period of 3-6 months. Repeated heart muscle biopsied revealed a significant diminution in the activity of intramitochondrial NAD-linked isocitrate dehydrogenase in the animals exposed to alcohol. Oxidative, phosphorylation of mitochondria was measured polarographically using a vibrating oxygen electrode; respiratory control index and mitochondrial oxygen consumption were markedly reduced (p less than 0.001). Myocardial ATP content was significantly diminished (p less than 0.025). Electron microscopic changes observed consisted of mitochondrial degeneration, dehiscence of intercalated discs, and dilatation of intercellular spaces. The average force velocity curve was shifted downward and to the left in afterloaded contractions with a significant depression of Vmax (p less than 0.01). Both calcium binding and calcium uptake of mitochondria and sarcoplasmic reticulum were inhibited. These results suggest that a disorder in the generation of energy and a defect in calcium binding by subcellular membranes may be the determinant events leading to impaired myocardial function in the course of chronic alcoholism.

Mitochondrial function and excitation-contraction coupling in the development of alcoholic cardiomyopathy.

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Mitochondrial function and excitation-contraction coupling in the development of alcoholic cardiomyopathy.