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Triglycerides/Hypertriglyceridemia
Published in Charles Theisler, Adjuvant Medical Care, 2023
Nicotinic Acid (Vitamin B3): Niacin is a first-line pharmacologic agent for treating hypertriglyceridemia.1 Niacin blocks the release of free fatty acid from adipose tissue and reduces the rate of secretion of very-low-density lipoprotein particles.4 Clinically, niacin reduces triglycerides by 30%–50%, raises HDL cholesterol by 20%–30%, and lowers LDL cholesterol levels by 5%–25%.1 Niacin is not as potent as fibrates for lowering triglyceride levels but is more effective at raising HDL cholesterol levels.1 Patients on nicotinic acid are usually started on low daily doses and gradually increased to an average daily dose of 1.5–3 gm/day to avoid hepatotoxicity.2 Flushing from nicotinic acid can be decreased by taking the extended-release form and by taking niacin during or after meals, or by the use of an aspirin 30 minutes before niacin ingestion.5 Patients should be made aware that niacin can interact with other medications and cause side effects. Low-dose niacin combined with a statin has been associated with a significant decrease in cardiovascular events.6
Micronutrient Supplementation and Ergogenesis — Vitamins
Published in Luke Bucci, Nutrients as Ergogenic Aids for Sports and Exercise, 2020
Niacin (nicotinic acid or niacinamide) was found to prevent the rise in plasma-free fatty acid (FFA) levels seen during exercise.208–210 Performance was not changed after niacin administration in those studies plus one other,208–211 and subjects administered niacin reported greater fatigue.211 Administration of niacin to glycogen-depleted subjects resulted in decreased endurance when compared to glycogen-depleted nonsupplemented subjects, supporting the hypothesis that FFA are an energy source during exercise and casting doubt about the use of excessive amounts of niacin alone as an ergogenic aid.212
Introduction to disorders of fatty acid oxidation
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop
The normal response to fasting and the oxidation of fat begins with lipolysis, which releases free-fatty acids. In patients with disorders of fatty acid oxidation, concentrations of free-fatty acids are usually higher than those of 3-hydroxybutyrate in blood at times of illness and metabolic stress. Thus, assessment of the concentrations of free fatty acids and 3-hydroxybutyrate in the blood is essential to the diagnosis of hypoketosis. Because fatty acids that accumulate in the presence of defective oxidation undergo ω-oxidation to dicarboxylic acids, a disproportionate ratio of dicarboxylic acids to 3-hydroxybutyrate in the organic acid analysis of the urine also indicates disordered fatty acid oxidation. Transport of long-chain fatty acids into the mitochondria, where ß-oxidation takes place, requires carnitine, and the entry of carnitine into cells such as muscle requires a specific transporter, which may be deficient in an inborn error of metabolism [6] (Chapter 35). Esterification of carnitine with fatty acyl CoA ester is catalyzed by acyltransferases, such as carnitine palmitoyl transferase (CPT) I (Chapter 37). The transport of the acylcarnitine across the mitochondrial membrane is catalyzed by carnitine translocase (Chapter 36); and then hydrolysis, releasing carnitine and the fatty acylCoA, is catalyzed by a second acyltransferase, CPT II (Chapters 37 and 38). Inborn errors are known for each of these three enzymatic steps. In ß-oxidation, the fatty acid is successively shortened by two carbons, releasing acetylCoA.
Novel model predicts diastolic cardiac dysfunction in type 2 diabetes
Published in Annals of Medicine, 2023
Mingyu Hao, Xiaohong Huang, Xueting Liu, Xiaokang Fang, Haiyan Li, Lingbo Lv, Liming Zhou, Tiecheng Guo, Dewen Yan
The myocardium of patients with diabetes is powered by free fatty acids [34]. The overuse of fatty acids in the myocardium will lead to the accumulation of fatty acids in the myocardium and lipotoxicity. Free fatty acids are the intermediate products of triglyceride metabolism in the body. In this study, TG was independently associated with diastolic cardiac dysfunction (OR = 1.1377, 95% CI 1.0435 − 1.2405). Previous studies have shown that hypertriglyceridemia affects glucose regulation and insulin sensitivity [35], and both high glucose levels and insulin resistance play an essential role in the pathogenesis of DCM [36,37]. Therefore, as a risk factor of DCM, TG affects the deterioration of the disease, to which clinicians should pay more attention. Of note, TG often increases before the onset of T2DM. Therefore, monitoring the TG level may help predict the occurrence of diabetes and its complications.
Protective effect of Qingluotongbi formula against Tripterygium wilfordii induced liver injury in mice by improving fatty acid β-oxidation and mitochondrial biosynthesis
Published in Pharmaceutical Biology, 2023
Jie Zhou, Ming Li, Zhichao Yu, Changqing Li, Lingling Zhou, Xueping Zhou
The compatibility of different traditional Chinese medicines exerts a synergistic effect, and is of proven effectiveness to reduce drug toxicity in clinical application. We have previously found that QLT and its ingredients could restore liver lipid metabolism homeostasis and reduce TW-induced liver injury in SD rats (Yu et al. 2022). In this study, we noted that the protective effects of QLT are closely related to mitochondrial function and fatty acid metabolism. TW-induced mice liver injury occurred with significant lipid accumulation and mitochondrial dysfunction. As the central organ of lipid metabolism, liver lipid metabolism homeostasis is crucial to normal liver function. Impaired fatty acid oxidation contributes to excessive lipid accumulation in the liver, which cannot be metabolic clearance in time will result in steatosis (Morio et al. 2021). Furthermore, increased free fatty acid concentrations can lead to lipotoxicity, causing cellular stress, apoptosis and necrosis (Hirsova et al. 2016). Besides direct cytotoxicity, enhanced insulin resistance that may be induced can result in further hepatic lipid accumulation and trigger inflammatory responses (Machado and Diehl 2016).
Comparative examination of levodopa pharmacokinetics during simultaneous administration with lactoferrin in healthy subjects and the relationship between lipids and COMT inhibitory activity in vitro
Published in Nutritional Neuroscience, 2022
Masahiro Nagai, Madoka Kubo, Rina Ando, Masayuki Ikeda, Hiroshi Iwamoto, Yasuhiro Takeda, Masahiro Nomoto
Free fatty acids in the blood are ∼0.24 mM in the early morning [28] and ∼0.33 mM at 100 μg/mL of sodium oleate (MW = 304). In this situation, there may be a region that is susceptible to changes in fatty acid concentrations in enhancing the COMT inhibitory activity of bLF by fatty acids (Figure 7A). In addition, the cholesterol concentration is approximately 65 mg/dL because approximately one-third of the total cholesterol laboratory values are present in free form [29]. Assuming that all cholesterols are dissolved in COMT inhibition assays, this level corresponds to a region that enhances the COMT inhibitory activity of bLF (Figure 6). Although a variety of factors may be involved, such as the presence of other binding molecules, high and low concentrations of these two fats may sensitively affect the effects of bLF. Many fats are bound to albumin [30]. In our experiments, the fatty acids used were free of albumin. Therefore, the increase in the COMT inhibitory activity of bLF may be weakened.