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Molecular sport nutrition
Published in Adam P. Sharples, James P. Morton, Henning Wackerhage, Molecular Exercise Physiology, 2022
Mark Hearris, Nathan Hodson, Javier Gonzalez, James P. Morton
Whilst glycogen forms the primary fuel source utilised during both prolonged and high-intensity endurance exercises, the capacity to store glycogen within human skeletal muscle is relatively limited (18). In contrast, even in the leanest of individuals, lipid storage within skeletal muscle, and in particular adipose tissue, is highly abundant. In fact, lipid storage within adipose tissue is sufficient for numerous days of continuous exercise. As such, there is increasing interest amongst athletes in strategies that increase the capacity to store and utilise lipids in the hope of sparing muscle glycogen and delaying the onset of fatigue during prolonged exercise (19). Although an increase in the ability to store, transport and oxidise fat forms one of the classical adaptations of endurance training (20), the adoption of a high-fat diet whilst undertaking daily training has the ability to further enhance such adaptation. This dietary strategy is more commonly referred to as fat adaptation or fat loading and is based upon the premise that such adaptations will promote higher rates of fat utilisation during exercise and allow for the sparing of the limited glycogen pool (21). Below, we look at how fatty acids derived from the diet activate the molecular signalling pathways that control the synthesis of proteins involved in the transport and utilisation of fat as a fuel during exercise.
Fuel Metabolism in the Fetus
Published in Emilio Herrera, Robert H. Knopp, Perinatal Biochemistry, 2020
Among mammalian species, lipid storage during the fetal life is the exception rather than the rule. In most mammals, the body fat content at birth is very low (Figure 4) and white adipose tissue is barely detectable.5 The human newborn is remarkable in this context since fat represents about 16% of the term-fetal body weight.
Glycogenosis type I – von Gierke disease
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
Pathologic examination [1, 43] (Figure 59.8) reveals that the hepatocytes and renal tubular cells are swollen and clear as stained with hematoxylin and eosin; staining with Best's carmine reveals the stored material to be glycogen. There may also be extensive lipid storage in the liver. In fact, the lipid may be so prominent that the referring pathologic diagnosis may be lipid storage disease, such as Wolman disease (Chapter 94). In the neonatal period, the histology of the liver can be so normal that one is led away from the diagnosis [16].
Dietary S. maltophilia induces supersized lipid droplets by enhancing lipogenesis and ER-LD contacts in C. elegans
Published in Gut Microbes, 2022
Kang Xie, Yangli Liu, Xixia Li, Hong Zhang, Shuyan Zhang, Ho Yi Mak, Pingsheng Liu
Metabolic syndromes are in fact a lipid storage disorder, ectopic lipid storage that originates from obesity. Obesity is a symptom of excessive accumulation of neutral lipids such as triacylglycerol (TAG) in white adipocytes. Adipose tissue governs the individual’s lipid homeostasis at the tissue level. However, at the cellular level, TAG is stored in LDs. The distribution of LDs in non-adipose tissues, the size and number of LDs in these cells, as well as the type and amount of fatty acids in TAG, are the key factors of metabolic disorders. In white adipose tissue, adipocytes contain unilocular lipid droplets with diameter between 50 μm and 150 μm and their cytoplasm only takes less than 15% of cell volume. Thereby, the LD size is typically considered synonymous for the adipocyte size.22,23 In other cells, such as liver cells, the number and size of LDs vary with the state of the cell.24–26 Therefore, morphological study of lipid droplets is of great significance for understanding obesity and ectopic lipid storage.
Mechanistically acting anti-obesity compositions/formulations of natural origin: a patent review (2010–2021)
Published in Expert Opinion on Therapeutic Patents, 2022
Pracheta Sengupta, Niyati Tiwari, Tanya Bhatt, Atish T. Paul
Adipose tissue, the main energy storage site, is receptive to both central and peripheral metabolic signals for regulating lipid storage and mobilization. Dietary fat is absorbed in the gastrointestinal tract by the formation of circulating chylomicrons. One part of this is metabolized to provide energy and the rest of the part enters the skeletal muscles and adipose tissues for long-term storage. This process results in the secretion of several adipokines, by adipose tissue. Excess fats are stored for short-term in liver. The liver plays an important role as a homeostat for transient energy fluctuation. It protects other tissues from postprandial triglyceridaemia by temporarily storing fatty acids (FAs) from the circulation as a benign derivative, triacylglycerol (TAG), and secreting them as very low-density lipoproteins (VLDL) when the period of maximum lipid load has passed. VLDL is reported to transport endogenous lipids to extrahepatic tissues. The liver is also an important site for energy conversion, exchanging energy sources from one form to another, such as glycogen to glucose, FA to TAG, and saturated FA to unsaturated FA [14]
High-carbohydrate diet-induced metabolic disorders in Gerbillus tarabuli (a new model of non-alcoholic fatty-liver disease). Protective effects of 20-hydroxyecdysone
Published in Archives of Physiology and Biochemistry, 2021
Hadjer Agoun, Nesrine Semiane, Aicha Mallek, Zineb Bellahreche, Soumia Hammadi, Maha Madjerab, Mohamed Abdlalli, Ali Khalkhal, Yasmina Dahmani
Co-administration of 20E with HCD for 5 months reduced all the adverse effects of HCD. The effects of 20E on the obesity induced by an excess of food have previously been investigated using high-fat diets: when given a high-fat diet, mice rapidly became obese, but when simultaneously given 20E (5 or 10 mg kg−1 d−1), they showed a much lower fat mass increase (Foucault et al. 2012, 2014). This effect did not result from a reduction of food intake. Adipocyte numbers were not modified, but their mean size was significantly reduced (Foucault et al. 2012). Their reduced lipid storage was related to a decreased uptake of circulating fatty acid via a reduced lipoprotein lipase expression. The effect of 20E on lipid storage was also observed for gerbil liver, and a similar reduction of liver TGs was also observed in 20E-treated diabetic rats (Sundaram et al. 2012).