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Nutrition and Metabolic Factors
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
The use of fat as an energy source is important during aerobic exercise (101) and can be a post-exercise consequence of anaerobic exercise, including resistance exercise (147, 160). As discussed in Chapter 2, fatty acids are oxidized within the mitochondria by the process of β-oxidation where acetyl-CoA is produced before entering the Krebs cycle. Like proteins and carbohydrate substrates, less complex fatty acids are oxidized faster than long-chain fatty acids (101, 167). It should be noted, however, that fat metabolism is significantly impacted by the endocrine system. Researchers have indicated that fat synthesis may be enhanced by insulin, whereas lipolysis may be enhanced by growth hormone, thyroxin, catecholamines, and cortisol (101, 147). Taking this into account, a variety of nutritional strategies have been proposed to enhance the mobilization and oxidation of fat during and after exercise.
The patient with acute endocrine problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Proteins are metabolised to amino acids, but some are able to donate their carbon atoms for glucose formation. Glucose generation from protein or from any other non-glucose source is called gluconeogenesis. With regard to fat metabolism, triglycerides release glycerol, which can be converted readily to glucose by the liver, but this accounts only for approximately 10% of the carbon atoms available from triglycerides, and thus has only a minor role in gluconeogenesis.
Fats, Fatty Acids, and Lipids
Published in Luke R. Bucci, Nutrition Applied to Injury Rehabilitation and Sports Medicine, 2020
Several properties make MCTs attractive as efficient energy sources. When ingested, MCTs are rapidly and completely absorbed into the portal blood system, not the lymphatic system like other fats. Medium-chain fatty acids are not reesterified and repackaged into chylomicrons. The liver readily takes up medium-chain fatty acids from the portal blood supply. Albumin is the chief carrier of medium-chain fatty acids, although some are dissolved in plasma. In the liver, medium-chain fatty acids do not need carnitine for transport into mitochondria. Medium-chain fatty acids are transported directly to oxidative sites in mitochondria.403,404,442,443 Medium-chain fatty acids are rapidly and, it seems, preferably oxidized to produce cellular energy and ketone bodies, which may be further oxidized or sent to peripheral tissues.442 Metabolism of medium-chain fatty acids resembles carbohydrate metabolism in some ways, rather than fat metabolism. Caloric yield of medium-chain fatty acids is 8 kcal/g, rather than 9 kcal/g usually associated with fats.170
Fat mass, weight and body shape changes at menopause – causes and consequences: a narrative review
Published in Climacteric, 2023
A. Fenton, C. Smart, L. Goldschmidt, V. Price, J. Scott
There are clearly some distinct changes that occur at menopause that appear to be directly related to hormonal changes and that do impact on body composition. Animal data have shown that estrogen deficiency is associated with transient hyperphagia and a reduction in spontaneous activity such as fidgeting [11]. These changes were reversed with estrogen replacement. Studies of mice who have undergone oophorectomy show that this procedure results in obesity, adipocyte inflammation and hepatic steatosis [12]. Supplemental estradiol protects the mice from insulin resistance, oxidative stress and fatty liver. Mice lacking the aromatase gene show a similar and early tendency to central visceral adiposity, adding support to the concept that estrogen deficiency plays an important role in these changes as well as the alterations in behavior noted earlier [12]. It appears that estrogen receptor α may play an important role in regulating some of the changes in fat metabolism [13].
Qushi Huayu decoction attenuated hepatic lipid accumulation via JAK2/STAT3/CPT-1A-related fatty acid β-oxidation in mice with non-alcoholic steatohepatitis
Published in Pharmaceutical Biology, 2022
QinMei Sun, Xin Wang, Xin Xin, ZiMing An, YiYang Hu, Qin Feng
Non-alcoholic fatty liver disease (NAFLD), characterized by excessive lipid deposition and metabolic dysfunction in hepatocytes, has become the most common chronic liver disease worldwide (Brunt et al. 2015). The spectrum of histopathology ranges from simple steatosis (non-alcoholic fatty liver, NAFL) to non-alcoholic steatohepatitis (NASH). Available evidence indicates that the risk factors contributing to the evolution of NAFL to NASH involve lipotoxicity, insulin resistance, chronic liver inflammation, oxidative damage, mitochondrial dysfunction and endoplasmic reticulum stress (Tilg and Moschen 2010; Suzuki and Diehl 2017). Despite progress in this field, the pathogenesis of NASH remains unclear. Lipid accumulation plays a pivotal role in NASH (Monsenego et al. 2012). Lipid levels maintain a dynamic balance between fat synthesis and fat consumption, and unbalanced lipid metabolism leads to fat accumulation in the liver, resulting in hepatic steatosis. Therefore, accelerating fat metabolism is an effective way to reduce lipid accumulation in the liver (Koo 2013).
Sodium–glucose cotransporter 2 inhibitors for the management of type 2 diabetes
Published in Expert Opinion on Pharmacotherapy, 2021
Maka Siamashvili, Stephen N. Davis
The prevalence of hypertension in T2DM is more than 50%. Thus, antihyperglycemic agents that also decrease blood pressure are especially advantageous. SGLT2 inhibitors have consistently shown improvements in systolic and diastolic blood pressure. This effect is thought to result from diuresis caused by appearance of glucose (an osmotically active molecule) in urine, natriuresis, reduction in arterial stiffness and improvement of endothelial dysfunction. Uric acid levels have been correlated with CV morbidity and mortality. Across several trials, the SGLT2 inhibitors have shown to lower this waste byproduct, thus potentially improving CV risk. Another proposed mechanism for CV protective effects of SGLT2 inhibitors include changes in cardiomyocyte energy metabolism [83]. Stimulation of fat metabolism can lead to decreased oxygen utilization, improved cardiac efficiency, and reduced oxidative stress caused by glucose toxicity. Additionally, glucagon (also increased by SGLT2 inhibitors) interacts with the receptors found in cardiomyocytes and improves cardiac inotropic and chronotropic effects.