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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
In adipocytes, there are two enzymes that are involved in degrading triglycerides: hormone-sensitive lipase and adipose triglyceride lipase. Adipose triglyceride lipase has a greater affinity for triglycerides compared to hormone sensitive lipase, and acts as the primary enzyme for triglyceride hydrolysis in adipocytes. Hormone sensitive lipase is found in small concentrations in muscle and can provide an intramuscular source of FFA and glycerol. In the sarcoplasm of muscle fibers, FFA are bound to CoA. Using a carnitine carrier, the FFA -acyl CoA molecule enters the mitochondria (35, 51, 129, 143). The triglyceride “backbone” glycerol can be converted to glycerol 3 phosphate and enter glycolysis for energy production.
Hormones of the Pancreas
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The most important consequence of the enhanced glucose uptake by adipose cells is an increased synthesis of α-glycerophosphate, which is used for esterification of fatty acids. α-Glycerophosphate is also derived from glucose. Hormone-sensitive lipase is also inhibited by insulin, and this reduces the hydrolysis of triglycerides stored in fat cells.
Emerging ergogenic aids for strength/power development
Published in Jay R Hoffman, Dietary Supplementation in Sport and Exercise, 2019
A number of mechanisms have been proposed to explain body composition changes subsequent to betaine supplementation and training. Regarding loss of fat, betaine has been suggested to: 1) promote fatty acid β-oxidation via increased muscle carnitine content and carnitine palmitoyl transferase-I mediated free fatty acid translocation into the mitochondria; 2) reduce acetyl-CoA for fatty acid synthesis; 3) decrease triglyceride synthesis via reduced acetyl-CoA carboxylase, fatty acid synthase, reduced fatty acid binding protein and mRNA expression of lipoprotein lipase; 4) increase hormone sensitive lipase activity; and 5) augment the GH response and improve insulin–insulin receptor signalling (11, 23). Regarding increased LBM, betaine has been suggested to: 1) conserve methionine for protein synthesis; 2) reduce homocysteine thiolactone (which inhibits insulin/IGF-1 mediated mRNA expression) to increase protein synthesis; 3) stimulate GH (via increased secretion of GH-releasing hormone), IGF-1, insulin–insulin–receptor signalling and reduce cortisol to increase anabolism; 4) increase cellular swelling from acting as an osmolyte, which increases protein synthesis via increased integrin-G-protein-stimulated gene transcription; and 5) stimulate mammalian target of rapamycin (mTOR) pathway-induced protein synthesis (2, 11, 31). So, betaine may be involved in a series of physiological mechanisms known to affect body composition. It appears betaine supplementation combined with training is needed to produce a desired effect.
Preparation and characterisation of a new form of silymarin as a potential antidiabetic agent in the adult male rat
Published in Archives of Physiology and Biochemistry, 2023
Elnaz Golestaneh, Abolfazl Aslani, Mahmoud Aghaei, Mohammad Hashemnia, Mohammad Hosein Aarabi
Several studies have shown that Silymarin induces alterations in the blood lipid profile by decreasing total cholesterol, triglyceride, and LDL of diabetic animals (Sajedianfard et al.2014, El-Far et al.2016, El-Tantawy and Temraz 2018). In the present study we induced diabetes leading to a significant increase in the amount of TG, TC compared to the normal group. These abnormalities were ameliorated by both SM and NFSM with the superiority of NFSM over SM in the reduction of TC. This is in agreement with the earlier studies (Sajedianfard et al.2014, El-Far et al.2016). The possible mechanism of hypolipidemic effects may be associated with insulin levels. Insulin deficiency or insulin resistance is related to hypercholesterolaemia and hypertriglyceridaemia. Indeed, insulin deficiency increases the mobilisation of free fatty acids from the peripheral lipid since insulin inhibits the hormone-sensitive lipase. A preliminary study also suggested that SM may be has a direct effect on liver cholesterol metabolism by inhibiting its biosynthesis (El-Tantawy et al.2015). Also, several studies have been shown an association between glucose/insulin regulations, oxidative stress, and free fatty acid in the diabetic state (Sajedianfard et al.2014, El-Far et al.2016). Brownlee et al. proposed that the elevation of glucose and free fatty acids in diabetic rats increases the generation of oxidative stress (Brownlee 2001).
Arsenic: an emerging role in adipose tissue dysfunction and muscle toxicity
Published in Toxin Reviews, 2022
Kaviyarasi Renu, Aditi Panda, Balachandar Vellingiri, Alex George, Abilash Valsala Gopalakrishnan
Adipose tissue is subdivided into two types, such as white adipose tissue (WAT) and brown adipose tissue (BAT). The distribution of the adipose tissue is mainly based on environmental factors and nutritional factors. In this, we have focused mainly on the storage of energy, communication by the endocrine, and sensitivity by insulin (Fantuzzi 2005, Frühbeck and Gómez-Ambrosi 2013, Choe et al.2016). Adipose tissue is mainly involved in the storage of fat, accumulation of energy excessively and releases it via lipogenesis [Triglyceride (TAG)] and lipolysis via [adipose triglyceride lipase (ATGL), Hormone-sensitive lipase (HSL), and monoglyceride lipase (MGL)]. The adipose tissue status is depending on the cellular composition changes, such as number, structure and site of deposit. Alteration of cell numbers of adipose (hyperplasia), size, and shape (hypertrophy) is the indication of the dysfunction of adipose tissue. Loss of fat or lipodystrophy is due to the attenuation of the number of adipocytes and the size of the adipocyte. These changes lead to the intolerance of glucose, hyperlipidemia, and insulin resistance (Choe et al.2016, Schoettl et al.2018, Henriques et al.2019, Recinella et al.2020). Adipose tissue acts as the main organ for the accumulation of arsenic. Augmented accumulation of arsenic in adipose tissue avert from differentiation of cells and mediates disproportion in the metabolism of fat, a function of mitochondria, and leads to obesity and diabetes (Bae et al.2019).
Galangin, a dietary flavonoid, ameliorates hyperglycaemia and lipid abnormalities in rats with streptozotocin-induced hyperglycaemia
Published in Pharmaceutical Biology, 2018
Amal A. Aloud, Veeramani Chinnadurai, Chandramohan Govindasamy, Mohammed A. Alsaif, Khalid S. Al-Numair
An increase in blood TG levels is a common problem in hyperglycaemic patients and plays a role in vascular complications (Naqvi et al. 2017). A previous study demonstrated defective lipoprotein lipase (LPL) activity may be responsible for hypertriglyceridemia in diabetics (Trent et al. 2014). In the present study, plasma and tissue TG levels increased significantly in diabetic rats, which might be due to defective LPL. Insulin plays an important role inhibiting hormone-sensitive lipase. In addition, glucagon and other hormones stimulate lipolysis. Therefore, higher serum lipid levels in patients with diabetes could be due to the lack of inhibition of lipolytic hormone activity on the depots (Trent et al. 2014). Antidiabetic drugs are associated with lowered plasma TG due to returning LPL to normal activity (Liu et al. 2018). Treatment with galangin led to decreased TG levels, which may be due to increased insulin secretion as a result of increased LPL activity.