China
Africa
Explore chapters and articles related to this topic
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
Fat oxidation: The most common form of fat storage in mammals are triglycerides. Triglycerides are primarily stored in fat cells (adipocytes) with small storage amounts in muscle. Triglycerides are degraded by hormone-sensitive lipase into energy substrates, three free fatty acid (FFA) chains and glycerol. FFA and glycerol released from triglyceride catabolism in adipocytes can be released into the circulation, taken up by muscle and used for energy (116, 138, 167).
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.
Adipocyte Development
Published in Fernand P. Bonnet, Adipose Tissue in Childhood, 2019
In summary, the authors obtain cells from a preparation which originally must be very heterogenous, and these cells collect more lipid granules than fibroblasts, but do not develop morphologically into adipocytes. The functional data show the presence of enzyme activities which are present in adipocytes as well as in several other types of cells, including those probably present in the original preparation (endothelial cells, blood cells, fibroblasts, smooth muscle cells). The best potential discriminator here seemed to be lipoprotein lipase, but the activity cannot be evaluated in quantitative terms. Hormone-sensitive lipase, an enzyme which is rather specific for adipocytes, was not measured.
Effects of different oxygen tensions on differentiated human preadipocytes lipid storage and mobilisation
Published in Archives of Physiology and Biochemistry, 2021
Bimit Mahat, Jean-François Mauger, Pascal Imbeault
Adipocytes, the signature cells of adipose tissue, play a central role in the regulation of lipid storage and lipid mobilisation (Luo and Liu 2016). Adipocytes store energy in excess of needs in the form of triglycerides (TG), a process termed lipogenesis that is partly driven by the lipoprotein lipase (LPL). LPL degrades lipoprotein-bound TG to fatty acids for their subsequent uptake by the adipocytes where they can be re-esterified into TG through the action of acyltransferases (MGAT (monoacylglycerol acyltransferase activity) and DGAT (diacylglycerol acyltransferase activity)) (Shi and Cheng 2009, Luo and Liu 2016). In addition, adipocytes can synthesise new fatty acids from other macronutrients, a process called de novo lipogenesis (DNL). Part of DNL regulation occurs at the transcriptional level through the nuclear factor carbohydrate response element-binding protein (ChREBP), which stimulates the expression of DNL rate-limiting enzymes acetyl-coA carboxylase (ACC) and fatty acid synthase (FASN) in response to increase in glucose availability (Shrago et al. 1969, Herman et al.2012). In time of increased metabolic need, stored lipids can be mobilised by converting adipocytes TG into fatty acids using a process called lipolysis, which depends mainly on the activation of two specific hydrolases, the adipose triglyceride lipase (ATGL) and the hormone-sensitive lipase (HSL) (Lass et al.2011). Fatty acids derived from intracellular lipolysis are released into circulation and delivered to peripheral tissues to sustain energy demand.
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.
4-Phenylbutyric acid and rapamycin improved diabetic status in high fat diet/streptozotocin-induced type 2 diabetes through activation of autophagy
Published in Archives of Physiology and Biochemistry, 2021
Shaimaa H. Gadallah, Hala M. Ghanem, Amany Abdel-Ghaffar, Fatma G. Metwaly, Laila K. Hanafy, Emad K. Ahmed
Also, hypertriglyceridemia, hypercholesterolemia, increase in LDL-C level, and decrease in HDL-C levels were also observed after induction of T2DM. The increased level of triglycerides in HFD/STZ-induced diabetes observed in the current study may be due to the disruptive and toxic effect of STZ on the insulin-producing β-cells of the pancreas. This results in a lack of insulin which normally activates the enzyme lipoprotein lipase that catalyses the hydrolysis of triacylglycerols in chylomicrons and VLDL. In addition, there is an increase in the activity of the hormone-sensitive lipase which catalyses the mobilization of fatty acids from the peripheral fat depots and its activity is normally inhibited by insulin (Cullen et al.1999).