Nutrition for health and sports performance
Nick Draper, Helen Marshall in Exercise Physiology, 2014
The lipid equivalent to glucose for energy production from fats is the fatty acid. Free fatty acids are long carbon chains with hydrogen atoms attached. As can be seen from Figure 2.11 one end of a fatty acid contains a COOH (carboxylic acid) unit and this is known as the head. The head will form bonds when in water because it is hydrophilic (water-friendly). However, the tail of a fatty acid is hydrophobic (water-fearing). While glucose is stored as glycogen in the muscles and liver, free fatty acids are stored as triglycerides within the adipocytes. Triglycerides are composed of a glycerol molecule attached to three fatty acids. Unlike the fatty acids, glycerol is a carbohydrate-based molecule that can be converted to glucose when a triglyceride is broken down. When fatty acids are required as an energy source the triglyceride can be catabolised (broken down) again to release the fatty acids. The process by which fats are released from their glycerol backbone is called lipolysis and during low-intensity exercise, when fat becomes the predominant fuel source for aerobic metabolism, the rate of lipolysis will increase. Fatty acids are released into the blood and attach to albumin, a blood protein, and travel to the exercising muscles as free fatty acids.
Experimental perturbations to investigate cardiovascular physiology
Neil Herring, David J. Paterson in Levick's Introduction to Cardiovascular Physiology, 2018
It is relatively simple to alter the composition of the perfusate when studying isolated cells or multicellular tissue in terms of the ion concentrations, blood gas tensions and pH to study their influence on cellular function. Multiple components can be changed simultaneously, for example, to mimic ischaemia. This is usually done with a perfusate containing high K+, low pH and low O2 tension. This does not mimic the tissue gradient of ion concentrations or temporal changes that occur in vivo during an ischaemic event. Many perfusate solutions contain glucose as the main metabolic substrate, but do not contain free fatty acids, ketone bodies or lactate. This is particularly relevant to the heart where under normal circumstances the main metabolic substrate for energy production are free fatty acids.
High Carbohydrate Diet-Induced Metabolic Syndrome in the Overweight Body
Nilanjana Maulik in Personalized Nutrition as Medical Therapy for High-Risk Diseases, 2020
It is well known that obesity with its accompanying morbidities, both in developed and underdeveloped societies has reached epidemic proportions, generally due to the high carbohydrate content in their daily diet and an unbalanced ratio between energy intake and utilization (Jung and Choi 2014; Fontes-Carvalho, Ladeiras-Lopes et al. 2015). In contrast to a positive energy balance, when energy is needed between meals or during physical exercise, triglycerides stored in adipocytes can be mobilized through lipolysis to release free fatty acids into circulation which are transported to other tissues to be used as an energy source. It is generally accepted that free fatty acids, a product of lipolysis, play a critical role in the development of obesity-related metabolic disturbances, especially insulin resistance (Jung and Choi 2014). In obesity, free fatty acids can directly enter the liver via portal circulation, and increased levels of hepatic free fatty acids induce increased lipid synthesis and gluconeogenesis as well as insulin resistance in the liver (Boden 1997). High levels of circulating free fatty acids can also cause peripheral insulin resistance in both animals and humans (Kelley, Mokan et al. 1993; Boden 1997). Although the exact mechanisms of the complex pathways of MetS are under investigation, it is generally accepted that the current food environment contributes to the development of MetS when our diet is mismatched with our biochemistry (Bremer, Mietus-Snyder et al. 2012).
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.
Electric pulse stimulation inhibited lipid accumulation on C2C12 myotubes incubated with oleic acid and palmitic acid
Published in Archives of Physiology and Biochemistry, 2021
Ling-Jie Li, Jin Ma, Song-Bo Li, Xue-Fei Chen, Jing Zhang
In this study, we treated C2C12 myotubes with OA and PA for 24 h to induce an increase of TG content and lipid droplet accumulation; low density EPS induced C2C12 myotubes to make rhythmical contraction for 3 h and decreased myotubes lipid content significantly. After that, we explored the reason for exercise promoting fatty acid oxidation through the process of fatty acid uptake, fatty acid re-esterification, and fatty acid oxidation. We observed that after OA + PA treatment, FATP1 and FABP3 expression were upregulated, and FASN expression increased significantly. The results indicated that under high fat conditions, fatty acid uptake and triglyceride synthesis both increased, while fatty acid oxidation induced no changes in fatty acid accumulation. In addition, exercise stimulation not only induced FAT/CD36, FATP4, FABP1 and FABP5 expression significantly but also promoted fatty acid key enzyme expression with significance, such as CPT1, ACOX1, UCP3 and PPARα. These results indicate that exercise not only stimulated fatty acid uptake, and inhibited synthesis of triglycerides but also increased fatty acid oxidation metabolism, and decreased lipid accumulation in skeletal muscle.
Effectiveness of a physical activity program on weight, physical fitness, occupational stress, job satisfaction and quality of life of overweight employees in high-tech industries: a randomized controlled study
Published in International Journal of Occupational Safety and Ergonomics, 2019
Yun-Ya Fang, Chien-Yuan Huang, Mei-Chi Hsu
In this study, we also observed a significant reduction of plasma triglyceride, total cholesterol and LDL-C levels after the intervention. The PA program significantly decreased the total cholesterol levels by 6%, triglyceride levels by 16% and LDL-C by 8% in the intervention group. On the contrary, there was an increase in total cholesterol levels by 6% and LDL-C by 14.3%, and an insignificant reduction of triglyceride levels by only 0.4% in the control group. The improvements in serum lipids could not be attributed to dietary changes as participants were advised not to change their dietary habit during the study. Our findings are consistent with a recent study indicating that exercise training lowered triglyceride and cholesterol levels among obese persons [22]. Our findings are also in agreement with the previous reports that reduced plasma cholesterol levels were associated with decreased body weight and percentage body fat [23], and that exercise raised serum HDL-C levels of middle-aged employees and improved lipid management and outcomes at the worksite [9]. Exercise facilitates alterations in lipid metabolism and influences fatty acid oxidation [10].
Related Knowledge Centers
- Biochemistry
- Carboxylic Acid
- Chemistry
- Cholesteryl Ester
- Diet
- Ester
- Phospholipid
- Aliphatic Compound
- Branched-Chain Fatty Acid
- Triglyceride