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Enzymes for Prodrug-Activation in Cancer Therapy
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2020
Lipoprotein lipase (LPL) hydrolyzes triglycerides (TG) in lipoproteins (found in lipoprotein particles such as chylomicrons and very low-density lipoproteins) into two free fatty acids and one monoacylglycerol molecule. The enzyme requires apolipoprotein C2 as cofactor for activation and is present among others in heart, adipose, and skeletal muscle tissue. The molecular mass of the glycoprotein LPL is between 55 and 58 kDa of which 12% are carbohydrates. Lipoprotein lipase provokes clearance of triglyceride-rich lipoproteins from the blood. Deficiencies or defects in LPL cause serious hypertriglyceridemia and susceptibility to chronic, life-threatening pancreatitis. Lipoprotein lipase deficiency, LPLD, is an ultra-rare autosomal recessive lipid disorder that results from a mutation in the gene encoding LPL lipoprotein lipase (Burnett et al., 2017). It is estimated that only 1 or two out of 1.000 000 people are affected.
Association of occupational exposure to pesticides with overweight and abdominal obesity in family farmers in southern Brazil
Published in International Journal of Environmental Health Research, 2022
Roberta Andressa Line Araújo, Cleber Cremonese, Ramison Santos, Camila Piccoli, Gabriela Carvalho, Carmen Freire, Raquel Canuto
Regarding insecticides and the outcomes of interest, only animal models and in vivo studies were found in the literature. An animal model study exposed mice to bifenthrin, a synthetic pyrethroid, for 6 weeks, resulting in increased body weight and fat mass. Hormone-sensitive protein lipase and adipose triglyceride lipase were downregulated, whereas lipoprotein lipase was upregulated after treatment. Similar effects were seen in 3T3-L1 cells treated with bifenthrin, thus validating the in vivo results (Wei et al. 2019). Similar results were also seen in cell models treated with cis-bifenthrin in a study conducted by Xiang et al. (2018) (Xiang et al. 2018). Shen et al. (2017) demonstrated that deltamethrin, a pyrethroid, increased the fat accumulation in 3T3-L1 adipocytes and Caenorhabditis elegans via aak-2 (an ortholog of AMPKα)-mediated mechanisms in an animal model (Shen et al. 2017). The results of these studies suggest that long-term exposure to pyrethroid insecticides disrupts the processes of fatty acid uptake and lipolysis, thus inducing fat deposition, which could cause obesity in humans as well.
Effect of an education-based workplace intervention (move in office with education) on sedentary behaviour and well-being in desk-based workers: a cluster randomized controlled trial
Published in International Journal of Occupational Safety and Ergonomics, 2022
Ashwini Kumar Patel, Chavinoor Banga, Baskaran Chandrasekaran
Computerization has led to increased sedentary behaviour (SB) – any waking behaviour characterized by an energy expenditure of less than 1.5 metabolic equivalents – in the occupational setting [1]. Desk-based office workers spend 65–75% of their waking hours sitting in the office and at home, and accrue 40% of this time in prolonged sitting bouts (a prolonged sitting bout can be operationally defined as a sitting time of more than 30 min) [2]. Contemporary evidence now exists proving that chronic uninterrupted SB is found to alter postprandial glycaemia, insulin resistance and triglyceridemia [3]. These risk factors are speculated to perpetuate the detrimental consequences associated with high SB such as diabetes, cardiovascular diseases, obesity and cancer due to suppression of skeletal muscle lipoprotein lipase [3,4]. Further, sedentary occupational time is associated positively with job dissatisfaction and fatigue, and negatively associated with work productivity [5] and mental well-being [6].
The effect of 10 days of energy-deficit diet and high-intensity exercise training on the plasma high-density-lipoprotein (HDL) level among healthy collegiate males
Published in European Journal of Sport Science, 2022
Mohamed Nashrudin Naharudin, Ashril Yusof
In the current study, although 8 min of high-intensity cycling exercise is considered to have mainly involved carbohydrate metabolism, a proportion of fat could still have been utilised out of the ∼125 kcal of total energy expenditure (van Loon, Greenhaff, Constantin-Teodosiu, Saris, & Wagenmakers, 2001). Therefore, a cumulative utilisation of fat during the series of high-intensity cycling performed over the 10 days of the experimental period could be the reason for the increase in HDL. Also, it is thought that the increase in HDL in response to exercise is due to an increase in the activity of lipoprotein lipase (which transfers other lipoproteins to HDL) and a reduction in the activity of hepatic lipase (which removes HDL in the blood) (Svendsen, Hassager, & Christiansen, 1994).