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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
An enhancement also occurs in the activity of lipoprotein lipase, which splits the triglyceride into fatty acids so that they can be absorbed and stored by fat cells. Lipoprotein lipase is therefore important in the formation of low-and high-density lipoproteins.
Lipoprotein lipase deficiency/type I hyperlipoproteinemia
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
Lipoprotein lipase deficiency is autosomal recessive in inheritance. Occurrence in a number of siblings has been reported [2], as has consanguinity [9]. Lipoprotein lipase activity of about 50 percent of normal has been reported in adipose tissue of parents of patients with deficiency [31]. Low levels of a lipolytic activity have also been observed in postheparin plasma of relatives, but heterozygosity cannot always be demonstrated by assay of the plasma [13]. Heterozygotes may have hypertriglyceridemia [31], but fasting levels of triglycerides are usually normal. In fact, it has been demonstrated by careful study of an extended pedigree [13] that hypertriglyceridemia of many genetic and other causes is so common in adults that the finding of an elevated concentration of triglycerides in a parent or relative cannot be equated with heterozygosity for lipoprotein lipase deficiency.
Atherosclerosis
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
Lipoprotein lipase is present in many tissues; adipose tissue and skeletal muscle constitute major sites. This lipase is primarily responsible for the hydrolysis of plasma lipoprotein triglyceride.351 Lipoprotein lipase differs from other lipases in that it needs apoC-II as a cofactor and is activated by low concentrations of heparin.629 Lipoprotein lipase activity can show wide fluctuations representing an adaptive mechanism whereby plasma triglyceride fatty acids are removed from circulation according to need.465 During postprandial triglyceride storage, the adipose tissue lipase activity is high. When triglycerides are mobilized as in starvation, lipase activity is low. This decrease in enzyme activity on the endothelial surface can result in an increased accumulation of VLDL and chylomicrons in the circulation. There are two pathological conditions connected with reduced lipoprotein lipase activity in adipose tissue: (1) uncontrolled diabetes mellitus317,332,507 and (2) familial hyperchylomicronemia (Type I hyperlipoproteinemia).566 In diabetes mellitus, lipase deficiency of adipose tissue is due to reduced levels of circulating insulin. Following treatment with this hormone, the enzyme activity returns to normal.329,360 There is an interaction between lipoprotein lipase and heparin-like polysaccharides.57
Effects of resistance training and nigella sativa on type 2 diabetes: implications for metabolic markers, low-grade inflammation and liver enzyme production
Published in Archives of Physiology and Biochemistry, 2023
Soheila Jangjo-Borazjani, Maryam Dastgheib, Efat Kiyamarsi, Roghayeh Jamshidi, Saleh Rahmati-Ahmadabad, Masoumeh Helalizadeh, Roya Iraji, Stephen M Cornish, Shiva Mohammadi-Darestani, Zohreh Khojasteh, Mohammad Ali Azarbayjani
The results of the present study are consistent with other studies (Prabhakaran et al.1999, Costa et al.2011, Vital et al.2016). Some studies have demonstrated that resistance training alone enhances glycemic control (Church et al.2010, Bacchi et al.2013) and muscle substrate metabolism in individuals with T2D (Sparks et al.2013). Factors such as improvements in insulin signalling and some molecular mechanism could be responsible for the resistance training-induced improvements in substrate metabolism and glycemic control (Holten et al.2004). Insulin resistance is one of the factors that may affect blood lipid levels. Some studies observed that insulin can affect how the liver regulates the enzymatic activity of lipoprotein lipase, apolipoprotein production and cholesterol ester transport protein, which causes dyslipidemia in diabetes mellitus. Moreover, with insulin deficiency, the activity of hepatic lipase and some steps in the production of biologically active lipoprotein lipase is reduced (Elnasri and Ahmed 2008, Mooradian 2009).
Stink bean (Parkia speciosa) empty pod: a potent natural antidiabetic agent for the prevention of pancreatic and hepatorenal dysfunction in high fat diet/streptozotocin-induced type 2 diabetes in rats
Published in Archives of Physiology and Biochemistry, 2023
Liwei Gao, Wenzhi Zhang, Leiyan Yang, Hong Fan, Opeyemi Joshua Olatunji
One of the main alteration experienced in diabetes is hyperlipidaemia, a condition that predisposes diabetic patient to cardiovascular diseases (Nandini and Naik 2019). Several studies have illustrated the prominent role insulin plays in lipid metabolism by stimulating lipogenesis and increasing the uptake of triglycerides in the blood to the muscles and adipose tissues, thus annihilating lipolysis through the action of lipoprotein lipase enzyme and subsequent reduction in the plasma level of triglycerides and fatty acids (Qaid and Abdelrahman 2016). In diabetes, the action of lipoprotein lipase enzyme is significantly reduced which leads to increase in adipose tissue lipolysis and high levels of triglycerides (Taskinen 1987; Eriksson et al. 2003; Huang et al. 2013). Furthermore, the increase in triglycerides promotes β-oxidation of fatty acids and cholesterol outputs leading to hypercholesterolaemia and hypertriglyceridaemia (Albasher et al. 2020). The results from this study indicated that diabetic rats showed significantly higher levels of triglycerides, total cholesterol, and LDL-C, while HDL was significantly reduced. However, treatment with PPS ameliorated hypercholesterolaemia and hypertriglyceridaemia, suggesting the protective role of PPS in hyperglycaemia-associated dyslipidemia.
Emerging lipid lowering agents targeting LDL cholesterol
Published in Postgraduate Medicine, 2020
The exact role of the ANGPTL3 protein in lipid metabolism is not yet fully clarified. It inhibits lipoprotein lipase and endothelial lipase activity, increasing levels of triglycerides and other lipids. Moreover, it may have proinflammatory, proangiogenic effects and a negative effect on cholesterol efflux, implying additional proatherosclerotic properties. Familial combined hypolipidemia is caused by homozygous loss of function ANGPTL3 mutations. It is associated with overall decrease in lipid levels including LDL-C, HDL-C, and triglycerides as well as reduced ASCVD risk [52]. Even heterozygous carriers of loss of function ANGPTL3 variants have reduced plasma levels of total cholesterol and triglycerides and are at lower risk of developing ASCVD, as compared to non-carriers [53]. In the DiscovEHR study, which involved ANGTPL3 gene sequencing of 58,335 participants, loss-of-function variants in ANGPTL3 were associated with significantly lower serum levels of triglycerides, HDL-C, and LDL-C. The loss of function heterozygosity was found in 0.33% of patients with coronary artery disease and in 0.45% of controls (adjusted odds ratio, 0.59; 95% confidence interval, 0.41 to 0.85; P = 0.004) [54].