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Metabolic Syndrome
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Small and dense HDL particles are not as protective to the heart as larger HDL particles, due to less capacity for reverse cholesterol transportation. The small particles also have fewer antioxidant and antiinflammatory effects. Endothelial function cannot be improved as much, and there is lower protection from oxidation of LDL particles. The liver more quickly metabolizes smaller, denser HDL particles. They do not exist for as long a time and are therefore lower in number. With metabolic syndrome, activity of hepatic lipase upon triglyceride-rich VLDL particles is higher.
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
Defective activity of the enzyme may be documented in postheparin plasma or in adipose tissue. Heparin also releases hepatic lipase into plasma. This enzyme has little activity against chylomicrons, and so it created no problem in the original assay of Havel and Gordon [3], but most modern assays are done with artificial emulsions of triglycerides. Selective assay requires inhibition of the lipoprotein lipase with protamine or concentrated saline and calculating the difference from total lipolytic activity [38], inhibition of the hepatic lipase by specific antiserum [31], or chromatographic separation of two enzymes [39]. In classic lipoprotein lipase deficiency, patients have marked triglyceridemia and virtually always have clinical symptoms before puberty, and they have defective enzyme activity in every tissue studied [40]. The enzyme may be measured in adipose tissue obtained by needle aspiration, which is of advantage because it does not contain hepatic lipase, but the assay must be done immediately thereafter. In patients with classic deficiency, the activity in adipose tissue is defective whether the patient is in the fed or fasted state [41].
Atherosclerosis
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
The lipid composition of lipoprotein a is similar to LDL, but it contains different proteins. The distribution of apolipoproteins in normal humans is given in Table 8. Although the presence of this lipoprotein has been confirmed in 75 to 78% of the population, it does not show any correlation with the occurence of coronary heart disease. Lipoprotein x was found in the serum of patients with lecithin: cholesterol acyl transferase deficiency and with biliary obstruction. It has been suggested that an altered apoA is the protein constituent which does not bind lipid. From the serum of cholestatic patients with significantly reduced hepatic lipase activity, a new lipoprotein was isolated which may mediate the disposition of chylomicrons.451 An abnormally low density lipoprotein has been isolated in obstructive jaundice,572 and the structure of a very high density lipoprotein in human serum has been elucidated.7
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).
Chemical compositions of Commiphora opobalsamum stem bark to alleviate liver complications in streptozotocin-induced diabetes in rats: Role of oxidative stress and DNA damage
Published in Biomarkers, 2022
Mai M. Farid, Asmaa F. Aboul Naser, Maha M. Salem, Yomna R. Ahmed, Mahmoud Emam, Manal A. Hamed
Our results showed substantial increases in cholesterol, TG and LDL-C levels, while significant decrease in HDL-C level of diabetic rats compared with the control group. These findings matched those of Ozder (2014), who noted that there are many factors in diabetes could modify blood lipid levels due to their interaction between carbohydrates and lipid metabolism. As a result, any disorder in glucose metabolism causes disturbance with lipid metabolism. Also, any disturbance in the insulin level is associated with a state of lipid metabolism disorder (Haffner et al. 2000). Additionally, insulin insufficiency also lowers hepatic lipase activity and many processes in the generation of physiologically active lipoprotein lipase (Elnasri and Ahmed 2008). Hashem et al. (2016) attributed the improvement in lipid profile after treatment with natural bioactive compounds to the reduction of hepatic triglyceride generation and the redistribution of cholesterol content among the lipoprotein molecules. We also noticed that, the decline in the total cholesterol by treatment with the plant extract was associated with a decrease of its LDL-C . This result suggested that the cholesterol-lowering activity of Commiphora opobalsamum butanol fraction result from the catabolism of LDL-C and its elimination in the form of bile acids.
Homozygous familial hypercholesterolemia and its treatment by inclisiran
Published in Expert Opinion on Orphan Drugs, 2020
A David Marais, Dirk J Blom, Frederick J Raal
The bulk of the cholesterol circulating in the blood plasma is in low-density lipoprotein (LDL) in which apolipoprotein B100 (apoB100) is practically the only protein. In the liver, apoB100 accepts triglyceride and cholesterol ester from microsomal triacylglycerol transfer protein (MTP) and the particle is secreted as very low-density lipoprotein (VLDL). In the circulation, the triglyceride contained in VLDL undergoes hydrolysis by lipoprotein lipase retained on the vascular endothelium of muscle, adipose tissue, and lactating breast tissue. Ultimately, hydrolysis of remnants by hepatic lipase yields smaller, cholesterol-rich LDL particles. Only once LDL is formed will apoB100 bind the LDL receptor on cells expressing the cognate receptors in response to intracellular depletion of cholesterol. The first description of a familial pattern of hypercholesterolemia, tendon xanthomata, and premature ischemic heart disease was published in 1938 [4]. Many years later the molecular pathophysiology of FH was proven to be due to the impaired uptake of LDL owing to defects in the LDL receptor. Brown and Goldstein were awarded the Nobel Prize for this work [5].