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Dyslipidemia
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Chylomicrons are large triglyceride-rich particles. They are manufactured in the intestines, and involved in transport of dietary triglycerides and cholesterol to the liver. Their size varies based on the amount of fat ingested. After a high-fat meal, large chylomicron particles form because of the higher amounts of triglyceride being carried. During fasting, chylomicron particles are small because less triglyceride is being carried. Chylomicron remnants are smaller particles resulting from the removal of triglyceride from the chylomicrons by the peripheral tissues. The remnants are high in cholesterol, and different from chylomicrons, are pro-atherogenic.
Functions of the Liver
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
After absorption, fat is either metabolized to yield energy or stored as triglyceride in fat deposits. Some 50% of triglycerides derived from the diet are hydrolysed to glycerol and fatty acids, whereas 40% are partially hydrolysed to monoglycerides. Short-chain fatty acids (fewer than 12 carbon atoms) are transported directly to the liver via the portal vein without re-esterification. Longer chain fatty acids are re-esterified after absorption and then covered with a phospholipid and protein layer to form chylomicrons. Lipoprotein lipases hydrolyse the chylomicrons, producing free fatty acids that may be taken up by adipocytes for storage or metabolized within body tissues as an energy source.
Features of Lipid Metabolism in Diabetes Mellitus and Ischemic Heart Disease
Published in E.I. Sokolov, Obesity and Diabetes Mellitus, 2020
The main functional role of chylomicrons is the transportation of triglycerides. They form in the walls of the small intestine and then along the lymph tracts get into a lymphatic duct and the blood. They are not atherogenic because they cannot penetrate into an artery wall owing to the large particle size [107, 167, 176, 292].
Enhanced dissolution and bioavailability of revaprazan using self-nanoemulsifying drug delivery system
Published in Pharmaceutical Development and Technology, 2022
Yoon Tae Goo, Cheol-Ki Sa, Min Song Kim, Gi Hyeong Sin, Chang Hyun Kim, Hyeon Kyun Kim, Myung Joo Kang, Sangkil Lee, Young Wook Choi
To examine the effect of SNEDDS on lymphatic transport, rats were pretreated with CYC, a well-known chylomicron blocking agent. Although the accurate mechanisms of lymphatic transport have not been fully understood, three theories can be postulated: via the paracellular route with absorption enhancers, via the gut-associated lymphoid tissues and M cells, and via a transcellular route in association with the triglyceride core of the chylomicrons (O’Driscoll 2002). Among these, the third route has been deemed a major mechanism of lymphatic delivery of lipophilic drugs with lipid-based formulations. Chylomicrons are extremely large, spherical particles that consist of a core of triglycerides (85–92%) and cholesterol (1–3%), and a monolayer of phospholipids (6–12%), and protein (1–2%) (Nakamura et al. 2016). Two steps are involved in the biosynthesis of chylomicrons. Synthesis of the primordial lipoprotein particle and the triglyceride-rich droplet occurs in the rough endoplasmic reticulum and smooth endoplasmic reticulum, respectively. Thereafter, core expansion occurs, which involves fusion of the primordial lipoprotein with the large triglyceride-rich droplets occurs. The biosynthesized chylomicron is transferred to the Golgi apparatus and is eventually secreted via the intracellular space into the lacteal ducts (Hussain 2000). By blocking the biosynthesis of chylomicron, CYC is able to completely block the lymphatic pathway (Li et al. 2017; Liao et al. 2019).
Safety and efficacy of therapies for chylomicronemia
Published in Expert Review of Clinical Pharmacology, 2022
Isabel Shamsudeen, Robert A. Hegele
Primary chylomicronemia refers to the pathological accumulation of chylomicrons in the plasma, resulting in severe HTG [1]. There are two main types of primary chylomicronemia: ultra-rare FCS and the more prevalent MCS [2]. The treatment of MCS relies on addressing secondary causes, and standard TG-lowering therapies have shown some efficacy in this population [2]. In contrast, FCS patients lack lipolytic capacity, and have a minimal response to conventional therapies [19]. Therefore, the treatment of FCS relies on a strict low-fat diet, which can be difficult to adhere to and leads to a reduced quality of life [5,19]. Apo C-III antagonists, specifically volanesorsen, olezarsen, and ARO-APOC3, are most promising in reducing TG levels in patients with FCS and patients with more common MCS. Anti-ANGPTL3 therapies appear to be effective in MCS but are perhaps less so in FCS. Although FCS is an ultra-rare disease, successful development of safe and effective therapies for these patients will likely be translatable for other more common and etiologically complex forms of severe HTG.
Mechanistically acting anti-obesity compositions/formulations of natural origin: a patent review (2010–2021)
Published in Expert Opinion on Therapeutic Patents, 2022
Pracheta Sengupta, Niyati Tiwari, Tanya Bhatt, Atish T. Paul
Adipose tissue, the main energy storage site, is receptive to both central and peripheral metabolic signals for regulating lipid storage and mobilization. Dietary fat is absorbed in the gastrointestinal tract by the formation of circulating chylomicrons. One part of this is metabolized to provide energy and the rest of the part enters the skeletal muscles and adipose tissues for long-term storage. This process results in the secretion of several adipokines, by adipose tissue. Excess fats are stored for short-term in liver. The liver plays an important role as a homeostat for transient energy fluctuation. It protects other tissues from postprandial triglyceridaemia by temporarily storing fatty acids (FAs) from the circulation as a benign derivative, triacylglycerol (TAG), and secreting them as very low-density lipoproteins (VLDL) when the period of maximum lipid load has passed. VLDL is reported to transport endogenous lipids to extrahepatic tissues. The liver is also an important site for energy conversion, exchanging energy sources from one form to another, such as glycogen to glucose, FA to TAG, and saturated FA to unsaturated FA [14]