synthesis in adipose tissue and liver, ..

Figure 2. Hepatic fatty acid transport and metabolism. Teaching points: many proteins are required in the liver for the import, transport and consumption of fatty acids (FA), the main component of triglycerides. Proteins located in the plasma membrane (FAT/CD36, FABPpm, and Caveolin-1) facilitate the transport FA from the bloodstream into the liver cells. FA imported or produced locally are modified by FATP or ACSL proteins to generate another lipid named acyl-CoA. Acyl-CoA is important because it is the form that is metabolized by enzymes within the liver cells. Acyl-CoA molecules can be converted back to FA by the activities of ACOT/Them proteins. In addition, FA and acyl-CoA interact with proteins (FABP, SCP2, and ACBP) that mediate their transport within liver cells.

We will review the role of triglyceride synthesis in ..

Interested to find and read your Q & A on people’s concerns re abnormal Liver Function Tests.

Fatty Acid Synthesis | Lipoprotein | Triglyceride

Figure 1. Major sources for hepatic lipids. This figure illustrates the origin of the triglyceride (a common form of fat) that is found in the liver in different physiological states. After a meal, the triglycerides obtained from the diet are modified in the intestine and exported to the bloodstream. Muscle and fat tissue can import and process the triglyceride molecules, modifying them according to their specific needs. The liver can also produce its own triglycerides from sugars and amino acids, in a process called lipogenesis (DNL). Within liver cells, the fat is metabolized in order to be stored in structures called lipid droplets (LDs) or to be exported to other organs via the bloodstream in association with particles called lipoproteins (in this case, very low density lipoprotein, VLDL). During fasting, the breakdown of triglyceride storage depots occurs, releasing fatty acids (the main breakdown products of triglycerides into the blood. When it reaches the liver, it can be used to provide energy through a process called fatty acid oxidation, or can be modified to produce VLDL. In the setting gf obesity or diabetes, the breakdown of triglyceride storage depots is stimulated and the synthesis of triglyceride in the liver increases. It results in the accumulation of triglyceride in the liver and increased levels in the blood, both of which are commonly observed in patients with a common condition known as nonalcoholic fatty liver disease.

Since triglyceride synthesis prevails ..

Figure 3. Hepatic triglyceride metabolism. This figure summarizes the cellular routes by FA are converted into more complex lipid forms, including triglycerides (TG). Mitochondrial proteins and those within the endoplasmic reticulum (GPAT, AGPAT, PAP, and DGAT) mediate a series of enzymatic reactions including addition of FA-derived intermediates and removal of a phosphate group, which culminates in the formation of TG. TG formed from FA that are synthesized within the liver cells are most likely exported to the bloodstream in VLDL for delivery to other organs. On the other hand, TG produced from FA that are delivered to the liver from the blood are destined for storage in the liver. Other enzymes (DGAT1 and DGAT2) may also regulate the differential usage of FAs.

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Figure 5. Lipolysis and fatty acid oxidation in hepatocytes. Teaching points: triglycerides (TG) stored in the liver can be metabolized to provide energy to the liver cell itself. This process is initiated by enzymes know as lipases (ATGL, HSL, and MGL) and culminates in the release of fatty acid (FA), the main constituent of TG. Autophagy, a lysosome-dependent pathway to recover and recycle cellular constituents, also mediates the breakdown of TG into FA. FA can also be produced from acyl-CoA lipids by enzymes referred to as ACOT/Them. In order to enter cellular metabolic pathways, FA must be converted to acyl-CoA by ACSL enzymes. They can then be used as a fuel when oxidized in the mitochondria, peroxisome, or endoplasmic reticulum, or can be used to build TG that will be exported to the bloodstream in VLDL particles.

Triglyceride Level: How to Lower High Triglycerides

Liver toxicity markers studied in rats included serum transaminases (AST and ALT), serum triglyceride (STG), hepatic triglyceride (HTG), TNF-alpha and IL-1beta together with histopathological examination.

June 2008 - Volume 19 - Issue 3

N2 - CTRP3 is a secreted plasma protein of the C1q family that helps regulate hepatic gluconeogenesis and is downregulated in a diet- induced obese state. However, the role of CTRP3 in regulating lipid metabolism has not been established. Here, we used a transgenic mouse model to address the potential function of CTRP3 in ameliorating high-fat diet-induced metabolic stress. Both transgenic and wild-type mice fed a high-fat diet showed similar body weight gain, food intake, and energy expenditure. Despite similar adiposity to wild-type mice upon diet-induced obesity (DIO), CTRP3 transgenic mice were strikingly resistant to the development of hepatic steatosis, had reduced serum TNF-a levels, and demonstrated a modest improvement in systemic insulin sensitivity. Additionally, reduced hepatic triglyceride levels were due to decreased expression of enzymes (GPAT, AGPAT, and DGAT) involved in triglyceride synthesis. Importantly, short-term daily administration of recombinant CTRP3 to DIO mice for 5 days was sufficient to improve the fatty liver phenotype, evident as reduced hepatic triglyceride content and expression of triglyceride synthesis genes. Consistent with a direct effect on liver cells, recombinant CTRP3 treatment reduced fatty acid synthesis and neutral lipid accumulation in cultured rat H4IIE hepa- tocytes. Together, these results establish a novel role for CTRP3 hormone in regulating hepatic lipid metabolism and highlight its protective function and therapeutic potential in attenuating hepatic steatosis.