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      ANGPTL8 in metabolic homeostasis: more friend than foe?

      review-article
      1 , 2 , 2 , 1 , 2 , 2 ,
      Open Biology
      The Royal Society
      ANGPTL8, betatrophin, T2DM, glucose metabolism, lipid metabolism

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          Abstract

          Abstract

          ANGPTL8 is an important cytokine, which is significantly increased in type 2 diabetes mellitus (T2DM), obesity and metabolic syndrome. Many studies have shown that ANGPTL8 can be used as a bio-marker of these metabolic disorders related diseases, and the baseline ANGPTL8 level has also been found to be positively correlated with retinopathy and all-cause mortality in patients with T2DM. This may be related to the inhibition of lipoprotein lipase activity and the reduction of circulating triglyceride (TG) clearance by ANGPTL8. Consistently, inhibition of ANGPTL8 seems to prevent or improve atherosclerosis. However, it is puzzling that ANGPTL8 seems to have a directing function for TG uptake in peripheral tissues; that is, ANGPTL8 specifically enhances the reserve and buffering function of white adipose tissue, which may alleviate the ectopic lipid accumulation to a certain extent. Furthermore, ANGPTL8 can improve insulin sensitivity and inhibit hepatic glucose production. These contradictory results lead to different opinions on the role of ANGPTL8 in metabolic disorders. In this paper, the correlation between ANGPTL8 and metabolic diseases, the regulation of ANGPTL8 and the physiological role of ANGPTL8 in the process of glucose and lipid metabolism were summarized, and the physiological/pathological significance of ANGPTL8 in the process of metabolic disorder was discussed.

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          Most cited references115

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          FAT SIGNALS - Lipases and Lipolysis in Lipid Metabolism and Signaling

          Lipolysis is defined as the catabolism of triacylglycerols stored in cellular lipid droplets. Recent discoveries of essential lipolytic enzymes and characterization of numerous regulatory proteins and mechanisms have fundamentally changed our perception of lipolysis and its impact on cellular metabolism. New findings that lipolytic products and intermediates participate in cellular signaling processes and that “lipolytic signaling” is particularly important in many nonadipose tissues unveil a previously underappreciated aspect of lipolysis, which may be relevant for human disease.
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            Energy metabolism in the liver.

            The liver is an essential metabolic organ, and its metabolic function is controlled by insulin and other metabolic hormones. Glucose is converted into pyruvate through glycolysis in the cytoplasm, and pyruvate is subsequently oxidized in the mitochondria to generate ATP through the TCA cycle and oxidative phosphorylation. In the fed state, glycolytic products are used to synthesize fatty acids through de novo lipogenesis. Long-chain fatty acids are incorporated into triacylglycerol, phospholipids, and/or cholesterol esters in hepatocytes. These complex lipids are stored in lipid droplets and membrane structures, or secreted into the circulation as very low-density lipoprotein particles. In the fasted state, the liver secretes glucose through both glycogenolysis and gluconeogenesis. During pronged fasting, hepatic gluconeogenesis is the primary source for endogenous glucose production. Fasting also promotes lipolysis in adipose tissue, resulting in release of nonesterified fatty acids which are converted into ketone bodies in hepatic mitochondria though β-oxidation and ketogenesis. Ketone bodies provide a metabolic fuel for extrahepatic tissues. Liver energy metabolism is tightly regulated by neuronal and hormonal signals. The sympathetic system stimulates, whereas the parasympathetic system suppresses, hepatic gluconeogenesis. Insulin stimulates glycolysis and lipogenesis but suppresses gluconeogenesis, and glucagon counteracts insulin action. Numerous transcription factors and coactivators, including CREB, FOXO1, ChREBP, SREBP, PGC-1α, and CRTC2, control the expression of the enzymes which catalyze key steps of metabolic pathways, thus controlling liver energy metabolism. Aberrant energy metabolism in the liver promotes insulin resistance, diabetes, and nonalcoholic fatty liver diseases.
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              Adipocyte dysfunctions linking obesity to insulin resistance and type 2 diabetes.

              Acquired resistance to the action of insulin to stimulate glucose transport in skeletal muscle is associated with obesity and promotes the development of type 2 diabetes. In skeletal muscle, insulin resistance can result from high levels of circulating fatty acids that disrupt insulin signalling pathways. However, the severity of insulin resistance varies greatly among obese people. Here we postulate that this variability might reflect differences in levels of lipid-droplet proteins that promote the sequestration of fatty acids within adipocytes in the form of triglycerides, thereby lowering exposure of skeletal muscle to the inhibitory effects of fatty acids.
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                Author and article information

                Contributors
                Journal
                Open Biol
                Open Biol
                RSOB
                royopenbio
                Open Biology
                The Royal Society
                2046-2441
                September 29, 2021
                September 2021
                : 11
                : 9
                : 210106
                Affiliations
                [ 1 ] Department of Nephrology, Affiliated Hospital of Jiangsu University, , 438 Jiefang Road, Zhenjiang 212001, Jiangsu, People's Republic of China
                [ 2 ] Department of Endocrinology, Affiliated Hospital of Jiangsu University, , 438 Jiefang Road, Zhenjiang 212001, Jiangsu, People's Republic of China
                Author notes
                [ † ]

                These authors contributed equally to this work.

                Author information
                http://orcid.org/0000-0003-3239-2080
                http://orcid.org/0000-0003-1806-9041
                http://orcid.org/0000-0003-0822-6066
                Article
                rsob210106
                10.1098/rsob.210106
                8478524
                34582711
                48ef3326-8a6f-4172-809f-6bd679e12006
                © 2021 The Authors.

                Published by the Royal Society under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/4.0/, which permits unrestricted use, provided the original author and source are credited.

                History
                : April 23, 2021
                : August 25, 2021
                Funding
                Funded by: High Caliber Medical Personnel Foundation of Jiangsu Province;
                Award ID: LGY2016053
                Funded by: Natural Science Foundation of Jiangsu Province, http://dx.doi.org/10.13039/501100004608;
                Award ID: BK20151331
                Award ID: BK2019222
                Funded by: Key Research and Development Projects of Social Development in Jiangsu Province, China;
                Award ID: BE2018692
                Funded by: 169-Phase V Science Research Project of Zhenjiang;
                Funded by: Scientific Research Projects of Jiangsu Health and Family Planning Commission;
                Award ID: Y2018109
                Funded by: Six Talent Peaks Project in Jiangsu Province, http://dx.doi.org/10.13039/501100010014;
                Award ID: 2015-WSN-006
                Funded by: National Natural Science Foundation of China, http://dx.doi.org/10.13039/501100001809;
                Award ID: 81570721
                Award ID: 81870548
                Categories
                15
                129
                Review
                Review Articles

                Life sciences
                angptl8,betatrophin,t2dm,glucose metabolism,lipid metabolism
                Life sciences
                angptl8, betatrophin, t2dm, glucose metabolism, lipid metabolism

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