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• W2148357813 abstract "HomeArteriosclerosis, Thrombosis, and Vascular BiologyVol. 31, No. 9The Complex Metabolic Mechanisms Relating Obesity to Hypertriglyceridemia Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBThe Complex Metabolic Mechanisms Relating Obesity to Hypertriglyceridemia Robert H. Eckel Robert H. EckelRobert H. Eckel From the Division of Endocrinology, Metabolism and Diabetes, and Cardiology, University of Colorado Anschutz Medical Campus, Aurora CO. Search for more papers by this author Originally published1 Sep 2011https://doi.org/10.1161/ATVBAHA.111.233049Arteriosclerosis, Thrombosis, and Vascular Biology. 2011;31:1946–1948The importance of hypertriglyceridemia as a cardiovascular disease risk factor continues to be a controversial topic,1 and patients with obesity frequently exhibit hypertriglyceridemia. In the Framingham Heart Study, the incidence of coronary heart disease was significantly greater with than without insulin resistance at either the lowest plasma high-density lipoprotein cholesterol values or the highest triglyceride values.2 The mechanism of hypertriglyceridemia in the setting of obesity has been linked to insulin resistance, wherein an increased flux of adipose tissue–derived free fatty acids (FFAs) gives rise to increased rates of hepatic triglyceride synthesis and secretion of very-low-density lipoprotein (VLDL) triglycerides (Figure).3,4 A recent report has also related increased FFA flux to the secretion of apolipoprotein CIII (apoCIII)-containing VLDL.4 Moreover, there is additional evidence that the hyperinsulinemia that ensues in the setting of insulin resistance is associated with increases in intrahepatic gene expression of genes of triglyceride biosynthesis, eg, sterol regulatory element-binding protein-1C.5 In the presence of increased intrahepatic triglycerides, nonalcoholic fatty liver disease or hypertriglyceridemia often occur, yet not all patients with obesity are insulin resistant.Download figureDownload PowerPointFigure. Insulin resistance is associated with an expanded adipose tissue mass. In this setting, many of the metabolic effects of insulin are reduced, including increases in basal lipolysis and less suppression of lipolysis by feeding and insulin. In addition, there is a reduction in the intrahepatic effects of insulin action that relate to apolipoprotein metabolism. Under physiological conditions, insulin suppresses apolipoprotein C-III (apo C-III) gene transcription and increases apolipoprotein B-100 (apo B-100) degradation, whereas in insulin-resistant states, both effects of insulin are reduced. However, the ability of insulin to increase sterol regulatory element-binding protein-1c gene transcription is preserved. Thus, with increased free fatty acid (FFA) flux and esterification to triglycerides (TG) and increased lipogenesis, hepatic steatosis frequently occurs. Moreover, in the presence of more TG, the increased availability of apo C-III and apo B-100 enhances the synthesis and secretion of very-low-density lipoprotein (VLDL). In addition, in the circulation the inhibitory effect of VLDL apo C-III on lipoprotein lipase (LPL) reduces the fractional catabolic rate of VLDL and contributes to the burden of the hypertriglyceridemia.See accompanying article on page 2144In the study by Taskinen et al published in the current issue of Arteriosclerosis, Thrombosis and Vascular Biology,6 both overproduction of large VLDL (VLDL1) and reduced VLDL1 fractional catabolic rate (FCR) were found to be associated with hypertriglyceridemia in obese subjects. A sophisticated multicompartmental model was used to simultaneously determine the kinetics of apoB and triglycerides in VLDL after a bolus injection of [(2)H(3)]leucine and [(2)H(5)]glycerol.7 Although the sample size was small, there were associations between large VLDL1 secretion and the amount of subcutaneous abdominal adipose tissue (measured by magnetic resonance imaging)+intrahepatic fat, and between VLDL1 FCR and plasma levels of apoCIII.The finding that <20% of the hypertriglyceridemia in these obese men was associated with increases in VLDL1 secretion but almost 50% related to impaired FCR is somewhat consistent with the literature. However, VLDL triglyceride overproduction is more emphasized as the pathophysiology of hypertriglyceridemia than defects in VLDL FCR.8,9 The association of plasma levels of apoCIII with reductions in VLDL1 FCR was of particular interest, noting the well-appreciated inhibitory effect of apoCIII on lipoprotein lipase (LPL).10 ApoCIII is a 79-amino-acid glycoprotein synthesized by the liver and intestines that is mostly associated with triglyceride-rich lipoproteins (VLDL and chylomicrons) and high-density lipoprotein, with rapid exchange of the apoprotein between these lipoprotein classes during lipolysis.11 Increased hepatic production of VLDL apoCIII is characteristic of subjects with higher body weights and insulin resistance and is strongly related to the plasma concentration and level of production of VLDL triglycerides.12,13 Because insulin is known to inhibit apoCIII gene transcription,14 overproduction of apoCIII may be a further manifestation of hepatic insulin resistance. Moreover, recent evidence indicates that once glucose intolerance develops, activation of apoCIII gene transcription by hyperglycemia could lead to worsening hypertriglyceridemia.15 Not to be dismissed is the role of insulin in increasing apoB degradation in the liver.16 Once insulin resistance occurs, this is another mechanism that could relate to the overproduction and secretion of VLDL in patients with obesity.The fact that the inverse relationship between VLDL1 FCR and apoCIII appeared to extend across the entire cohort suggests that a continuous relationship exists between apoCIII production and plasma triglycerides.6 However, not stated was whether or not levels of apoCIII also related to VLDL1 production or hepatic fat. There was, however, no evidence of any apoCIII variants in the study participants that have recently been linked to fatty liver.17 Although it is presumed that the effect on clearance of VLDL1 in the obese hypertriglyceridemic group was an inhibitory effect on LPL, only LPL mass was quantified. Because most of the LPL in plasma is inactive mass and there is no predictability of postheparin LPL activity by LPL activity in preheparin plasma,18 additional studies are needed to discern whether or not the presumed inhibitory effect of apoCIII on LPL as a contributor to the hypertriglyceridemia can be distinguished from simply a defect in FCR related to VLDL pool size.The debate continues as to the relative importance of increases in intraabdominal or visceral fat versus subcutaneous fat in hepatic FFA delivery. Although in this study the subcutaneous adipose tissue depot appeared to relate to VLDL1 secretion rate more than visceral adipose tissue, increases in lipolysis and fatty acid flux from the visceral depot seems more etiologic in explaining fatty liver and hypertriglyceridemia. Despite the direct link between the visceral depot and the liver, intraabdominal adipose tissue quantitatively remains a relatively minor contributor. In 1 study in obese men, splanchnic FFA levels ranged from <10% to almost 50%, with an increasing contribution as visceral adipose tissue volume increased.19 When obese subjects with nonalcoholic fatty liver disease were compared with those with normal levels of intrahepatic fat, the increased VLDL triglyceride secretion was primarily due to fatty acid sources other than the systemic circulation, ie, from visceral or intrahepatic sites.20Both obese groups appeared to be hyperinsulinemic, although the sample size limited the distinction between the nonobese fasting insulin of 5.7±0.8 mU/L in the nonobese normotriglyceridemic group from 10.0±1.9 mU/L in the obese normotriglyceridemic group.6 The fasting insulin of 12.9±1.7 mU/L in the hypertriglyceridemic obese group was clearly not different from that in the obese normotriglyceridemic group, as was the homeostasis model assessment of insulin resistance. Thus, these crude assessments of insulin sensitivity do not appear to be related to the mechanism of the hypertriglyceridemia. Despite the sample size and lack of robust tests of insulin action, some attempt to relate VLDL kinetics to fasting insulin and homeostasis model assessment of insulin resistance may have helped clarify whether a gradient or threshold relationship existed. Moreover, a euglycemic clamp with stepwise increments in the insulin infusion rate assessing both the effects of insulin on antilipolysis and FFA flux, in addition to hepatic and peripheral insulin resistance in glucose metabolism, would be informative.Overall, Taskinen et al6 appropriately stress a simplistic approach to identifying patients at high cardiometabolic risk by measuring waist circumference and fasting triglycerides, revisiting the hypertriglyceridemic waist, a concept developed by the Després group more than a decade ago.21 Defined as a waist circumference of ≥90 cm and a triglyceride level of ≥2.0 mmol/L in men and a waist circumference of ≥85 cm and a triglyceride level of ≥1.5 mmol/L in women, this easily quantified metric has been used to identify patients with added metabolic disturbances related to insulin resistance and higher risk for coronary heart disease.22,23 Finally, apoCIII remains a fascinating lipoprotein constituent that demands further characterization and epidemiology before its measurement is ready for prime time.AcknowledgmentsThe author thanks Dr Hong Wang for her assistance with the figure.DisclosuresNone.FootnotesCorrespondence to Robert H. Eckel, Division of Endocrinology, Metabolism and Diabetes, and Cardiology, University of Colorado Anschutz Medical Campus, Mail Stop 8106, 12801 East 17th Ave, Rm 7107, Research Complex 1, Aurora CO. E-mail robert.[email protected]eduReferences1. Goldberg IJ, Eckel RH, McPherson R. Triglycerides and heart disease: still a hypothesis?Arterioscler Thromb Vasc Biol. 2011; 31[Epub ahead of print]. LinkGoogle Scholar2. Robins SJ, Lyass A, Zachariah JP, Massaro JM, Vasan RS. Insulin resistance and the relationship of a dyslipidemia to coronary heart disease: the Framingham Heart Study. Arterioscler Thromb Vasc Biol. 2011; 31: 1208– 1214. LinkGoogle Scholar3. Yki-Jarvinen H, Taskinen MR. Interrelationships among insulin's antilipolytic and glucoregulatory effects and plasma triglycerides in nondiabetic and diabetic patients with endogenous hypertriglyceridemia. Diabetes. 1988; 37: 1271– 1278. CrossrefMedlineGoogle Scholar4. Pavlic M, Valero R, Duez H, Xiao C, Szeto L, Patterson BW, Lewis GF. Triglyceride-rich lipoprotein-associated apolipoprotein C-III production is stimulated by plasma free fatty acids in humans. Arterioscler Thromb Vasc Biol. 2008; 28: 1660– 1665. LinkGoogle Scholar5. Shimomura I, Bashmakov Y, Ikemoto S, Horton JD, Brown MS, Goldstein JL. Insulin selectively increases SREBP-1c mRNA in the livers of rats with streptozotocin-induced diabetes. Proc Natl Acad Sci U S A1999; 96: 13656– 13661. CrossrefMedlineGoogle Scholar6. Taskinen M-R, Adiels M, Westerbacka J, Söderlund S, Kahri J, Lundbom N, Lundbom J, Hakkarainen A, Olofsson S-O, Orho-Melander M, Boren J. Dual metabolic defects are required to produce hypertriglyceridemia in obese subjects. Arterioscler Thromb Vasc Biol.2011; 31: 2144– 2150. LinkGoogle Scholar7. Adiels M, Packard C, Caslake MJ, Stewart P, Soro A, Westerbacka J, Wennberg B, Olofsson SO, Taskinen MR, Boren J. A new combined multicompartmental model for apolipoprotein B-100 and triglyceride metabolism in VLDL subfractions. J Lipid Res. 2005; 46: 58– 67. CrossrefMedlineGoogle Scholar8. Adiels M, Olofsson SO, Taskinen MR, Boren J. Overproduction of very low-density lipoproteins is the hallmark of the dyslipidemia in the metabolic syndrome. Arterioscler Thromb Vasc Biol. 2008; 28: 1225– 1236. LinkGoogle Scholar9. Ginsberg HN, Zhang YL, Hernandez-Ono A. Regulation of plasma triglycerides in insulin resistance and diabetes. Arch Med Res. 2005; 36: 232– 240. CrossrefMedlineGoogle Scholar10. Ginsberg HN, Le NA, Goldberg IJ, Gibson JC, Rubinstein A, Wang-Iverson P, Norum R, Brown WV. Apolipoprotein B metabolism in subjects with deficiency of apolipoproteins CIII and AI: evidence that apolipoprotein CIII inhibits catabolism of triglyceride-rich lipoproteins by lipoprotein lipase in vivo. J Clin Invest. 1986; 78: 1287– 1295. CrossrefMedlineGoogle Scholar11. Ooi EM, Barrett PH, Chan DC, Watts GF. Apolipoprotein C-III: understanding an emerging cardiovascular risk factor. Clin Sci (Lond). 2008; 114: 611– 624. CrossrefMedlineGoogle Scholar12. Cohn JS, Patterson BW, Uffelman KD, Davignon J, Steiner G. Rate of production of plasma and very-low-density lipoprotein (VLDL) apolipoprotein C-III is strongly related to the concentration and level of production of VLDL triglyceride in male subjects with different body weights and levels of insulin sensitivity. J Clin Endocrinol Metab. 2004; 89: 3949– 3955. CrossrefMedlineGoogle Scholar13. Cohn JS, Tremblay M, Batal R, Jacques H, Rodriguez C, Steiner G, Mamer O, Davignon J. Increased apoC-III production is a characteristic feature of patients with hypertriglyceridemia. Atherosclerosis. 2004; 177: 137– 145. CrossrefMedlineGoogle Scholar14. Altomonte J, Cong L, Harbaran S, Richter A, Xu J, Meseck M, Dong HH. Foxo1 mediates insulin action on apoC-III and triglyceride metabolism. J Clin Invest. 2004; 114: 1493– 1503. CrossrefMedlineGoogle Scholar15. Caron S, Verrijken A, Mertens I, Samanez CH, Mautino G, Haas JT, Duran-Sandoval D, Prawitt J, Francque S, Vallez E, Muhr-Tailleux A, Berard I, Kuipers F, Kuivenhoven JA, Biddinger SB, Taskinen MR, Van GL, Staels B. Transcriptional activation of apolipoprotein CIII expression by glucose may contribute to diabetic dyslipidemia. Arterioscler Thromb Vasc Biol. 2011; 31: 513– 519. LinkGoogle Scholar16. Sparks JD, Sparks CE. Insulin modulation of hepatic synthesis and secretion of apolipoprotein B by rat hepatocytes. J Biol Chem. 1990; 265: 8854– 8862. CrossrefMedlineGoogle Scholar17. Petersen KF, Dufour S, Hariri A, Nelson-Williams C, Foo JN, Zhang XM, Dziura J, Lifton RP, Shulman GI. Apolipoprotein C3 gene variants in nonalcoholic fatty liver disease. N Engl J Med. 2010; 362: 1082– 1089. CrossrefMedlineGoogle Scholar18. Eckel RH, Goldberg IJ, Steiner L, Yost TJ, Paterniti JR. Plasma lipolytic activity: relationship to postheparin lipolytic activity and evidence for metabolic regulation. Diabetes. 1988; 37: 610– 615. CrossrefMedlineGoogle Scholar19. Nielsen S, Guo Z, Johnson CM, Hensrud DD, Jensen MD. Splanchnic lipolysis in human obesity. J Clin Invest. 2004; 113: 1582– 1588. CrossrefMedlineGoogle Scholar20. Fabbrini E, Mohammed BS, Magkos F, Korenblat KM, Patterson BW, Klein S. Alterations in adipose tissue and hepatic lipid kinetics in obese men and women with nonalcoholic fatty liver disease. Gastroenterology. 2008; 134: 424– 431. CrossrefMedlineGoogle Scholar21. Lemieux I, Pascot A, Couillard C, Lamarche B, Tchernof A, Almeras N, Bergeron J, Gaudet D, Tremblay G, Prud'homme D, Nadeau A, Després JP. Hypertriglyceridemic waist: A marker of the atherogenic metabolic triad (hyperinsulinemia; hyperapolipoprotein B; small, dense LDL) in men?Circulation. 2000; 102: 179– 184. LinkGoogle Scholar22. de Graaf FR, Schuijf JD, Scholte AJ, Djaberi R, van Velzen JE, Roos CJ, Kroft LJ, de RA, van der Wall EE, Wouter JJ, Després JP, Bax JJ. Usefulness of hypertriglyceridemic waist phenotype in type 2 diabetes mellitus to predict the presence of coronary artery disease as assessed by computed tomographic coronary angiography. Am J Cardiol. 2010; 106: 1747– 1753. CrossrefMedlineGoogle Scholar23. St-Pierre J, Lemieux I, Vohl MC, Perron P, Tremblay G, Després JP, Gaudet D. Contribution of abdominal obesity and hypertriglyceridemia to impaired fasting glucose and coronary artery disease. Am J Cardiol. 2002; 90: 15– 18. CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Gaba P, Bhatt D, Mason R, Miller M, Verma S, Steg P and Boden W (2022) Benefits of icosapent ethyl for enhancing residual cardiovascular risk reduction: A review of key findings from REDUCE-IT, Journal of Clinical Lipidology, 10.1016/j.jacl.2022.05.067, Online publication date: 1-Jun-2022. Wu J, Liu J and Wang D (2020) Effects of body condition on the insulin resistance, lipid metabolism and oxidative stress of lactating dairy cows, Lipids in Health and Disease, 10.1186/s12944-020-01233-7, 19:1, Online publication date: 1-Dec-2020. Shin K, Hwang I, Choe S, Park J, Ji Y, Kim J, Lee G, Choi S, Ching J, Kovalik J and Kim J (2017) Macrophage VLDLR mediates obesity-induced insulin resistance with adipose tissue inflammation, Nature Communications, 10.1038/s41467-017-01232-w, 8:1, Online publication date: 1-Dec-2017. Welty F, Alfaddagh A and Elajami T (2016) Targeting inflammation in metabolic syndrome, Translational Research, 10.1016/j.trsl.2015.06.017, 167:1, (257-280), Online publication date: 1-Jan-2016. 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