Lipoprotein effects of incretin analogs and dipeptidyl peptidase 4 inhibitors

References

• Ng M, Fleming T, Robinson M et al. Global, regional, and national prevalence of overweight and obesity in children and adults during 1980–2013: a systematic analysis for the Global Burden of Disease Study 2013. Lancet 384, 766–781 (2014).
   Google Scholar
• Krauss RM. Lipids and lipoproteins in patients with Type 2 diabetes. Diabetes Care 27, 1496–1504 (2004).
   Google Scholar
• Ginsberg HN. Insulin resistance and cardiovascular disease. J. Clin. Invest. 106(4), 453–458 (2000).
   Google Scholar
• Bansal S, Buring JE, Rifai N, Mora S, Sacks FM, Ridker PM. Fasting compared with nonfasting triglycerides and risk of cardiovascular events in women. JAMA 298(3), 309–316 (2007).
   Google Scholar
• Nordestgaard BG, Benn M, Schnohr P, Tybjaerg-Hansen A. Nonfasting triglycerides and risk of myocardial infarction, ischemic heart disease, and death in men and women. JAMA 298(3), 299–308 (2007).
   Google Scholar
• Pang J, Chan DC, Barrett PHR, Watts GF. Postprandial dyslipidaemia and diabetes: mechanistic and therapeutic aspects. Curr. Opin. Lipidol. 23(4), 303–309 (2012).
   Google Scholar
• Zilversmit DB. Atherogenesis: a postprandial phenomenon. Circulation 60(3), 473–485 (1979).
   Google Scholar
• Imke C, Rodriguez BL, Grove JS et al. Are remnant-like particles independent predictors of coronary heart disease incidence? The Honolulu Heart study. Arterioscler. Thromb. Vasc. Biol. 25(8), 1718–1722 (2005).
   Google Scholar
• Varbo A, Benn M, Tybjærg-Hansen A, Nordestgaard BG. Elevated remnant cholesterol causes both low-grade inflammation and ischemic heart disease, whereas elevated low-density lipoprotein cholesterol causes ischemic heart disease without inflammation. Circulation 128(12), 1298–1309 (2013).
   Google Scholar
• Gerstein HC, Miller ME, Genuth S et al. Long-term effects of intensive glucose lowering on cardiovascular outcomes. N. Engl. J. Med. 364(9), 818–828 (2011).
   Google Scholar
• Rivellese AA, De Natale C, Di Marino L et al. Exogenous and endogenous postprandial lipid abnormalities in Type 2 diabetic patients with optimal blood glucose control and optimal fasting triglyceride levels. J. Clin. Endocrinol. Metab. 89(5), 2153–2159 (2004).
   Google Scholar
• Rivellese AA. Exogenous and endogenous postprandial lipid abnormalities in Type 2 diabetic patients with optimal blood glucose control and optimal fasting triglyceride levels. J. Clin. Endocrinol. Metab. 89(5), 2153–2159 (2004).
   Google Scholar
• Masuda D, Sakai N, Sugimoto T et al. Fasting serum apolipoprotein B-48 can be a marker of postprandial hyperlipidemia. J. Atheroscler. Thromb. 18(12), 1062–1070 (2011).
   Google Scholar
• Hogue J-C, Lamarche B, Tremblay AJ, Bergeron J, Gagné C, Couture P. Evidence of increased secretion of apolipoprotein B-48-containing lipoproteins in subjects with Type 2 diabetes. J. Lipid Res. 48(6), 1336–1342 (2007).
   Google Scholar
• Schaefer EJ, McNamara JR, Shah PK et al. Elevated remnant-like particle cholesterol and triglyceride levels in diabetic men and women in the Framingham Offspring Study. Diabetes Care 25(6), 989–994 (2002).
   Google Scholar
• Chan DC, Wong ATY, Yamashita S, Watts GF. Apolipoprotein B-48 as a determinant of endothelial function in obese subjects with Type 2 diabetes mellitus: effect of fenofibrate treatment. Atherosclerosis 221(2), 484–409 (2012).
   Google Scholar
• Lapice E, Cipriano P, Patti L, Romano G, Vaccaro O, Rivellese AA. Fasting apolipoprotein B48 is associated with asymptomatic peripheral arterial disease in Type 2 diabetic subjects: a case–control study. Atherosclerosis 223(2), 504–506 (2012).
   Google Scholar
• Masuda D, Sugimoto T, Tsujii K-I et al. Correlation of fasting serum apolipoprotein B-48 with coronary artery disease prevalence. Eur. J. Clin. Invest. 42(9), 992–999 (2012).
   Google Scholar
• Nakatani K, Sugimoto T, Masuda D et al. Serum apolipoprotein B-48 levels are correlated with carotid intima-media thickness in subjects with normal serum triglyceride levels. Atherosclerosis 218(1), 226–232 (2011).
   Google Scholar
• Alipour A, Valdivielso P, Elte JWF et al. Exploring the value of apoB48 as a marker for atherosclerosis in clinical practice. Eur. J. Clin. Invest. 42(7), 702–708 (2012).
   Google Scholar
• Fisher EA, Feig JE, Hewing B, Hazen SL, Smith JD. High-density lipoprotein function, dysfunction, and reverse cholesterol transport. Arterioscler. Thromb. Vasc. Biol. 32(12), 2813–2820 (2012).
   Google Scholar
• D’Alessio DA, Vogel R, Prigeon R et al. Elimination of the action of glucagon-like peptide 1 causes an impairment of glucose tolerance after nutrient ingestion by healthy baboons. J. Clin. Invest. 97(1), 133–138 (1996).
   Google Scholar
• Ayala JE, Bracy DP, James FD, Julien BM, Wasserman DH, Drucker DJ. The glucagon-like peptide-1 receptor regulates endogenous glucose production and muscle glucose uptake independent of its incretin action. Endocrinology 150(3), 1155–1164 (2009).
   Google Scholar
• Ussher JR, Drucker DJ. Cardiovascular biology of the incretin system. Endocr. Rev. 33(2), 187–215 (2012).
   Google Scholar
• Dupre J, Ross SA, Watson D, Brown JC. Stimulation of insulin secretion by gastric inhibitory polypeptide in man. J. Clin. Endocrinol. Metab. 37(5), 826–828 (1973).
   Google Scholar
• Nauck MA. Unraveling the science of incretin biology. Am. J. Med. 122(6 Suppl.), S3–S10 (2009).
   Google Scholar
• Kreymann B, Williams G, Ghatei MA, Bloom SR. Glucagon-like peptide-1 7–36: a physiological incretin in man. Lancet 2(8571), 1300–1304 (1987).
   Google Scholar
• Knauf C, Cani PD, Perrin C et al. Brain glucagon-like peptide-1 increases insulin secretion and muscle insulin resistance to favor hepatic glycogen storage. J. Clin. Invest. 115(12), 3554–3563 (2005).
   Google Scholar
• D’Alessio DA, Sandoval DA, Seeley RJ. New ways in which GLP-1 can regulate glucose homeostasis. J. Clin. Invest. 115(12), 3406–3408 (2005).
   Google Scholar
• Sisley S, Gutierrez-Aguilar R, Scott M, D’Alessio DA, Sandoval DA, Seeley RJ. Neuronal GLP1R mediates liraglutide’s anorectic but not glucose-lowering effect. J. Clin. Invest. 124(6), 2456–2463 (2014).
   Google Scholar
• Qin X, Shen H, Liu M, Yang Q. GLP-1 reduces intestinal lymph flow, triglyceride absorption, and apolipoprotein production in rats. Am. J. Physiol. Gastrointest. Liver Physiol. 288(5), G943–G949 (2005).
   Google Scholar
• Meier JJ, Gethmann A, Götze O et al. Glucagon-like peptide 1 abolishes the postprandial rise in triglyceride concentrations and lowers levels of non-esterified fatty acids in humans. Diabetologia 49(3), 452–458 (2006).
   Google Scholar
• Vella A, Bock G, Giesler PD et al. The effect of dipeptidyl peptidase-4 inhibition on gastric volume, satiation and enteroendocrine secretion in Type 2 diabetes: a double-blind, placebo-controlled crossover study. Clin. Endocrinol. 69(5), 737–744 (2008).
   Google Scholar
• Hsieh J, Longuet C, Baker CL et al. The glucagon-like peptide 1 receptor is essential for postprandial lipoprotein synthesis and secretion in hamsters and mice. Diabetologia 53, 552–561 (2010).
   Google Scholar
• Lee Y-S, Shin S, Shigihara T et al. Glucagon-like peptide-1 gene therapy in obese diabetic mice results in long-term cure of diabetes by improving insulin sensitivity and reducing hepatic gluconeogenesis. Diabetes 56(6), 1671–1679 (2007).
   Google Scholar
• Svegliati-Baroni G, Saccomanno S, Rychlicki C et al. Glucagon-like peptide-1 receptor activation stimulates hepatic lipid oxidation and restores hepatic signalling alteration induced by a high-fat diet in nonalcoholic steatohepatitis. Liver Int. 31(9), 1285–1297 (2011).
   Google Scholar
• Parlevliet ET, Wang Y, Geerling JJ et al. GLP-1 receptor activation inhibits VLDL production and reverses hepatic steatosis by decreasing hepatic lipogenesis in high-fat-fed APOE*3-Leiden mice. PLoS ONE 7(11), e49152 (2012).
   Google Scholar
• Panjwani N, Mulvihill EE, Longuet C et al. GLP-1 receptor activation indirectly reduces hepatic lipid accumulation but does not attenuate development of atherosclerosis in diabetic male ApoE(-/-) mice. Endocrinology 154(1), 127–139 (2013).
   Google Scholar
• Shirazi R, Palsdottir V, Collander J et al. Glucagon-like peptide 1 receptor induced suppression of food intake, and body weight is mediated by central IL-1 and IL-6. Proc. Natl Acad. Sci. USA 110, 16199–16204 (2013).
   Google Scholar
• Schwartz EA, Koska J, Mullin MP, Syoufi I, Schwenke DC, Reaven PD. Exenatide suppresses postprandial elevations in lipids and lipoproteins in individuals with impaired glucose tolerance and recent onset Type 2 diabetes mellitus. Atherosclerosis 212(1), 217–222 (2010).
   Google Scholar
• Xiao C, Bandsma RHJ, Dash S, Szeto L, Lewis GF. Exenatide, a glucagon-like peptide-1 receptor agonist, acutely inhibits intestinal lipoprotein production in healthy humans. Arterioscler. Thromb. Vasc. Biol. 32(6), 1513–1519 (2012).
   Google Scholar
• Van Bloemendaal L, IJzerman RG, Ten Kulve JS et al. GLP-1 receptor activation modulates appetite- and reward-related brain areas in humans. Diabetes 63 (12), 4186–96 (2014). www.ncbi.nlm.nih.gov
   Google Scholar
• Matikainen N, Mänttäri S, Schweizer A et al. Vildagliptin therapy reduces postprandial intestinal triglyceride-rich lipoprotein particles in patients with Type 2 diabetes. Diabetologia 49(9), 2049–2057 (2006).
   Google Scholar
• Noda Y, Miyoshi T, Oe H et al. Alogliptin ameliorates postprandial lipemia and postprandial endothelial dysfunction in non-diabetic subjects: a preliminary report. Cardiovasc. Diabetol. 12(1), 8 (2013).
   Google Scholar
• Tremblay AJ, Lamarche B, Deacon CF, Weisnagel SJ, Couture P. Effect of sitagliptin therapy on postprandial lipoprotein levels in patients with Type 2 diabetes. Diabetes. Obes. Metab. 13(4), 366–373 (2011).
   Google Scholar
• Xiao C, Dash S, Morgantini C, Patterson BW, Lewis GF. Sitagliptin, a DPP-4 inhibitor, acutely inhibits intestinal lipoprotein particle secretion in healthy humans. Diabetes 63(7), 2394–2401 (2014).
   Google Scholar
• Bobik A. Apolipoprotein CIII and atherosclerosis: beyond effects on lipid metabolism. Circulation 118(7), 702–704 (2008).
   Google Scholar
• Azuma K, Radikova Z, Mancino J et al. Measurements of islet function and glucose metabolism with the dipeptidyl peptidase 4 inhibitor vildagliptin in patients with Type 2 diabetes. J. Clin. Endocrinol. Metab. 93(2), 459–464 (2008).
   Google Scholar
• Boschmann M, Engeli S, Dobberstein K et al. Dipeptidylpeptidase-IV inhibition augments postprandial lipid mobilization and oxidation in Type 2 diabetic patients. J. Clin. Endocrinol. Metab. 94(3), 846–852 (2009).
   Google Scholar
• Xiao C, Dash S, Morgantini C, Lewis GF. New and emerging regulators of intestinal lipoprotein secretion. Atherosclerosis 233(2), 608–615 (2014).
   Google Scholar
• Hsieh J, Longuet C, Maida A et al. Glucagon-like peptide-2 increases intestinal lipid absorption and chylomicron production via CD36. Gastroenterology 137(3), 997–1005, 1005.e1–e4 (2009).
   Google Scholar
• Meier JJ, Nauck MA, Pott A et al. Glucagon-like peptide 2 stimulates glucagon secretion, enhances lipid absorption, and inhibits gastric acid secretion in humans. Gastroenterology 130(1), 44–54 (2006).
   Google Scholar
• Hein GJ, Baker C, Hsieh J, Farr S, Adeli K. GLP-1 and GLP-2 as yin and yang of intestinal lipoprotein production: evidence for predominance of GLP-2-stimulated postprandial lipemia in normal and insulin-resistant states. Diabetes 62(2), 373–381 (2013).
   Google Scholar
• Finan B, Ma T, Ottaway N et al. Unimolecular dual incretins maximize metabolic benefits in rodents, monkeys, and humans. Sci. Transl. Med. 5(209), 209ra151 (2013).
   Google Scholar