Postprandial hyperglycemia and postprandial hypertriglyceridemia in type 2 diabetes

Toru Hiyoshi, Mutsunori Fujiwara, Zemin Yao

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Journal of Biomedical Research ›› 2019, Vol. 33 ›› Issue (1) : 1-16. DOI: 10.7555/JBR.31.20160164
Review Article
Review Article

Postprandial hyperglycemia and postprandial hypertriglyceridemia in type 2 diabetes

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Abstract

Postprandial glucose level is an independent risk factor for cardiovascular disease that exerts effects greater than glucose levels at fasting state, whereas increase in serum triglyceride level, under both fasting and postprandial conditions, contributes to the development of arteriosclerosis. Insulin resistance is a prevailing cause of abnormalities in postabsorptive excursion of blood glucose and postprandial lipid profile. Excess fat deposition renders a vicious cycle of hyperglycemia and hypertriglyceridemia in the postprandial state, and both of which are contributors to atherosclerotic change of vessels especially in patients with type 2 diabetes mellitus. Several therapeutic approaches for ameliorating each of these abnormalities have been attempted, including various antidiabetic agents or new compounds targeting lipid metabolism.

Keywords

postprandial hyperglycemia / postprandial hypertriglyceridemia / Type 2 diabetes mellitus / atherosclerosis

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Toru Hiyoshi, Mutsunori Fujiwara, Zemin Yao. Postprandial hyperglycemia and postprandial hypertriglyceridemia in type 2 diabetes. Journal of Biomedical Research, 2019, 33(1): 1‒16 https://doi.org/10.7555/JBR.31.20160164

References

[1]
Group TDS, and the The DECODE Study Group. Group on behalf of the EDE. Is the current definition for diabetes relevant to mortality risk from all causes and cardiovascular and noncardiovascular diseases[J]? Diabetes Care, 2003, 26(3): 688–696
CrossRef Google scholar
[2]
Levitan EB, Song Y, Ford ES, Is nondiabetic hyperglycemia a risk factor for cardiovascular disease[J]? Arch Intern Med, 2004, 164(19): 2147–2155
CrossRef Google scholar
[3]
DECODE Study Group, and the European Diabetes Epidemiology Group. Glucose tolerance and cardiovascular mortality: comparison of fasting and 2-hour diagnostic criteria[J]. Arch Intern Med, 2001, 161(3): 397–405
CrossRef Google scholar
[4]
Sone H, Tanaka S, Tanaka S, Serum level of triglycerides is a potent risk factor comparable to LDL cholesterol for coronary heart disease in Japanese patients with type 2 diabetes: Subanalysis of the Japan Diabetes Complications Study (JDCS)[J]. J Clin Endocrinol Metab, 2011, 96(11): 3448–3456
CrossRef Google scholar
[5]
Nakamura H, Arakawa K, Itakura H, Primary prevention of cardiovascular disease with pravastatin in Japan (MEGA Study): a prospective randomised controlled trial[J]. Lancet, 2006, 368(9452): 1155–1163
CrossRef Google scholar
[6]
Iso H, Imano H, Yamagishi K, Fasting and non-fasting triglycerides and risk of ischemic cardiovascular disease in Japanese men and women: the Circulatory Risk in Communities Study (CIRCS)[J]. Atherosclerosis, 2014, 237(1): 361–368
CrossRef Google scholar
[7]
Zilversmit DB. Atherogenesis: a postprandial phenomenon[J]. Circulation, 1979, 60(3): 473–485
CrossRef Google scholar
[8]
Monnier L, Colette C, Dunseath GJ, The loss of postprandial glycemic control precedes stepwise deterioration of fasting with worsening diabetes[J]. Diabetes Care, 2007, 30(2): 263–269
CrossRef Google scholar
[9]
International Diabetes Federation GUIDELINE FOR MANAGEMENT OF POSTMEAL GLUCOSE IN DIABETES[J]. 2011, http://www.idf.org/2011-guideline-management-postmeal-glucose-diabetes.
[10]
Kodama K, Tojjar D, Yamada S, Ethnic differences in the relationship between insulin sensitivity and insulin response: A systematic review and meta-analysis[J]. Diabetes Care, 2013, 36(6): 1789–1796
CrossRef Google scholar
[11]
Wu L, Parhofer KG. Diabetic dyslipidemia[J]. Metabolism, 2014, 63(12): 1469–1479
CrossRef Google scholar
[12]
Node K, Inoue T. Postprandial hyperglycemia as an etiological factor in vascular failure[J]. Cardiovasc Diabetol, 2009, 8(1): 23
CrossRef Google scholar
[13]
Tomkin GH, Owens D. Dyslipidaemia of diabetes and the intestine[J]. World J Diabetes, 2015, 6(7): 970–977
CrossRef Google scholar
[14]
Ceriello A, Genovese S. Atherogenicity of postprandial hyperglycemia and lipotoxicity[J]. Rev Endocr Metab Disord, 2016, 17(1): 111–116
CrossRef Google scholar
[15]
Rizza RA. Pathogenesis of fasting and postprandial hyperglycemia in type 2 diabetes: Implications for therapy[J]. Diabetes, 2010, 59(11): 2697–2707
CrossRef Google scholar
[16]
Ginsberg HN. Review: Efficacy and mechanisms of action of statins in the treatment of diabetic dyslipidemia[J]. J Clin Endocrinol Metab, 2006, 91(2): 383–392
CrossRef Google scholar
[17]
Bonora E, Corrao G, Bagnardi V, Prevalence and correlates of post-prandial hyperglycaemia in a large sample of patients with type 2 diabetes mellitus[J]. Diabetologia, 2006, 49(5): 846–854
CrossRef Google scholar
[18]
Pratley RE, Weyer C. The role of impaired early insulin secretion in the pathogenesis of Type II diabetes mellitus[J]. Diabetologia, 2001, 44(8): 929–945
CrossRef Google scholar
[19]
Fineman MS, Koda JE, Shen LZ, The human amylin analog, pramlintide, corrects postprandial hyperglucagonemia in patients with type 1 diabetes[J]. Metabolism, 2002, 51(5): 636–641
CrossRef Google scholar
[20]
Koda JE, Fineman M, Rink TJ, Amylin concentrations and glucose control[J]. Lancet, 1992, 339(8802): 1179–1180
CrossRef Google scholar
[21]
Holst JJ, Gromada J. Role of incretin hormones in the regulation of insulin secretion in diabetic and nondiabetic humans[J]. Am J Physiol Endocrinol Metab, 2004, 287(2): E199–E206
CrossRef Google scholar
[22]
Toft-Nielsen MB, Damholt MB, Madsbad S, Determinants of the impaired secretion of glucagon- like peptide-1 in type 2 diabetic patients[J]. J Clin Endocrinol Metab, 2001, 86(8): 3717–3723
CrossRef Google scholar
[23]
Meier JJ, Nauck MA. Is the diminished incretin effect in type 2 diabetes just an epi-phenomenon of impaired beta-cell function[J]? Diabetes, 2010, 59(5): 1117–1125
CrossRef Google scholar
[24]
Little TJ, Pilichiewicz AN, Russo A, Effects of intravenous glucagon-like peptide-1 on gastric emptying and intragastric distribution in healthy subjects: relationships with postprandial glycemic and insulinemic responses[J]. J Clin Endocrinol Metab, 2006, 91(5): 1916–1923
CrossRef Google scholar
[25]
Drucker DJ, Nauck MA. The incretin system: glucagon-like peptide-1 receptor agonists and dipeptidyl peptidase-4 inhibitors in type 2 diabetes[J]. Lancet, 2006, 368(9548): 1696–1705
CrossRef Google scholar
[26]
Haller H, Lindschau C, Quass P, Differentiation of vascular smooth muscle cells and the regulation of protein kinase C-alpha[J]. Circ Res, 1995, 76(1): 21–29
CrossRef Google scholar
[27]
Goetze S, Xi XP, Kawano Y, TNF-alpha-induced migration of vascular smooth muscle cells is MAPK dependent[J]. Hypertension, 1999, 33(1): 183–189
CrossRef Google scholar
[28]
Anderson TJ. Assessment and treatment of endothelial dysfunction in humans[J]. J Am Coll Cardiol, 1999, 34(3): 631–638
CrossRef Google scholar
[29]
Giacco F, Brownlee M. Oxidative stress and diabetic complications[J]. Circ Res, 2010, 107(9): 1058–1070
CrossRef Google scholar
[30]
Wu J, Xia S, Kalionis B, The role of oxidative stress and inflammation in cardiovascular aging[J]. BioMed Res Int, 2014(2): 615312.
[31]
Harrison DG. Cellular and molecular mechanisms of endothelial cell dysfunction[J]. J Clin Invest, 1997, 100(9): 2153–2157
CrossRef Google scholar
[32]
Monnier L, Mas E, Ginet C, Activation of oxidative stress by acute glucose fluctuations compared with sustained chronic hyperglycemia in patients with type 2 diabetes[J]. JAMA, 2006, 295(14): 1681–1687
CrossRef Google scholar
[33]
Monnier L, Lapinski H, Colette C. Contributions of fasting and postprandial plasma glucose increments to the overall diurnal hyperglycemia of type 2 diabetic patients: Variations with increasing levels of HbA1c[J]. Diabetes Care, 2003, 26(3): 881–885
CrossRef Google scholar
[34]
Ceriello A, Falleti E, Motz E, Hyperglycemia-induced circulating ICAM-1 increase in diabetes mellitus: the possible role of oxidative stress[J]. Horm Metab Res, 1998, 30(3): 146–149
CrossRef Google scholar
[35]
Shuto Y, Asai A, Nagao M, Repetitive glucose spikes accelerate atherosclerotic lesion formation in C57BL/6 mice[J]. PLoS One, 2015, 10(8): e0136840
CrossRef Google scholar
[36]
Mandosi E, Giannetta E, Filardi T, Endothelial dysfunction markers as a therapeutic target for Sildenafil treatment and effects on metabolic control in type 2 diabetes[J]. Expert Opin Ther Targets, 2015, 19(12): 1617–1622
CrossRef Google scholar
[37]
Firth RG, Bell PM, Marsh HM, Postprandial hyperglycemia in patients with noninsulin-dependent diabetes mellitus. Role of hepatic and extrahepatic tissues[J]. J Clin Invest, 1986, 77(5): 1525–1532
CrossRef Google scholar
[38]
Unger RH, Orci L. The essential role of glucagon in the pathogenesis of diabetes mellitus[J]. Lancet, 1975, 1(7897): 14–16
CrossRef Google scholar
[39]
Kawamori D, Kurpad AJ, Hu J, Insulin signaling in alpha cells modulates glucagon secretion in vivo[J]. Cell Metab, 2009, 9(4): 350–361
CrossRef Google scholar
[40]
Ahren B. Beta- and alpha-cell dysfunction in subjects developing impaired glucose tolerance: outcome of a 12-year prospective study in postmenopausal Caucasian women[J]. Diabetes, 2009, 58(3): 726–731
CrossRef Google scholar
[41]
Henquin JC, Rahier J. Pancreatic alpha cell mass in European subjects with type 2 diabetes[J]. Diabetologia, 2011, 54(7): 1720–1725
CrossRef Google scholar
[42]
Kubota N, Kubota T, Itoh S, Dynamic functional relay between insulin receptor substrate 1 and 2 in hepatic insulin signaling during fasting and feeding[J]. Cell Metab, 2008, 8(1): 49–64
CrossRef Google scholar
[43]
Kubota T, Kubota N, Kumagai H, Impaired insulin signaling in endothelial cells reduces insulin-induced glucose uptake by skeletal muscle[J]. Cell Metab, 2011, 13(3): 294–307
CrossRef Google scholar
[44]
The Diabetes Control and Complications Trial Research Group. The Effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus[J]. N Engl J Med, 1993, 329(14): 977–986
CrossRef Google scholar
[45]
UK Prospective Diabetes Study (UKPDS) Group. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33)[J]. Lancet, 1998, 352(9131): 837–853
CrossRef Google scholar
[46]
Ohkubo Y, Kishikawa H, Araki E, Intensive insulin therapy prevents the progression of diabetic microvascular complications in Japanese patients with non-insulin-dependent diabetes mellitus: a randomized prospective 6-year study[J]. Diabetes Res Clin Pract, 1995, 28(2): 103–117
CrossRef Google scholar
[47]
Turner RC, Millns H, Holman RR, Risk factors for coronary artery disease in non-insulin dependent diabetes mellitus: United Kingdom prospective diabetes study (UKPDS: 23)[J]. BMJ, 1998, 316(7134): 823–828
CrossRef Google scholar
[48]
Tominaga M, Eguchi H, Manaka H, Impaired glucose tolerance is a risk factor for cardiovascular disease, but not impaired fasting glucose. The Funagata Diabetes Study[J]. Diabetes Care, 1999, 22(6): 920–924
CrossRef Google scholar
[49]
Nakagami T, Qiao Q, Tuomilehto J, Screen-detected diabetes, hypertension and hypercholesterolemia as predictors of cardiovascular mortality in five populations of Asian origin: the DECODA study[J]. Eur J Cardiovasc Prev Rehabil, 2006, 13(4): 555–561
CrossRef Google scholar
[50]
Hanefeld M, Cagatay M, Petrowitsch T, Acarbose reduces the risk for myocardial infarction in type 2 diabetic patients: meta-analysis of seven long-term studies[J]. Eur Heart J, 2004, 25(1): 10–16
CrossRef Google scholar
[51]
Ceriello A, Esposito K, Piconi L, Oscillating glucose is more deleterious to endothelial function and oxidative stress than mean glucose in normal and type 2 diabetic patients[J]. Diabetes, 2008, 57(5): 1349–1354
CrossRef Google scholar
[52]
de Vries M, Klop B, Castro Cabezas M. The use of the non-fasting lipid profile for lipid-lowering therapy in clinical practice- point of view[J]. Atherosclerosis, 2014, 234(2): 473–475
CrossRef Google scholar
[53]
Rosenson RS, Davidson MH, Hirsh BJ, Genetics and causality of triglyceride-rich lipoproteins in atherosclerotic cardiovascular disease[J]. J Am Coll Cardiol, 2014, 64(23): 2525–2540
CrossRef Google scholar
[54]
White KT, Moorthy MV, Akinkuolie AO, Identifying an optimal cutpoint for the diagnosis of hypertriglyceridemia in the nonfasting state[J]. Clin Chem, 2015, 61(9): 1156–1163
CrossRef Google scholar
[55]
Langsted A, Nordestgaard BG. Nonfasting Lipid Profiles: The Way of the Future[J]. Clin Chem, 2015, 61(9): 1123–1125
CrossRef Google scholar
[56]
Syvänne M, Taskinen MR. Lipids and lipoproteins as coronary risk factors in non-insulin-dependent diabetes mellitus[J]. Lancet, 1997, 350(Suppl): SI20–SI23
CrossRef Google scholar
[57]
Adiels M, Boren J, Caslake MJ, Overproduction of VLDL1 driven by hyperglycemia is a dominant feature of diabetic dyslipidemia[J]. Arterioscler Thromb Vasc Biol, 2005, 25(8): 1697–1703
CrossRef Google scholar
[58]
Bansal S, Buring JE, Rifai N, Fasting compared with nonfasting triglycerides and risk of cardiovascular events in women[J]. JAMA, 2007, 298(3): 309–316
CrossRef Google scholar
[59]
Harchaoui KEL, Visser ME, Kastelein JJP, Triglycerides and cardiovascular risk[J]. Curr Cardiol Rev, 2009, 5(3): 216–222
CrossRef Google scholar
[60]
Eberly LE, Stamler J, Neaton JD. Relation of triglyceride levels, fasting and nonfasting, to fatal and nonfatal coronary heart disease[J]. Arch Intern Med, 2003, 163(9): 1077–1083
CrossRef Google scholar
[61]
Yao Z, Wang Y. Apolipoprotein C–III and hepatic triglyceride-rich lipoprotein production[J]. Curr Opin Lipidol, 2012, 23(3): 206–212
CrossRef Google scholar
[62]
Gaudet D, Brisson D, Tremblay K, Targeting APOC3 in the Familial Chylomicronemia Syndrome[J]. N Engl J Med, 2014, 371(23): 2200–2206
CrossRef Google scholar
[63]
Gaudet D, Alexander VJ, Baker BF, Antisense Inhibition of Apolipoprotein C–III in Patients with Hypertriglyceridemia[J]. N Engl J Med, 2015, 373(5): 438–447
CrossRef Google scholar
[64]
Graham MJ, Lee RG, Bell TA, Antisense oligonucleotide inhibition of apolipoprotein c-iii reduces plasma triglycerides in rodents, nonhuman primates, and humans[J]. Circ Res, 2013, 112(11): 1479–1490
CrossRef Google scholar
[65]
TG and HDL Working Group of the Exome Sequencing Project, National Heart, Lung, and Blood Institute, Crosby J, Loss-of-function mutations in APOC3, triglycerides, and coronary disease[J]. N Engl J Med, 2014, 371(1): 22–31
CrossRef Google scholar
[66]
Caron S, Verrijken A, Mertens I, Transcriptional activation of apolipoprotein CIII expression by glucose may contribute to diabetic dyslipidemia[J]. Arterioscler Thromb Vasc Biol, 2011, 31(3): 513–519
CrossRef Google scholar
[67]
Gleeson A, Anderton K, Owens D, The role of microsomal triglyceride transfer protein and dietary cholesterol in chylomicron production in diabetes[J]. Diabetologia, 1999, 42(8): 944–948
CrossRef Google scholar
[68]
Qin B, Qiu W, Avramoglu RK, Tumor necrosis factor-α induces intestinal insulin resistance and stimulates the overproduction of intestinal apolipoprotein b48-containing lipoproteins[J]. Diabetes, 2007, 56(2): 450–461
CrossRef Google scholar
[69]
Zoltowska M, Ziv E, Delvin E, Cellular aspects of intestinal lipoprotein assembly in Psammomys obesus: a model of insulin resistance and type 2 diabetes[J]. Diabetes, 2003, 52(10): 2539–2545
CrossRef Google scholar
[70]
Phillips C, Bennett A, Anderton K, Intestinal rather than hepatic microsomal triglyceride transfer protein as a cause of postprandial dyslipidemia in diabetes[J]. Metabolism, 2002, 51(7): 847–852
CrossRef Google scholar
[71]
Phillips C, Mullan K, Owens D, Intestinal microsomal triglyceride transfer protein in type 2 diabetic and non-diabetic subjects: the relationship to triglyceride-rich postprandial lipoprotein composition[J]. Atherosclerosis, 2006, 187(1): 57–64
CrossRef Google scholar
[72]
Lally S, Tan CY, Owens D, Messenger RNA levels of genes involved in dysregulation of postprandial lipoproteins in type 2 diabetes: the role of Niemann-Pick C1-like 1, ATP-binding cassette, transporters G5 and G8, and of microsomal triglyceride transfer protein[J]. Diabetologia, 2006, 49(5): 1008–1016
CrossRef Google scholar
[73]
Sparks JD, Chamberlain JM, O’Dell C, Acute suppression of apo B secretion by insulin occurs independently of MTP[J]. Biochem Biophys Res Commun, 2011, 406(2): 252–256
CrossRef Google scholar
[74]
Sarwar N, Gao P, Seshasai SRK, , and the The Emerging Risk Factors Collaboration. Diabetes mellitus, fasting blood glucose concentration, and risk of vascular disease: a collaborative meta-analysis of 102 prospective studies[J]. Lancet, 2010, 375(9733): 2215–2222
CrossRef Google scholar
[75]
Kadowaki S, Okamura T, Hozawa A, Relationship of elevated casual blood glucose level with coronary heart disease, cardiovascular disease and all-cause mortality in a representative sample of the Japanese population. NIPPON DATA80[J]. Diabetologia, 2008, 51(4): 575–582
CrossRef Google scholar
[76]
Fujishima M, Kiyohara Y, Kato I, Diabetes and Cardiovascular Disease in a Prospective Population Survey in Japan: The Hisayama Study[J]. Diabetes, 1996, 45(Supplement 3): S14–S16
CrossRef Google scholar
[77]
Nakamura K, Miyoshi T, Yunoki K, Postprandial hyperlipidemia as a potential residual risk factor[J]. J Cardiol, 2016, 67(4): 335–339
CrossRef Google scholar
[78]
Gordin D, Saraheimo M, Tuomikangas J, Influence of postprandial hyperglycemic conditions on arterial stiffness in patients with type 2 diabetes[J]. J Clin Endocrinol Metab, 2016, 101(3): 1134–1143
CrossRef Google scholar
[79]
Hokanson JE, Austin MA. Plasma triglyceride level is a risk factor for cardiovascular disease independent of high-density lipoprotein cholesterol level: a meta-analysis of population-based prospective studies[J]. J Cardiovasc Risk, 1996, 3(2): 213–219
CrossRef Google scholar
[80]
Labreuche J, Touboul PJ, Amarenco P. Plasma triglyceride levels and risk of stroke and carotid atherosclerosis: a systematic review of the epidemiological studies[J]. Atherosclerosis, 2009, 203(2): 331–345
CrossRef Google scholar
[81]
Noda H, Iso H, Saito I, The impact of the metabolic syndrome and its components on the incidence of ischemic heart disease and stroke: the Japan public health center-based study[J]. Hypertens Res, 2009, 32(4): 289–298
CrossRef Google scholar
[82]
Patel A, Barzi F, Jamrozik K, Serum triglycerides as a risk factor for cardiovascular diseases in the Asia-Pacific region[J]. Circulation, 2004, 110(17): 2678–2686
CrossRef Google scholar
[83]
Sarwar N, Danesh J, Eiriksdottir G, Triglycerides and the risk of coronary heart disease: 10,158 incident cases among 262,525 participants in 29 Western prospective studies[J]. Circulation, 2007, 115(4): 450–458
CrossRef Google scholar
[84]
Gæde P, Lund-Andersen H, Parving HH, Effect of a multifactorial intervention on mortality in type 2 diabetes[J]. N Engl J Med, 2008, 358(6): 580–591
CrossRef Google scholar
[85]
Ma KL, Varghese Z, Ku Y, Sirolimus inhibits endogenous cholesterol synthesis induced by inflammatory stress in human vascular smooth muscle cells[J]. Am J Physiol Heart Circ Physiol, 2010, 298(6): H1646–H1651
CrossRef Google scholar
[86]
Zhao L, Chen Y, Tang R, Inflammatory stress exacerbates hepatic cholesterol accumulation via increasing cholesterol uptake and de novo synthesis[J]. J Gastroenterol Hepatol, 2011, 26(5): 875–883
CrossRef Google scholar
[87]
Walenbergh SMA, Koek GH, Bieghs V, Non-alcoholic steatohepatitis: The role of oxidized low-density lipoproteins[J]. J Hepatol, 2013, 58(4): 801–810
CrossRef Google scholar
[88]
Tanaka M, Ikeda K, Suganami T, Macrophage-inducible C-type lectin underlies obesity-induced adipose tissue fibrosis[J]. Nat Commun, 2014, 5: 4982
CrossRef Google scholar
[89]
Itoh M, Kato H, Suganami T, Hepatic crown-like structure: A unique histological feature in non-alcoholic steatohepatitis in mice and humans[J]. PLoS One, 2013, 8(12): e82163
CrossRef Google scholar
[90]
Brenner C, Galluzzi L, Kepp O, Decoding cell death signals in liver inflammation[J]. J Hepatol, 2013, 59(3): 583–594
CrossRef Google scholar
[91]
Chiasson JL, Josse RG, Gomis R, Acarbose for the prevention of Type 2 diabetes, hypertension and cardiovascular disease in subjects with impaired glucose tolerance: facts and interpretations concerning the critical analysis of the STOP-NIDDM Trial data[J]. Diabetologia, 2004, 47(6): 969–975., discussion 976–977.
CrossRef Google scholar
[92]
Barrett ML, Udani JK. A proprietary alpha-amylase inhibitor from white bean (Phaseolus vulgaris): a review of clinical studies on weight loss and glycemic control[J]. Nutr J, 2011, 10(1): 24
CrossRef Google scholar
[93]
Fujitani Y, Fujimoto S, Takahashi K, Effects of linagliptin monotherapy compared with voglibose on postprandial blood glucose responses in Japanese patients with type 2 diabetes: Linagliptin Study of Effects on Postprandial blood glucose (L-STEP)[J]. Diabetes Res Clin Pract, 2016, 121: 146–156
CrossRef Google scholar
[94]
Pratley RE, Hagberg JM, Dengel DR, Aerobic exercise training-induced reductions in abdominal fat and glucose-stimulated insulin responses in middle-aged and older men[J]. J Am Geriatr Soc, 2000, 48(9): 1055–1061
CrossRef Google scholar
[95]
Pratley RE, Weyer C. The role of impaired early insulin secretion in the pathogenesis of Type II diabetes mellitus[J]. Diabetologia, 2001, 44(8): 929–945
CrossRef Google scholar
[96]
Teva, Product Information: Glyburide (Glibenclamide), 2009, https://www.accessdata.fda.gov/drugsatfda_docs/label/2009/017532s030lbl.pdf.
[97]
Sanofi-Aventis, Product Information: Glimepiride, 2012., www.accessdata.fda.gov/drugsatfda.../020496s018s019lbl.pdf.
[98]
Hu S, Boettcher B, Dunning B. The mechanisms underlying the unique pharmacodynamics of nateglinide[J]. Diabetologia, 2003, 46(S1): M37–M43
CrossRef Google scholar
[99]
Prasad-Reddy L, Isaacs D. A clinical review of GLP-1 receptor agonists: efficacy and safety in diabetes and beyond[J]. Drugs Context, 2015, 4(212283): 1–19
CrossRef Google scholar
[100]
Fisman E, Tenenbaum A. Antidiabetic treatment with gliptins: focus on cardiovascular effects and outcomes[J]. Cardiovasc Diabetol, 2015, 14(1): 129
CrossRef Google scholar
[101]
Green J, Bethel M, Armstrong P, Effect of Sitagliptin on Cardiovascular Outcomes in Type 2 Diabetes[J]. N Engl J Med, 2015, 373(3): 232–242
CrossRef Google scholar
[102]
Zannad F, Cannon C, Cushman W, Heart failure and mortality outcomes in patients with type 2 diabetes taking alogliptin versus placebo in EXAMINE: a multicentre, randomised, double-blind trial[J]. Lancet, 2015, 385(9982): 2067–2076
CrossRef Google scholar
[103]
The ACCORD Study Group, Long-term effects of intensive glucose lowering on cardiovascular outcomes[J]. N Engl J Med, 2011, 364(9): 818–828
CrossRef Google scholar
[104]
Colhoun , Helen M. Primary prevention of cardiovascular disease with atorvastatin in type 2 diabetes in the Collaborative Atorvastatin Diabetes Study (CARDS): multicentre randomised placebo-controlled trial[J]. Lancet,2004, 364(9435): 685–696.
[105]
Sever PS, Poulter NR, Dahlof B, Reduction in cardiovascular events with atorvastatin in 2,532 patients with type 2 diabetes: Anglo-Scandinavian Cardiac Outcomes Trial–lipid-lowering arm (ASCOT-LLA)[J]. Diabetes Care, 2005, 28(5): 1151–1157
CrossRef Google scholar
[106]
Borén J, Matikainen N, Adiels M, Postprandial hypertriglyceridemia as a coronary risk factor[J]. Clin Chim Acta, 2014, 431: 131–142
CrossRef Google scholar
[107]
Scott R, O’Brien R, Fulcher G, Effects of fenofibrate treatment on cardiovascular disease risk in 9,795 individuals with type 2 diabetes and various components of the metabolic syndrome: the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study[J]. Diabetes Care, 2009, 32(3): 493–498
CrossRef Google scholar
[108]
Sabatine MS, Giugliano RP, Wiviott SD, Efficacy and Safety of Evolocumab in Reducing Lipids and Cardiovascular Events[J]. N Engl J Med, 2015, 372(16): 1500–1509
CrossRef Google scholar
[109]
Blom DJ, Hala T, Bolognese M, A 52-Week Placebo-Controlled Trial of Evolocumab in Hyperlipidemia[J]. N Engl J Med, 2014, 370(19): 1809–1819
CrossRef Google scholar
[110]
Chandler CE, Wilder DE, Pettini JL, CP-346086: an MTP inhibitor that lowers plasma cholesterol and triglycerides in experimental animals and in humans[J]. J Lipid Res, 2003, 44(10): 1887–1901
CrossRef Google scholar
[111]
Mera Y, Kawai T, Ogawa N, JTT-130, a novel intestine-specific inhibitor of microsomal triglyceride transfer protein, ameliorates lipid metabolism and attenuates atherosclerosis in hyperlipidemic animal models[J]. J Pharmacol Sci, 2015, 129(3): 169–176
CrossRef Google scholar
[112]
Filippov S, Pinkosky SL, Newton RS. LDL-cholesterol reduction in patients with hypercholesterolemia by modulation of adenosine triphosphate-citrate lyase and adenosine monophosphate-activated protein kinase[J]. Curr Opin Lipidol, 2014, 25(4): 309–315
CrossRef Google scholar
[113]
Lemus HN, Mendivil CO. Adenosine triphosphate citrate lyase: Emerging target in the treatment of dyslipidemia[J]. J Clin Lipidol, 2015, 9(3): 384–389
CrossRef Google scholar
[114]
Chen JS, Chen YH, Huang PH, Ginkgo biloba extract reduces high-glucose-induced endothelial adhesion by inhibiting the redox-dependent interleukin-6 pathways[J]. Cardiovasc Diabetol, 2012, 11(1): 49
CrossRef Google scholar
[115]
Siegel G, Ermilov E, Knes O, Combined lowering of low grade systemic inflammation and insulin resistance in metabolic syndrome patients treated with Ginkgo biloba[J]. Atherosclerosis, 2014, 237(2): 584–588
CrossRef Google scholar
[116]
Zhou YH, Yu JP, Liu YF, Effects of Ginkgo biloba extract on inflammatory mediators (SOD, MDA, TNF-alpha, NF-kappaBp65, IL-6) in TNBS-induced colitis in rats[J]. Mediators Inflamm, 2006, 2006(5): 92642.
[117]
Xie Z, Liang G, Zhang L, Molecular mechanisms underlying the cholesterol-lowering effect of Ginkgo biloba extract in hepatocytes: a comparative study with lovastatin[J]. Acta Pharmacol Sin, 2009, 30(9): 1262–1275
CrossRef Google scholar
[118]
Schultz O, Oberhauser F, Saech J, Effects of inhibition of interleukin-6 signalling on insulin sensitivity and lipoprotein (a) levels in human subjects with rheumatoid diseases[J]. PLoS One, 2010, 5(12): e14328
CrossRef Google scholar
[119]
Strang AC, Bisoendial RJ, Kootte RS, Pro-atherogenic lipid changes and decreased hepatic LDL receptor expression by tocilizumab in rheumatoid arthritis. Atherosclerosis, 2013, 229(1): 174–181
CrossRef Google scholar
[120]
Ridker PM. From C-reactive protein to interleukin-6 to interleukin-1: moving upstream to identify novel targets for atheroprotection[J]. Circ Res, 2016, 118(1): 145–156
CrossRef Google scholar
[121]
Lippi G, Targher G. Optimal therapy for reduction of lipoprotein(a)[J]. J Clin Pharm Ther, 2012, 37(1): 1–3
CrossRef Google scholar
[122]
Mohammadpour AH, Akhlaghi F. Future of cholesteryl ester transfer protein (CETP) inhibitors: a pharmacological perspective[J]. Clin Pharmacokinet, 2013, 52(8): 615–626
CrossRef Google scholar
[123]
Kumashiro N, Beddow SA, Vatner DF, Targeting pyruvate carboxylase reduces gluconeogenesis and adiposity and improves insulin resistance[J]. Diabetes, 2013, 62(7): 2183–2194
CrossRef Google scholar
[124]
Kiyosue A, Hayashi N, Komori H, Dose-ranging study with the glucokinase activator AZD1656 as monotherapy in Japanese patients with type 2 diabetes mellitus[J]. Diabetes Obes Metab, 2013, 15(10): 923–930
CrossRef Google scholar
[125]
Lloyd DJ, St Jean DJJ, Kurzeja RJM, Antidiabetic effects of glucokinase regulatory protein small-molecule disruptors[J]. Nature, 2013, 504(7480): 437–440
CrossRef Google scholar
[126]
van Poelje PD, Potter SC, Erion MD. Fructose-1, 6-bisphosphatase inhibitors for reducing excessive endogenous glucose production in type 2 diabetes[J]. Handb Exp Pharmacol, 2011, 203: 279–301
CrossRef Google scholar
[127]
Swarbrick MM, Havel PJ, Levin AA, Inhibition of protein tyrosine phosphatase-1B with antisense oligonucleotides improves insulin sensitivity and increases adiponectin concentrations in monkeys[J]. Endocrinology, 2009, 150(4): 1670–1679
CrossRef Google scholar
[128]
Agius L. New hepatic targets for glycaemic control in diabetes[J]. Best Pract Res Clin Endocrinol Metab, 2007, 21(4): 587–605
CrossRef Google scholar
[129]
Baker DJ, Timmons JA, Greenhaff PL. Glycogen phosphorylase inhibition in type 2 diabetes therapy: A systematic evaluation of metabolic and functional effects in rat skeletal muscle[J]. Diabetes, 2005, 54(8): 2453–2459
CrossRef Google scholar
[130]
Kazda CM, Ding Y, Kelly RP, Evaluation of efficacy and eafety of the glucagon receptor antagonist LY2409021 in patients with type 2 diabetes: 12- and 24-week phase 2 studies[J]. Diabetes Care, 2016, 39(7): 1241–1249
CrossRef Google scholar
[131]
Girard J. The inhibitory effects of insulin on hepatic glucose production are both direct and indirect[J]. Diabetes, 2006, 55(Supplement 2): S65–S69
CrossRef Google scholar
[132]
Gray LR, Sultana MR, Rauckhorst AJ, Hepatic mitochondrial pyruvate carrier 1 is required for efficient regulation of gluconeogenesis and whole-body glucose homeostasis[J]. Cell Metab, 2015, 22(4): 669–681
CrossRef Google scholar
[133]
Divakaruni AS, Wiley SE, Rogers GW, Thiazolidinediones are acute, specific inhibitors of the mitochondrial pyruvate carrier[J]. Proc Natl Acad Sci USA, 2013, 110(14): 5422–5427
CrossRef Google scholar
[134]
DiTullio NW, Berkoff CE, Blank B, 3-Mercaptopicolinic Acid, an Inhibitor of Gluconeogenesis[J]. Biochem J, 1974, 138(3): 387–394
CrossRef Google scholar
[135]
Altomonte J, Richter A, Harbaran S, Inhibition of Foxo1 function is associated with improved fasting glycemia in diabetic mice[J]. Am J Physiol Endocrinol Metab, 2003, 285(4): E718–E728
CrossRef Google scholar
[136]
Perry RJ, Kim T, Zhang XM, Reversal of hypertriglyceridemia, fatty liver disease, and insulin resistance by a liver-targeted mitochondrial uncoupler[J]. Cell Metab, 2013, 18(5): 740–748
CrossRef Google scholar
[137]
Perry RJ, Zhang D, Zhang XM, Controlled-release mitochondrial protonophore reverses diabetes and steatohepatitis in rats[J]. Science, 2015, 347(6227): 1253–1256
CrossRef Google scholar
[138]
Yamauchi T, Nio Y, Maki T, Targeted disruption of AdipoR1 and AdipoR2 causes abrogation of adiponectin binding and metabolic actions[J]. Nat Med, 2007, 13(3): 332–339
CrossRef Google scholar
[139]
Iwabu M, Yamauchi T, Okada-Iwabu M, Adiponectin and AdipoR1 regulate PGC-1alpha and mitochondria by Ca(2+) and AMPK/SIRT1[J]. Nature, 2010, 464(7293): 1313–1319
CrossRef Google scholar
[140]
Okada-Iwabu M, Yamauchi T, Iwabu M, A small-molecule AdipoR agonist for type 2 diabetes and short life in obesity[J]. Nature, 2013, 503(7477): 493–499
CrossRef Google scholar

Acknowledgments

The authors wish to thank all members of each department.

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2017 2017 by the Journal of Biomedical Research.
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