Abstract
Background: For more than three decades, it has been known that manipulation of dopaminergic system could affect glucose homesotasis in experimental animals. The notion that glucose homeostasis in human might be influenced by dopaminergic drugs has attracted a great deal of attention in the past two decades. In spite of rapid advancements in revealing involvement of dopaminergic neurotransmission in insulin release, glucose up-take and pancreatic beta cell function in general through centrally and peripherally controlled mechanisms, there are discrepancies among observations on experimental animals and human subjects.
Conclusion: With the expansion of pharmacotherapy in psychotic conditions, depression and endocrine abnormalities along with a sharp increase in prevalence of type two diabetes and disturbances of glucose homeostasis as a major risk factor for many cardiovascular complications and associated mortalities; it seems a critical analysis of recent investigations on drugs which act as agonists or antagonists of dopaminergic receptors in various tissues and organs may provide better insight into how safe and efficient these medicines could be prescribed. Furthermore, the other main objective of present review is to compare clinical data on significance of changes in blood glucose and insulin levels during short term and after long term treatment with these agents. This in turn would be beneficial for determining adequate strategies to combat or to avoid adverse effects associated with dopaminergic drug therapy.
Keywords: Dopamine receptor, glucose up-take, hepatic glucose output, Insulin secretion, dopamine agonists, homesotasis.
[1]
Sachdev Y, Gopal K, Garg VK. Bromocriptine therapy in acromegaly. A long-term review of 35 cases. BMJ 1981; 57: 210-6.
[2]
Kamran A, Doraiswamy PM, Jane JL, Hammett EB, Dunn L. Severe hyperglycemia associated with high doses of clozapine. Am J Psychiatry 1994; 151: 1395.
[3]
Wirshing DA, Spellberg BJ, Erhart SM, Marder SR, Wirshing WC. Novel antipsychotics and new onset diabetes. Biol Psychiatry 1998; 44(8): 778-83.
[4]
Henderson DC, Cagliero E, Gray C, et al. Clozapine, diabetes mellitus, weight gain, and lipid abnormalities: A five-year naturalistic study. Am J Psychiatry 2000; 157(6): 975-81.
[5]
Dwyer DS, Donohoe D. Induction of hyperglycemia in mice with atypical antipsychotic drugs that inhibit glucose uptake. Pharmacol Biochem Behav 2003; 75(2): 255-60.
[6]
Girgis RR, Javitch JA, Lieberman JA. Antipsychotic drug mechanisms: links between therapeutic effects, metabolic side effects and the insulin signaling pathway. Mol Psychiatry 2008; 13(10): 918-29.
[7]
Bahar A, Kashi Z, Daneshpour E, Akha O, Ala S. Effects of cabergoline on blood glucose levels in type 2 diabetic patients: A double-blind controlled clinical trial. Medicine 2016; 95(40): e4818.
[8]
Lopez Vicchi F, Luque GM, Brie B, Nogueira JP, Garcia Tornadu I, Becu-Villalobos D. Dopaminergic drugs in type 2 diabetes and glucose homeostasis. Pharmacol Res 2016; 109: 74-80.
[9]
Mezey E, Eisenhofer G, Harta G, et al. A novel nonneuronal catecholaminergic system: Exocrine pancreas synthesizes and releases dopamine. Proc Natl Acad Sci USA 1996; 93: 10377-82.
[10]
Goldstein DS, Eisenhofer G, Kopin IJ. Sources and significance of plasma levels of catechols and their metabolites in humans. J Pharmacol Exp Ther 2003; 305(3): 800-11.
[11]
Cincotta AH, Meier AH, Southern LL. Bromocriptine alters hormone rhythms and lipid metabolism in swine. Ann Nutr Metab 1989; 33(6): 305-14.
[12]
Kvernmo T, Härtter S, Burger E. A review of the receptor-binding and pharmacokinetic properties of dopamine agonists. Clin Ther 2006; 28(8): 1065-78.
[13]
DeFronzo RA. From the triumvirate to the ominous octet: A new paradigm for the treatment of type 2 diabetes mellitus. Diabetes 2009; 58(4): 773-95.
[14]
Chamarthi B, Cincotta AH. Effect of bromocriptine-QR therapy on glycemic control in subjects with type 2 diabetes mellitus whose dysglycemia is inadequately controlled on insulin. Postgrad Med 2017; 129(4): 446-55.
[15]
Ustione A, Piston DW, Harris PE. Minireview: Dopaminergic Regulation of Insulin Secretion from the Pancreatic Islet. Mol Endocrinol 2013; 27(8): 1198-207.
[16]
Lamos EM, Levitt DL, Munir KM. A review of dopamine agonist therapy in type 2 diabetes and effects on cardio-metabolic parameters. Prim Care Diabetes 2016; 10: 60-5.
[17]
Rubí B, Ljubicic S, Pournourmohammadi S, et al. Dopamine D2-like receptors are expressed in pancreatic beta cells and mediate inhibition of insulin secretion. J Biol Chem 2005; 280(44): 36824-32.
[18]
Shankar E, Santhosh KT, Paulose CS. Dopaminergic regulation of glucose-induced insulin secretion through dopamine D2 receptors in the pancreatic islets in vitro. IUBMB Life 2006; 58(3): 157-63.
[19]
Contreras F, Foullioux C, Pacheco B, et al. Effect of drugs interacting with the dopaminergic receptors on glucose levels and insulin release in healthy and type 2 diabetic subjects. Am J Ther 2008; 15(4): 397-402.
[20]
Ericson LE, Hakanson R, Lundquist I. Accumulation of dopamine in mouse pancreatic B-cells following injection of L-DOPA. Localization to secretory granules and inhibition of insulin secretion. Diabetologia 1977; 13(2): 117-24.
[21]
Sims H, Smith KH, Bramlage P, Minguet J. Sotagliflozin: A dual
sodium-glucose co-transporter-1 and -2 inhibitor for the management
of Type 1 and Type 2 diabetes mellitus. Available from: www.ncbi.nlm.nih.gov/pubmed/29637608 (Accessed on: Apr 10,
2018).
[22]
Schubert D, Tarikas H, LaCorbiere M. Neurotransmitter regulation of adenosine 3′,5′-monophosphate in clonal nerve, glia, and muscle cell lines. Science 1976; 192: 471-3.
[23]
Lee AD, Hansen PA, Schluter J, Gulve EA, Gao J, Holloszy JO. Effects of epinephrine on insulin-stimulated glucose uptake and GLUT-4 phosphorylation in muscle. Am J Physiol 1997; 273(3 Pt 1): C1082-7.
[24]
Hunt DG, Ding Z, Ivy JL. Clenbuterol prevents epinephrine from antagonizing insulin-stimulated muscle glucose uptake. J Appl Physiol 2002; 92(3): 1285-92.
[25]
Aviles-Olmos I, Limousin P, Lees A, Foltynie T. Parkinson’s disease, insulin resistance and novel agents of neuroprotection. Brain 2013; 136(Pt 2): 374-84.
[26]
Korner J, Lo J, Freda PU, Wardlaw SL. Treatment with cabergoline is associated with weight loss in patients with hyperprolactinemia. Obes Res 2003; 11: 311-2.
[27]
Gibson CD, Karmally W, McMahon DJ, Wardlaw SL, Korner J. Randomized pilot study of cabergoline, a dopamine receptor agonist: effects on body weight and glucose tolerance in obese adults. Diabetes Obes Metab 2012; 14(4): 335-40.
[28]
Taghavi SM, Fatemi SS, Rokni H. Cabergoline effect on blood sugar in type 2 diabetic patients with oral agent failure. Med J Malaysia 2012; 67(4): 390-2.
[29]
Saadat N, Eesmaily H, Abbasinazari M, et al. Does twice-weekly cabergoline improve anthropometrical and biochemical profiles in prediabetes? A randomized double-blind clinical trial pilot study. Iran J Pharm Res 2015; 14(Suppl.): 77-86.
[30]
Johns DW, Ayers CR, Williams SC. Dilation of forearm blood vessels after angiotensin-converting-enzyme inhibition by captopril in hypertensive patients. Hypertension 1984; 6(4): 545-50.
[31]
Kodama J, Katayama S, Tanaka K, Itabashi A, Kawazu S, Ishii J. Effect of captopril on glucose concentration: Possible role of augmented postprandial forearm blood flow. Diabetes Care 1990; 13(11): 1109-11.
[32]
Dwyer DS, Liu Y, Bradley RJ. Dopamine receptor antagonists modulate glucose uptake in rat pheochromocytoma (PC12) cells. Neurosci Lett 1999; 274(3): 151-4.
[33]
Dwyer DS, Pinkofsky HB, Liu Y, Bradley RJ. Antipsychotic drugs affect glucose uptake and the expression of glucose transporters in PC12 cells. Prog Neuropsychopharmacol Biol Psychiatry 1999; 23(1): 69-80.
[34]
Ardizzone TD, Bradley RJ, Freeman AM, Dwyer DS. Inhibition of glucose transport in PC12 cells by the atypical antipsychotic drugs risperidone and clozapine, and structural analogs of clozapine. Brain Res 2001; 923(1–2): 82-90.
[35]
Dwyer DS. Model of the 3-D structure of the GLUT3 glucose transporter and molecular dynamics simulation of glucose transport. Proteins Struct Funct Genet 2001; 42: 531-41.
[36]
Dwyer DS, Ardizzone TD, Bradley RJ. Psychoactive drugs affect glucose transport and the regulation of glucose metabolism. Int Rev Neurobiol 2002; 51: 503-30.
[37]
Gaziano JM, Cincotta AH, Vinik A, Blonde L, Bohannon N, Scranton R. Effect of bromocriptine-QR (a quick-release formulation of bromocriptine mesylate) on major adverse cardiovascular events in type 2 diabetes subjects. J Am Heart Assoc 2012; 1(5): e002279.
[38]
Gaziano JM, Cincotta AH, O’Connor CM, et al. Randomized clinical trial of quick-release bromocriptine among patients with type 2 diabetes on overall safety and cardiovascular outcomes. Diabetes Care 2010; 33(7): 1503-8.
[39]
Chamarthi B, Gaziano JM, Blonde L, et al. Timed bromocriptine-QR therapy reduces progression of cardiovascular disease and dysglycemia in subjects with well-controlled type 2 diabetes mellitus. J Diabetes Res 2015; 2015: 157698.
[40]
Garber AJ, Blonde L, Bloomgarden ZT, Handelsman Y, Dagogo-Jack S. The role of bromocriptine-QR in the management of type 2 diabetes expert panel recommendations. Endocr Pract 2013; 19(1): 100-6.
[41]
Chamarthi B, Ezrokhi M, Rutty D, Cincotta AH. Impact of bromocriptine-QR therapy on cardiovascular outcomes in type 2 diabetes mellitus subjects on metformin. Postgrad Med 2016; 128(8): 761-9.
[42]
Coomans CP, Van Den Berg SAA, Lucassen EA, et al. The suprachiasmatic nucleus controls circadian energy metabolism and hepatic insulin sensitivity. Diabetes 2013; 62(4): 1102-8.
[43]
Holt RIG. Barnett a H, Bailey CJ. Bromocriptine: Old drug, new formulation and new indication. Diabetes Obes Metab 2010; 12(12): 1048-57.
[44]
Schwartz SS, Zangeneh F. Evidence-based practice use of quick-release bromocriptine across the natural history of type 2 diabetes mellitus. Postgrad Med 2016; 128: 828-38.
[45]
Reaven GM, Lithell H, Landsberg L. Hypertension and associated metabolic abnormalities-the role of insulin resistance and the sympathoadrenal system. N Engl J Med 1996; 334(6): 374-81.
[46]
De Mattia G, Ferri C, Laurenti O, Cassone-Faldetta M, Piccoli A, Santucci A. Circulating catecholamines and metabolic effects of captopril in NIDDM patients. Diabetes Care 1996; 19(3): 226-30.
[47]
Moan A, Risanger T, Eide I, Kjeldsen SE. The effect of angiotensin II receptor blockade on insulin sensitivity and sympathetic nervous system activity in primary hypertension. Blood Press 1994; 3(3): 185-8.
[48]
Dwyer DS, Ardizzone TD, Bradley RJ. Psychoactive drugs affect glucose transport and the regulation of glucose metabolism In: Glucose Metabolism in the Brain 2002 p 503–30 Available from: 2002.http://www.sciencedirect.com/science/article/pii/S0074774202510151
[49]
Cincotta AH, Meier AH. Bromocriptine inhibits in vivo free fatty acid oxidation and hepatic glucose output in seasonally obese hamsters (Mesocricetus auratus). Metabolism 1995; 44(10): 1349-55.
[50]
Scranton RE, Gaziano JM, Rutty D, Ezrokhi M, Cincotta A. A randomized, double-blind, placebo-controlled trial to assess safety and tolerability during treatment of type 2 diabetes with usual diabetes therapy and either Cycloset or placebo. BMC Endocr Disord 2007; 7: 3.
[51]
Rummel-Kluge C, Komossa K, Schwarz S, et al. Head-to-head comparisons of metabolic side effects of second generation antipsychotics in the treatment of schizophrenia: A systematic review and meta-analysis. Schizophr Res 2010; 123(2–3): 225-33.
[52]
Boden R, Edman G, Reutfors J, Ostenson CG, Osby U. A comparison of cardiovascular risk factors for ten antipsychotic drugs in clinical practice. Neuropsychiatr Dis Treat 2013; 9: 371-7.
[53]
Ehret M, Goethe J, Lanosa M, Coleman CI. The effect of metformin on anthropometrics and insulin resistance in patients receiving atypical antipsychotic agents: A meta-analysis. J Clin Psychiatry 2010; 71(10): 1286-92.
[54]
Klein DJ, Saldaña SN. Review: Metformin is effective at attenuating the metabolic risks associated with use of atypical antipsychotics. Evid Based Ment Health 2011; 14: 55.
[55]
de Silva VA, Suraweera C, Ratnatunga SS, Dayabandara M, Wanniarachchi N, Hanwella R. Metformin in prevention and treatment of antipsychotic induced weight gain: A systematic review and meta-analysis. BMC Psychiatry 2016; 16(1): 341.
[56]
Volkow ND, Wang GJ, Fowler JS, et al. “Nonhedonic” food motivation in humans involves dopamine in the dorsal striatum and methylphenidate amplifies this effect. Synapse 2002; 44(3): 175-80.
[57]
Small DM, Jones-Gotman M, Dagher A. Feeding-induced dopamine release in dorsal striatum correlates with meal pleasantness ratings in healthy human volunteers. Neuroimage 2003; 19(4): 1709-15.
[58]
Pepino MY, Eisenstein SA, Bischoff AN, et al. Sweet dopamine: Sucrose preferences relate differentially to striatal D2 receptor binding and age in obesity. Diabetes 2016; 65(9): 2618-23.
[59]
Travers JB, Akey LR, Chen SC, Rosen S, Paulson G, Travers SP. Taste preferences in Parkinson’s disease patients. Chem Senses 1993; 18(1): 47-55.
[60]
Xenakis S, Sclafani A. The dopaminergic mediation of a sweet reward in normal and VMH hyperphagic rats. Pharmacol Biochem Behav 1982; 16(2): 293-302.
[61]
Paolisso G, Scheen A, D’Onofrio F, Lefèbvre P. Magnesium and glucose homeostasis. Diabetologia 1990; 33: 511-4.
[62]
Paolisso G, Passariello N, Pizza G, et al. Dietary magnesium supplements improve B-cell response to glucose and arginine in elderly non-insulin dependent diabetic subjects. Acta Endocrinol, (Copenh) 1989; 121(1): 16–20.
[63]
Haenni A, Berglund L, Reneland R, Anderssson PE, Lind L, Lithell H. The alterations in insulin sensitivity during angiotensin converting enzyme inhibitor treatment are related to changes in the calcium/magnesium balance. Am J Hypertens 1997; 10(2): 145-51.
[64]
Martínez Martín FJ. Manidipine in hypertensive patients with metabolic syndrome: The MARIMBA study. Expert Rev Cardiovasc Ther 2009; 7(7): 863-9.
[65]
Fogari R, Zoppi A, Corradi L, Preti P, Malalamani GD, Mugellini A. Effects of different dihydropyridine calcium antagonists on plasma norepinephrine in essential hypertension. J Hypertens 2000; 18(12): 1871-5.
[66]
Besnard I, Auclair V, Callery G, Gabriel-Bordenave C, Roberge C. Antipsychotic-drug-induced hyperprolactinemia: Physiopathology, clinical features and guidance. Encephale 2014; 40(1): 86-94.
[67]
Krysiak R, Gilowski W, Szkrobka W, Okopien B. The effect of atorvastatin on cardiometabolic risk factors in bromocriptine-treated premenopausal women with isolated hypercholesterolemia. Cardiovasc Ther 2015; 33(5): 282-7.
[68]
Krysiak R, Okopien B. Different effects of cabergoline and bromocriptine on metabolic and cardiovascular risk factors in patients with elevated prolactin levels. Basic Clin Pharmacol Toxicol 2015; 116(3): 251-6.
[69]
Brunerova L, Potockova J, Horacek J, Suchy J, Andel M. Central dopaminergic activity influences metabolic parameters in healthy men. Neuroendocrinology 2013; 97(2): 132-8.
[70]
Berinder K, Nyström T, Höybye C, Hall K, Hulting AL. Insulin sensitivity and lipid profile in prolactinoma patients before and after normalization of prolactin by dopamine agonist therapy. Pituitary 2011; 14(3): 199-207.
[71]
Holt RIG, Barnett AH, Bailey CJ. Bromocriptine: Old drug, new formulation and new indication. Diabetes Obes Metab 2010; 12: 1048-57.
[72]
Scranton R, Cincotta A. Bromocriptine--unique formulation of a dopamine agonist for the treatment of type 2 diabetes. Expert Opin Pharmacother 2010; 11(2): 269-79.
[73]
Kok P, Roelfsema F, Frolich M, et al. Activation of dopamine D2 receptors simultaneously ameliorates various metabolic features of obese women. AJP Endocrinol Metab 2006; 291(5): E1038-43.
[74]
Garcia BMJ, Iglesias OMC, Blanco EJ, et al. Dopamine modulates insulin release and is involved in the survival of rat pancreatic beta cells. PLoS One 2015; 10(4): e0123197.
Article Metrics
43
3