PUBLICATIONS
Cincotta AH, Meier AH, Cincotta Jr M.
Bromocriptine improves glycaemic control and serum lipid profile in obese Type 2 diabetic subjects: a new approach in the treatment of diabetes.
Expert Opin Investig Drugs. 1999 Oct;8(10):1683-1707.
Pijl H, Ohashi S, Matsuda M, Miyazaki Y, Mahankali A, Kumar V, Pipek R, Iozzo P, Lancaster JL, Cincotta AH, DeFronzo RA.
Bromocriptine: a novel approach to the treatment of type 2 diabetes.
Diabetes Care. 2000 Aug;23(8):1154-61.
Kamath V, Jones CN, Yip JC, Varasteh BB, Cincotta AH, Reaven GM, Chen YD.
Effects of a quick-release form of bromocriptine (Ergoset) on fasting and postprandial plasma glucose, insulin, lipid, and lipoprotein concentrations in obese nondiabetic hyperinsulinemic women.
Diabetes Care. 1997 Nov;20(11):1697-701.
Cincotta AH, Meier AH.
Bromocriptine (Ergoset) reduces body weight and improves glucose tolerance in obese subjects.
Diabetes Care. 1996 Jun;19(6):667-70.
Meier AH, Cincotta AH, Lovell WC.
Timed bromocriptine administration reduces body fat stores in obese subjects and hyperglycemia in type II diabetics.
Experientia. 1992 Mar 15;48(3):248-53.
Jetton TL, Liang Y, Cincotta AH.
Systemic treatment with sympatholytic dopamine agonists improves aberrant beta-cell hyperplasia and GLUT2, glucokinase, and insulin immunoreactive levels in ob/ob mice.
Metabolism. 2001 Nov;50(11):1377-84.
Liang Y, Cincotta AH.
Increased responsiveness to the hyperglycemic, hyperglucagonemic and hyperinsulinemic effects of circulating norepinephrine in ob/ob mice.
Int J Obes Relat Metab Disord. 2001 May;25(5):698-704.
Boundy VA, Cincotta AH.
Hypothalamic adrenergic receptor changes in the metabolic syndrome of genetically obese (ob/ob) mice.
Am J Physiol Regul Integr Comp Physiol. 2000 Aug;279(2):R505-14.
Luo S, Luo J, Cincotta AH.
Association of the antidiabetic effects of bromocriptine with a shift in the daily rhythm of monoamine metabolism within the suprachiasmatic nuclei of the Syrian hamster.
Chronobiol Int. 2000 Mar;17(2):155-72.
Cincotta AH, Luo S, Liang Y.
Hyperinsulinemia increases norepinephrine metabolism in the ventromedial hypothalamus of rats.
Neuroreport. 2000 Feb 7;11(2):383-7.
Bina KG, Cincotta AH.
Dopaminergic agonists normalize elevated hypothalamic neuropeptide Y and corticotropin-releasing hormone, body weight gain, and hyperglycemia in ob/ob mice.
Neuroendocrinology. 2000 Jan;71(1):68-78.
Liang Y, Luo S, Cincotta AH.
Long-term infusion of norepinephrine plus serotonin into the ventromedial hypothalamus impairs pancreatic islet function.
Metabolism. 1999 Oct;48(10):1287-9.
Zhang Y, Scislowski PW, Prevelige R, Phaneuf S, Cincotta AH.
Bromocriptine/SKF38393 treatment ameliorates dyslipidemia in ob/ob mice.
Metabolism. 1999 Aug;48(8):1033-40.
Luo S, Liang Y, Cincotta AH.
Intracerebroventricular administration of bromocriptine ameliorates the insulin-resistant/glucose-intolerant state in hamsters.
Neuroendocrinology. 1999 Mar;69(3):160-6.
Luo S, Meier AH, Cincotta AH.
Bromocriptine reduces obesity, glucose intolerance and extracellular monoamine metabolite levels in the ventromedial hypothalamus of Syrian hamsters.
Neuroendocrinology. 1998 Jul;68(1):1-10.
Cincotta AH, Meier AH.
Reductions of body fat stores and total plasma cholesterol and triglyceride concentrations in several species by bromocriptine treatment.
Life Sci. 1989;45(23):2247-54.
Cincotta L, Szeto D, Lampros E, Hasan T, Cincotta AH.
Benzophenothiazine and benzoporphyrin derivative combination phototherapy effectively eradicates large murine sarcomas.
Photochem Photobiol. 1996 Feb;63(2):229-37.
Keisari Y, Cincotta E, Meier AH, Cincotta AH.
Timed daily administration of prolactin and corticosteroid hormone reduces murine tumor growth and enhances immune reactivity.
Chronobiol Int. 1999 May;16(3):315-33.
Hendrzak-Henion JA, Knisely TL, Cincotta L, Cincotta E, Cincotta AH.
Role of the immune system in mediating the antitumor effect of benzophenothiazine photodynamic therapy.
Photochem Photobiol. 1999 May;69(5):575-81.
RESEARCH
Metabolic Disease
By employing methods that mimic the neurobiochemical physiology responsible for the seasonal shift from the obese, insulin resistant condition to the lean, insulin sensitive state common among vertebrate species in the wild, it is possible to develop new treatment strategies for human metabolic diseases such as type 2 diabetes, obesity, and metabolic syndrome. Changes in the circadian phase relations of distinct neuroendocrine rhythms drive the annual cycle of metabolism among vertebrates in the wild.
Consequently, it is not merely supplying the neuroendocrine factors of the “lean” season that produces leanness but rather supplying the circadian neuroendocrine blueprint that accomplishes this shift. Methods aimed at doing so, can function to alleviate and induce the obese, insulin resistant condition as is the case in the wild. We are developing different ways of applying this science to provide effective and practical means of treating human metabolic diseases.
Immune Disorders
Immuno-suppression and autoimmune diseases are both associated with derangements in the circadian neuroendocrine axis. Once again, it is the critical role of the brain-neuroendocrine axis to regulate and orchestrate the complex immunological interactions that occur at the cellular and tissue levels for the production of an organismal level immunocompetence.
Rather than focusing on specific immuno-modulators such chemokines or lymphkines to boost immuno-reactivity, we focus on resetting circadian neuroendocrine events that organize overall global immunophysiology to treat immuno-suppressed states. Similarly, autoimmune disorders with genetic components manifest as alterations in the neuroendocrine axis which in turn potentiate the underlying disorder.
Consequently, autoimmune diseases may be improved by appropriately resetting specific aberrations in the circadian neuroendocrine axis. Our interventions are not just pharmaceutical compounds but rather therapeutic treatment regimens employing such compounds in a particular manner to reprogram the master control centers in the brain for the production of whole-body immunological status.