Nihal Tümer, Ph.D.

Dr. Tumer

Emeritus Professor
Office: ARB R5-114
Phone: 352- 273-9424 (Office); 273-9143 (Lab)
Publications: Search PubMed


Research Interests

  • Discovery of neuronal mechanisms underlying diet and aged-induced obesity. Obesity is occurring at epidemic rates with frightful health consequences. Our hypothesis is that leptin resistance is an important causative factor in both diet-induced and age-related obesity. We demonstrated that both types of obesity are associated with leptin resistance and this resistance resides within the first order hypothalamic neurons that contain leptin receptors, and we provided strong evidence that the leptin receptor-signaling cascade is impaired. One current area of focus is to restore leptin receptor function with gene delivery/programmed of the leptin in a circadian/intermittent fashion to specific brain regions. A second area of focus is the role of specific dietary components such as fat or sugar as causative factors in leptin resistance independent of caloric intake or body weight.
  • Chronic consequences of Traumatic Brain Injury (TBI) on cerebrovascular function. One deleterious consequence of brain injury is cerebral vascular dysfunction. Human studies indicate that severe traumatic brain injury leads to decreased blood flow and hypoperfusion of the brain tissue. Our hypothesis is that long-term consequences of TBI are the results of impaired cerebral blood flow and due to chronic oxidative stress and inflammation. Secondarily, we propose there is elevated sympathetic nervous system activity leading to systemic cardiovascular problems including hypertension.
  • A third area of focus in elucidation of the mechanisms underlying increased hypertension with age. Elevated blood pressure is a major contributor to cardiovascular diseases in the elderly which is the number one killer in the United States. We are examining the role of oxidative stress and inflammation in age-related sympathetic nervous activation and blood pressure elevation.

Recent Publications:

  • Côté I, Green SM, Morgan D, Carter CS, Tümer N, Scarpace PJ. Activation of the central melanocortin system in rats persistently reduces body and fat mass independently of caloric reduction. Can J Physiol Pharmacol. 2017 Nov 13:1-5. doi: 10.1139/cjpp-2017-0440.
  • Côté I, Green SM, Toklu HZ, Morgan D, Carter CS, Tümer N, Scarpace PJ. Differential physiological responses to central leptin overexpression in male and female rats. J Neuroendocrinol. 2017 Dec;29(12). doi: 10.1111/jne.12552.
  • Basgut B, Whidden MA, Kirichenko N, Woods M, Erdos B, Scarpace PJ, Tümer N. Effect of High-Salt Diet on Age-Related High Blood Pressure and Hypothalamic Redox Signaling. Pharmacology. 2017;100(3-4):105-114. doi: 10.1159/000472259. Epub 2017 May 19.
  •  Toklu HZ, Sakarya Y, Tümer N. A Proteomic Evaluation of Sympathetic Activity Biomarkers of the Hypothalamus-Pituitary-Adrenal Axis by Western Blotting Technique Following Experimental Traumatic Brain Injury. Methods Mol Biol. 2017;1598:313-325. doi: 10.1007/978-1-4939-6952-4_16.
  • Côté I, Sakarya Y, Kirichenko N, Morgan D, Carter CS, Tümer N, Scarpace PJ. Activation of the central melanocortin system chronically reduces body mass without the necessity of long-term caloric restriction. Can J Physiol Pharmacol. 2017 Feb;95(2):206-214. doi: 10.1139/cjpp-2016-0290. Epub 2016 Oct 19.
  • Toklu HZ, Scarpace PJ, Sakarya Y, Kirichenko N, Matheny M, Bruce EB, Carter CS, Morgan D, Tümer N. Intracerebroventricular tempol administration in older rats reduces oxidative stress in the hypothalamus but does not change STAT3 signalling or SIRT1/AMPK pathway. Appl Physiol Nutr Metab. 2017 Jan;42(1):59-67. doi: 10.1139/apnm-2016-0067. Epub 2016 Oct 6.
  • Gocmez SS, Scarpace PJ, Whidden MA, Erdos B, Kirichenko N, Sakarya Y, Utkan T, Tumer N. Age Impaired endothelium-dependent vasodilation is improved by resveratrol in rat mesenteric arteries. J Exerc Nutrition Biochem. 2016 Mar 31;20(1):41-8. doi: 10.20463/jenb.2016.