Education

  • BS, Biological Sciences, Louisiana State University, 1999
  • BA, Psychology, Louisiana State University, 2001
  • PhD, Vision Sciences, University of Alabama - Birmingham, 2008
  • MS, Clinical Research, Tulane University, 2020

Curriculum Vitae

Research Interests

Dr. McDougal’s research investigates why individuals with diabetes often lose the body’s natural defenses against low blood sugar (glucose). Under normal conditions, the brain detects falling glucose levels and activates hormonal and behavioral responses to restore balance. In diabetes, however, this protective mechanism frequently breaks down, increasing the risk of dangerous hypoglycemic (low glucose) episodes. This breakdown is known as hypoglycemia-associated autonomic failure (HAAF), a condition marked by blunted hormonal responses and diminished physical symptoms of low blood sugar. It is commonly referred to as impaired awareness of hypoglycemia (IAH). As HAAF/IAH develops, individuals become less able to recognize and respond to hypoglycemia, leading to progressively more severe and potentially life-threatening episodes.

 

A central question guiding the lab is how adaptations in the brain drive this breakdown in defense. Early work from Dr. McDougal and others revealed that glial cells — long thought to play only a supportive role — actively sense glucose and signal during hypoglycemia. Disruptions in glial metabolism are now linked to the development of HAAF/IAH in both humans and animal models. Building on these insights, his group employs approaches ranging from magnetic resonance spectroscopy (MRS) and live-cell imaging to hyperinsulinemic clamps and transgenic mouse models, seeking to connect mechanistic discoveries with clinical relevance.

 

Nutrition and dietary state have emerged as powerful modifiers of this biology. Dr. McDougal’s lab has shown that caloric restriction and ketogenic diets alter hypoglycemic defenses, and that leptin treatment can restore counterregulation under these nutritional stresses. In metabolically healthy men, a 72-hour fast increased glial acetate metabolism, providing evidence that brain fuel use shifts with diet and may influence hypoglycemia risk. More recently, his team has validated methods using whole-room calorimetry to measure metabolic flexibility after overnight fasting or high-fat meals, offering new ways to link diet, energy balance, and autonomic control.

This nutrition-focused dimension complements the lab’s mechanistic and translational work.

 

Ongoing experiments test whether recurrent hypoglycemia produces a “false starvation” signal by lowering leptin, suppressing normal defenses. At the same time, human studies pair dietary manipulations with advanced metabolic phenotyping to define how the brain interprets changes in fuel availability. Through these integrated efforts, Dr. McDougal is building a unified picture of how brain circuits, glial metabolism, leptin signaling, and nutrition interact to regulate glucose homeostasis. The ultimate goal is to identify therapeutic strategies — informed by diet, lifestyle, and pharmacology — that reduce hypoglycemia risk and improve outcomes for people with diabetes.

Lab: Neurobiology of Metabolic Dysfunction

Selected Publications

  1. McDougal DH, Sanchez-Delgado G, Flanagan EW, Marlatt KL, Sparks JR, Yang S, Redman LM, Ravussin E. Validation of a novel approach to assess metabolic flexibility to a high-fat meal in a whole-body room calorimeter. Obesity (Silver Spring). 2025 Apr;33(4):743-753.  PMID: 40051190.

  2. DuVall MA, Coulter CE, Gosey JL, Herrera MJ, Hill CM, Jariwala RR, Maisano LE, Moldovan LA, Morrison CD, Nwabueze NV, Sikaffy HX, McDougal DH. Leptin treatment prevents impaired hypoglycemic counterregulation induced by exposure to severe caloric restriction or exposure to recurrent hypoglycemia. Auton Neurosci. 2021 Nov;235:102853.  PMC8532139.

  3. Morrison CD, DuVall MA, Hill CM, Spann RA, McDougal DH. Leptin receptor signaling is required for intact hypoglycemic counterregulation: A study in male Zucker rats. J Diabetes Complications. 2021 Oct;35(10):107994 PMCID: PMC8435018.

  4. Morrison CD, Hill CM, DuVall MA, Coulter CE, Gosey JL, Herrera MJ, Maisano LE, Sikaffy HX, McDougal DH. Consuming a ketogenic diet leads to altered hypoglycemic counter-regulation in mice. J Diabetes Complications. 2020 May;34(5):107557.  PMCID: PMC7299499.

  5. McDougal DH, Darpolor MM, DuVall MA, Sutton EF, Morrison CD, Gadde KM, Redman LM, Carmichael OT. Glial acetate metabolism is increased following a 72-h fast in metabolically healthy men and correlates with susceptibility to hypoglycemia. Acta Diabetol. 2018 Oct;55(10):1029-1036.  PMCID: PMC6153507.

  6. McDougal DH, Hermann GE, Rogers RC. Astrocytes in the nucleus of the solitary tract are activated by low glucose or glucoprivation: evidence for glial involvement in glucose homeostasis. Front Neurosci. 2013;7:249.  PMCID: PMC3868892.

  7. McDougal DH, Hermann GE, Rogers RC. Vagal afferent stimulation activates astrocytes in the nucleus of the solitary tract via AMPA receptors: evidence of an atypical neural-glial interaction in the brainstem. J Neurosci. 2011 Sep 28;31(39):14037-45 PMCID: PMC3445261.

NCBI Bibliography