Stress-level glucocorticoids increase fasting hunger and decrease cerebral blood flow in regions regulating eating

• Published in: NeuroImage clinical 2022-01, Vol.36, p.103202-103202, Article 103202
• Main Authors: Bini, Jason, Parikh, Lisa, Lacadie, Cheryl, Hwang, Janice J., Shah, Saloni, Rosenberg, Samuel B., Seo, Dongju, Lam, Katherine, Hamza, Muhammad, De Aguiar, Renata Belfort, Constable, Todd, Sherwin, Robert S., Sinha, Rajita, Jastreboff, Ania M.
• Format: Article
• Language: English
• Subjects: Appetite - physiology; Cerebrovascular Circulation; Cortisol; fMRI; Glucocorticoids; Glucocorticoids - pharmacology; Humans; Hunger; Hunger - physiology; Hydrocortisone; Insulin - metabolism; Magnetic Resonance Imaging; Regular; Stress
• ISSN: 2213-1582; 2213-1582
• DOI: 10.1016/j.nicl.2022.103202

•Does stress-level hydrocortisone administration have effects on metabolic, neural and behavioral factors that could underlie the association between glucocorticoids, appetite and obesity risk?•Hydrocortisone relative to saline significantly decreased whole brain voxel based cerebral blood flow responses in the hypothalamus and related cortico-striatal-limbic regions, while increasing hunger, glucose, insulin and leptin.•Such hydrocortisone-related increases in hunger were predicted by less reduction of CBF in the medial OFC, medial brainstem and thalamus, and several cortical regions.•Increased glucocorticoids at levels of psychological stress, increase hunger and decrease cerebral blood flow in neural regions that regulate food intake. The neural regulation of appetite and energy homeostasis significantly overlaps with the neurobiology of stress. Frequent exposure to repeated acute stressors may cause increased allostatic load and subsequent dysregulation of the cortico-limbic striatal system leading to inefficient integration of postprandial homeostatic and hedonic signals. It is therefore important to understand the neural mechanisms by which stress generates alterations in appetite that may drive weight gain. To determine glucocorticoid effects on metabolic, neural and behavioral factors that may underlie the association between glucocorticoids, appetite and obesity risk. A randomized double-blind cross-over design of overnight infusion of hydrocortisone or saline followed by a fasting morning perfusion magnetic resonance imaging to assess regional cerebral blood flow (CBF) was completed. Visual Analog Scale (VAS) hunger, cortisol and metabolic hormones were also measured. Hydrocortisone relative to saline significantly decreased whole brain voxel based CBF responses in the hypothalamus and related cortico-striatal-limbic regions. Hydrocortisone significantly increased hunger VAS pre-scan, insulin, glucose and leptin, but not other metabolic hormones versus saline CBF groups. Hydrocortisone related increases in hunger were predicted by less reduction of CBF (hydrocortisone minus saline) in the medial OFC, medial brainstem and thalamus, left primary sensory cortex and right superior and medial temporal gyrus. Hunger ratings were also positively associated with plasma insulin on hydrocortisone but not saline day. Increased glucocorticoids at levels akin to those experienced during psychological stress, result in increased fasting hunger and decreased re