The dawn phenomenon in diabetes: pathophysiology from periphery to central nervous system and circadian rhythm-based therapeutic strategies.

The Dawn Phenomenon (DP) denotes the occurrence of spontaneous early-morning hyperglycemia in the absence of overnight hypoglycemia, or that necessitating an elevation in insulin to sustain normal morning blood glucose levels. Studies exhibit considerable variability, with some indicating that DP is a spontaneous occurrence reported in a substantial percentage of individuals. Patients with DP demonstrate increased average blood glucose variability over a 24-h period compared to those without DP, presenting considerable problems for clinical diabetes pharmacotherapy and nutritional regulation. Moreover, given the ambiguity surrounding the precise pathophysiology and targeted therapies for DP, therapeutic care predominantly emphasizes symptom alleviation. Conventional perspectives ascribe DP to physiological surges in the secretion of counterregulatory hormones, including cortisol, catecholamines, and growth hormone, in the early morning hours. These hormones enhance hepatic glucose production while concurrently diminishing peripheral tissue sensitivity to insulin. This article examines the contemporary pathophysiological underpinnings of DP to offer insights for clinical diagnosis and treatment in diabetes. This article focuses mainly on the dawn phenomenon in type 2 diabetes (T2DM), while evidence related to type 1 diabetes (T1DM) is addressed independently.