Although not yet completely understood, the<unk>  is thought to be caused by an exaggeration of the normal physiologic hormonal processes that occur overnight. Overnight the human body sees increased levels of several hormones, most notably growth hormone and catecholamines, that lead to increased rates of glucose production and release from the liver. These hormones also inhibit the effects of insulin, leading to an overall increase in circulating blood glucose. This effect is amplified in patients with islet β-cell dysfunction such as diabetics. Notably throughout this process glucagon levels remain unchanged and the increased levels of cortisol observed overnight do not appear to be involved. Observed hyperglycemia secondary to the<unk>  is often defined as an increase in blood glucose of at least >1.1mmol/L (20mg/dL) between the lowest level at night and the highest level before breakfast; however, actual ranges may vary. The physiologic process involved in causing the<unk>  has been shown to occur in most people. In non-diabetic patients there is a modest increase in insulin secretion just before<unk>  which compensates for the increased glucose being released from the liver to prevent hyperglycemia. However, studies have shown that diabetic patients fail to compensate for this transiently increased blood glucose release, resulting in hyperglycemia. This resulting hyperglycemia is clinically relevant in diabetic patients as its lasting effects can lead to overall poor glycemic control. In Type 1 diabetics hyperglycemia due to the<unk>  can persist despite adequate insulin compensation overnight, while in Type 2 diabetics the<unk>  has been shown to be resistant to treatment with both oral medications and diet modifications. An "extended"<unk>  has also been observed in which the abnormal increase in blood glucose levels continues after breakfast. This prolonged duration is thought to be caused by the compounding effects of absorbing and metabolizing breakfast carbohydrates during this period. Both the<unk>  and its extended period have been shown to be significantly more difficult to control when a patient's HbA1c is greater than 7%.
Dawn phenomenon
Ashman phenomenon
Tullio phenomenon
Azzopardi phenomenon
Marcus Gunn phenomenon
Entoptic phenomenon
Inverted binocular phenomenon
Renbök phenomenon