The following pathways are three ways in which intermittent fasting contributes to the reduction of Type II Diabetes symptoms on a molecular level.

1. Phosphorylation of cAMP Response Element Binding Protein (CREB)

CREB is a transcription factor that deals with stress responses. In Type II diabetics, patterns of overconsumption lead to persistent phosphorylation of this protein and increased glucose mobilization into the bloodstream. Intermittent fasting improves the circadian rhythm of the phosphorylation of CREB and improves regulation of blood glucose.

2. Ketone Body Reduction of Oxidative Stress

Ketone bodies arise from periods of prolonged fasting and breakdown of fats in the body. In addition to providing energy, these molecules also play a role in fighting oxidative stress that arises from eating . Additionally, insulin resistance is directly improved with reduced oxidative stress.

3. Glucagon-Mediated Insulin Secretion After Fasting

Intermittent fasting impacts the secretion of glucagon and insulin by specified cells in the pancreas. In a fasted state, essential metabolites for gluconeogenesis lead to improved secretion of hormones responsible for glucose metabolism. This pathway describes the effect of intermittent fasting on insulin secretion.