The details of our described metabolic pathways are inspired heavily by several published scientific papers that give insight into the molecular methods used to study intermittent fasting and its effects on the body.

The first of these papers, Time of feeding and the intrinsic circadian clock drive rhythms in hepatic gene expression (Vollmers, et al., 2009), describes the methods used to study the connections between circadian rhythm, intermittent fasting, and phosphorylation of the CREB protein. This paper was crucial in our understanding of this specific molecular pathway, and clearly demonstrates how time-restricted feeding impacts the regulation of glucose metabolism via the internal clock. The findings and methods used in this study are further described in this section, Circadian Regulation of Hepatic Gene Expression.

The second paper, Reactive oxygen species have a casual role in multiple forms of insulin resistance (Houstis, 2006), demonstrates the connection between oxidative stress and insulin resistance through pro-inflammatory treatments. This paper provided key evidence to understand the Ketone Body Reduction of Oxidative Stress pathway, especially how constant feeding can increase the risk of insulin resistance. The findings and methods used in this study are further described in this section, Insulin Resistance Induced by Oxidative Stress.

The third and final paper, GIP mediates the incretin effect and glucose tolerance by dual actions on α cells and β cells (El, et al., 2021), discusses the communication between alpha and beta cells in the pancreas. This molecular pathway is described in the Glucagon-Mediated Insulin Secretion After Fasting section. Each cell type is responsible for secreting a specific hormone, glucagon and insulin, respectively. Although these hormones are perceived to have adverse effects, the communication between them is essential for maintaining glucose homeostasis. This specific pathway gives evidence that intermittent fasting can impact insulin secretion, to help those with insufficiencies from type II diabetes. The findings and methods used in this study are further described in this section, GIP-Mediated Communication of Pancreatic α-cells and β-cells Leads to Increased Insulin Secretion.