FIGURE 3.

Dim ALAN abolishes the rhythm of glucose and changes the expression of genes involved in glucose uptake and processing. Rats were kept either in the standard LD regime (CTRL; grey) or exposed to dim light at night (ALAN; blue) for 2 weeks. Plasma levels of insulin (A) and glucose (B). Hepatic glycogen concentration (C). Scheme of glucose metabolism in the hepatocyte (D). Glucose enters a hepatocyte via glucose transporter 2 (GLUT2) and subsequently is processed by glucokinase (GCK) which results in glucose-6-phosphate (G-6-P). G-6-P can be stored as glycogen or processed in the glycolysis and pentose phosphate pathway. Gluconeogenesis in the liver is regulated by forkhead box protein 1 (FOXO1) which is under the control of metabolic sensors. Glycogen phosphorylase L (the liver form, PYGL) releases glucose-1-phosphate from glycogen stores. Relative mRNA expression of Glut2, Gck, Foxo1, and Pygl in the liver (E–H). Relative mRNA levels of Glut4 in the adipose tissue (I). Grey area indicates the dark/dim light phase. Data represent mean ± SEM with n = 5–6 per group. Solid lines indicate the significant daily rhythms (p < 0.05) and dashed lines show rhythms with a trend to significance (p-value between 0.05 and 0.1). Missing lines represent non-significant 24-h rhythm. Significant changes in amplitude (A) and acrophase (φ) revealed by Wald tests are specified by **p < 0.01 and # a trend to significance (p-value between 0.05 and 0.1).