For example, the hormone leptin circulates throughout the body, gauging fat deposition and docking onto neurons to convey that the body has adequate food.
If, for example, the hormone auxin is prevented, by experimental means, from influencing the plant, the plant lives longer than normal and undergoes an atypical prolonged pattern of senescent change.
For example, the hormone prolactin increases synthesis of milk proteins in tissue by causing a twofold rise in the rate of mRNA synthesis; but it also causes a 17-fold rise in mRNA lifetime, so that in this case the main cause of increased protein synthesis is the prolonged availability of mRNA.
In voles, for example, the hormone is key to attachment behavior: Males with higher levels of oxytocin are more likely to be faithful to their mates.
For example, the hormone level of androstane-3 α-17 β-diol glucuronide, an index of 5 α-reductase activity, and IGF-binding protein-3, which modulates the effect of IGF-1, differs according to ethnicity (Platz et al, 1999; Wu et al, 2001).
For example, the hormone changes during pregnancy and the postpartum period are thought to underlie improved cognitive abilities, with reproductive experience enhancing spatial memory (reviewed in Kinsley et al. 1999), as well as other hippocampal functions (reviewed in Galea et al. 2014).
For example, the steroid hormone receptors family of TFs (NR5A1, NR4A1, and NR5A2) regulated the steroid hormone biosynthesis pathway (pathway: 00140, Figure 6(b)).
It has become obvious that many of the hormones previously ascribed only to vertebrates are secreted by invertebrates as well (for example, the pancreatic hormone insulin).
For example, the steroid hormone estradiol may enhance LTP by driving CREB phosphorylation and subsequent dendritic spine growth.
For example, the pancreatic hormone glucagon activates the CREB-mediated gluconeogenetic program in the liver in response to a low glucose level during fasting.
For example, the incretin hormone glucagon-like peptide-1 (GLP-1) is secreted in a taste receptor-dependent manner by gut enteroendocrine L cells in response to stimulation with natural and artificial sweeteners [15].
