Gene expression profiling in rat pancreas after ventromedial hypothalamic lesioning

• Published in: Pancreas Vol. 39; no. 5; pp. 627 - 632
• Main Authors: Kiba, Takayoshi, Kintaka, Yuri, Suzuki, Yoko, Ishizuka, Noriko, Ishigaki, Yasuhito, Inoue, Shuji
• Format: Journal Article
• Language: English
• Published: United States 01-07-2010
• Subjects: Animals; Apelin Receptors; Cell Proliferation; Down-Regulation; Female; Gene Expression Profiling; Pancreas - innervation; Pancreas - metabolism; Rats; Rats, Sprague-Dawley; Receptors, G-Protein-Coupled - genetics; Ventromedial Hypothalamic Nucleus - injuries; Ventromedial Hypothalamic Nucleus - physiology
• ISSN: 0885-3177; 1536-4828
• DOI: 10.1097/mpa.0b013e3181c52bc5

We previously reported that vagal hyperactivity produced by ventromedial hypothalamic (VMH) lesions stimulated cell proliferation of rat pancreatic islet B and acinar cells primarily through a cholinergic receptor mechanism.
This study examined how gene families involved in cell proliferation are regulated after VMH lesions formation. Total pancreatic RNA was extracted, and differences in the gene expression profiles between rats at day 3 after VMH lesioning and sham-VMH-lesioned rats were investigated using DNA microarray and real-time polymerase chain reaction.
The VMH lesions regulated the genes that are involved in functions related to cellular growth and proliferation and neuronal development in the pancreas. Real-time polymerase chain reaction also confirmed that gene expressions of angiotensin II receptor-like 1 (AGTRL1) and proline rich 15 (PRR15) were down-regulated at day 3 after the VMH lesions.
Ventromedial hypothalamic lesions may change the expression of cell proliferation-related genes and neuron-related genes in a rat pancreas.