Somatostatin inhibits insulin-gene expression through a posttranscriptional mechanism in a hamster islet cell line.
Insulin secretion is regulated by the interplay of nutrients, local intraislet factors, and hormones. Nutrients involved in the positive control of insulin secretion, such as glucose and amino acid, also act on insulin biosynthesis. SRIF is one of the most potent inhibitors of insulin secretion. To determine whether SRIF also regulates insulin biosynthesis, we studied its effects on insulin-gene expression. SRIF decreases steady-state insulin mRNA levels in a clonal hamster islet cell line, HIT-T15, in a dose- and time-dependent manner; this decrease does not occur at the transcriptional level but essentially at a posttranscriptional level. We conclude that SRIF not only modulates insulin secretion but also affects insulin-gene expression.
Philippe
J
J
Department of Genetics and Microbiology, Centre Médical Universitaire, Geneva, Switzerland.
D000818:Animals; D002467:Cell Nucleus / Q000187:drug effects / Q000502:physiology; D006224:Cricetinae; D004305:Dose-Response Relationship, Drug; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects*; D006207:Half-Life; D007328:Insulin / Q000096:biosynthesis / Q000235:genetics*; D007340:Insulinoma; D007700:Kinetics; D010190:Pancreatic Neoplasms; D012323:RNA Processing, Post-Transcriptional / Q000187:drug effects; D012333:RNA, Messenger / Q000378:metabolism*; D013004:Somatostatin / Q000494:pharmacology*; D013997:Time Factors; D014158:Transcription, Genetic / Q000187:drug effects; D014407:Tumor Cells, Cultured
D007328:Insulin; D012333:RNA, Messenger; D013004:Somatostatin