The Neglected Insulin: IGF-II, a Metabolic Regulator with Implications for Diabetes, Obesity, and Cancer
When originally discovered, one of the initial observations was that, when all of the insulin peptide was depleted from serum, the vast majority of the insulin activity remained and this was due to a single additional peptide, IGF-II. The IGF-II gene is adjacent to the insulin gene, which is a resul...
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| Published in: | Cells (Basel, Switzerland) Vol. 8; no. 10; p. 1207 |
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| Main Authors: | , , |
| Format: | Journal Article |
| Language: | English |
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| ISSN: | 2073-4409, 2073-4409 |
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| Abstract | When originally discovered, one of the initial observations was that, when all of the insulin peptide was depleted from serum, the vast majority of the insulin activity remained and this was due to a single additional peptide, IGF-II. The IGF-II gene is adjacent to the insulin gene, which is a result of gene duplication, but has evolved to be considerably more complicated. It was one of the first genes recognised to be imprinted and expressed in a parent-of-origin specific manner. The gene codes for IGF-II mRNA, but, in addition, also codes for antisense RNA, long non-coding RNA, and several micro RNA. Recent evidence suggests that each of these have important independent roles in metabolic regulation. It has also become clear that an alternatively spliced form of the insulin receptor may be the principle IGF-II receptor. These recent discoveries have important implications for metabolic disorders and also for cancer, for which there is renewed acknowledgement of the importance of metabolic reprogramming. |
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| AbstractList | When originally discovered, one of the initial observations was that, when all of the insulin peptide was depleted from serum, the vast majority of the insulin activity remained and this was due to a single additional peptide, IGF-II. The IGF-II gene is adjacent to the insulin gene, which is a result of gene duplication, but has evolved to be considerably more complicated. It was one of the first genes recognised to be imprinted and expressed in a parent-of-origin specific manner. The gene codes for IGF-II mRNA, but, in addition, also codes for antisense RNA, long non-coding RNA, and several micro RNA. Recent evidence suggests that each of these have important independent roles in metabolic regulation. It has also become clear that an alternatively spliced form of the insulin receptor may be the principle IGF-II receptor. These recent discoveries have important implications for metabolic disorders and also for cancer, for which there is renewed acknowledgement of the importance of metabolic reprogramming.When originally discovered, one of the initial observations was that, when all of the insulin peptide was depleted from serum, the vast majority of the insulin activity remained and this was due to a single additional peptide, IGF-II. The IGF-II gene is adjacent to the insulin gene, which is a result of gene duplication, but has evolved to be considerably more complicated. It was one of the first genes recognised to be imprinted and expressed in a parent-of-origin specific manner. The gene codes for IGF-II mRNA, but, in addition, also codes for antisense RNA, long non-coding RNA, and several micro RNA. Recent evidence suggests that each of these have important independent roles in metabolic regulation. It has also become clear that an alternatively spliced form of the insulin receptor may be the principle IGF-II receptor. These recent discoveries have important implications for metabolic disorders and also for cancer, for which there is renewed acknowledgement of the importance of metabolic reprogramming. When originally discovered, one of the initial observations was that, when all of the insulin peptide was depleted from serum, the vast majority of the insulin activity remained and this was due to a single additional peptide, IGF-II. The IGF-II gene is adjacent to the insulin gene, which is a result of gene duplication, but has evolved to be considerably more complicated. It was one of the first genes recognised to be imprinted and expressed in a parent-of-origin specific manner. The gene codes for IGF-II mRNA, but, in addition, also codes for antisense RNA, long non-coding RNA, and several micro RNA. Recent evidence suggests that each of these have important independent roles in metabolic regulation. It has also become clear that an alternatively spliced form of the insulin receptor may be the principle IGF-II receptor. These recent discoveries have important implications for metabolic disorders and also for cancer, for which there is renewed acknowledgement of the importance of metabolic reprogramming. |
| Author | Holly, Jeff M. P. Perks, Claire M. Biernacka, Kalina |
| AuthorAffiliation | Department of Translational Health Science, Bristol Medical School, Faculty of Health Sciences, University of Bristol, Learning & Research Building, Southmead Hospital, Bristol BS10 5NB, UK; mdxkz@bristol.ac.uk (K.B.); claire.m.perks@bristol.ac.uk (C.M.P.) |
| AuthorAffiliation_xml | – name: Department of Translational Health Science, Bristol Medical School, Faculty of Health Sciences, University of Bristol, Learning & Research Building, Southmead Hospital, Bristol BS10 5NB, UK; mdxkz@bristol.ac.uk (K.B.); claire.m.perks@bristol.ac.uk (C.M.P.) |
| Author_xml | – sequence: 1 givenname: Jeff M. P. surname: Holly fullname: Holly, Jeff M. P. – sequence: 2 givenname: Kalina surname: Biernacka fullname: Biernacka, Kalina – sequence: 3 givenname: Claire M. surname: Perks fullname: Perks, Claire M. |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31590432$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Alternative splicing Amino acids Antisense RNA cancer Chromosomes Diabetes Diabetes mellitus Gene duplication Gene loci Hypoglycemia igf-ii Insulin Insulin-like growth factor II Insulin-like growth factors Metabolic disorders Metabolism mRNA Non-coding RNA obesity Peptides Physiology Review Tumors |
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