ArticleCell & bioscience2016
Disruption of the Golgi protein Otg1 gene causes defective hormone secretion and aberrant glucose homeostasis in mice.
Article in Cell & bioscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 6 citations in OpenAlex.
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Authors and funding
8 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundConcerted hormone secretion is essential for glucose homeostasis and growth. The oocyte testis gene 1 (Otg1) has limited information in mammals before. Human OTG1 has been identified as an antigen associated with cutaneous T cell lymphoma, while worm Otg1 is recently reported to be a vesicle trafficking regulator in neurons. To understand the physiological role of Otg1 and its potential relation to hormone secretion, we characterized a mutation caused by the piggyBac transposon (PB) insertion in mice.
resultsOocyte testis gene 1 encodes a Golgi localized protein that is expressed with a broad tissue distribution in mice. The PB insertion effectively blocks Otg1 expression, which results in postnatal lethality, growth retardation, hypoglycemia and improved insulin sensitivity in mice. Otg1 mutants exhibit decreased levels of insulin, leptin and growth hormone in the circulation and reduced hepatic IGF-1 expression. Decreased expression of Otg1 in pituitary GH3 cells causes reduced grow hormone expression and secretion, as well as the traffic of the VSVG protein marker.
conclusionsOur data support the hypothesis that Otg1 impacts hormone secretion by regulating vesicle trafficking. These results revealed a previously unknown and important role of Otg1 in hormone secretion and glucose homeostasis in mammals.
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