Insulin Resistance and Growth Retardation in Mice Lacking Insulin Receptor Substrate‐1 and Identification of Insulin Receptor Substrate‐2

Kadowaki, Takuya; Tamemoto, Hiroyuki; Tobe, K.; Terauchi, Yasuhiro; Ueki, Katsuji; Kaburagi, Yasushi; Yamauchi, Teruaki; Satoh, Shinobu; Sekihara, Hisahiko; Aizawa, Shin-Ichi; Yazaki, Y

doi:10.1002/dme.1996.13.s6.103

Cited by 26 publications

(5 citation statements)

References 7 publications

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“…The treated db/db mice developed overt obesity in the end stage despite nearnormal glucose level and increased insulin secretion, as seen in nondiabetic obesity. 51 On the other hand, systemic delivery of FST driven by ubiquitous promoter (which is out of scope of this manuscript) efficiently improved whole-body insulin sensitivity in addition to overcoming insulin insufficiency in the db/db mice. Future attempts of FST therapy may require ubiquitous expression of FST to overcome insulin insufficiency as well as insulin resistance.…”

Section: Discussionmentioning

confidence: 99%

Overcoming Insulin Insufficiency by Forced Follistatin Expression in β -cells of db/db Mice

et al. 2015

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Diabetes poses a substantial burden to society as it can lead to serious complications and premature death. The number of cases continues to increase worldwide. Two major causes of diabetes are insulin resistance and insulin insufficiency. Currently, there are few antidiabetic drugs available that can preserve or protect β-cell function to overcome insulin insufficiency in diabetes. We describe a therapeutic strategy to preserve β-cell function by overexpression of follistatin (FST) using an AAV vector (AAV8-Ins-FST) in diabetic mouse model. Overexpression of FST in the pancreas of db/db mouse increased β-cell islet mass, decreased fasting glucose level, alleviated diabetic symptoms, and essentially doubled lifespan of the treated mice. The observed islet enlargement was attributed to β-cell proliferation as a result of bioneutralization of myostatin and activin by FST. Overall, our study indicates overexpression of FST in the diabetic pancreas preserves β-cell function by promoting β-cell proliferation, opening up a new therapeutic avenue for the treatment of diabetes.

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Section: Discussionmentioning

confidence: 99%

Overcoming Insulin Insufficiency by Forced Follistatin Expression in β -cells of db/db Mice

et al. 2015

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“…IRS1 is reported to be involved in insulin responses, notably mitogenesis (71). A lack of IRS1 in mice leads to defective reproductive function (72).…”

Section: Discussionmentioning

confidence: 99%

Analysis of circRNA and miRNA expression profiles in IGF3-induced ovarian maturation in spotted scat (Scatophagus argus)

Guo²,

Ndandala³

et al. 2022

Front. Endocrinol.

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Insulin-like growth factor 3 (IGF3) induces ovarian maturation in teleosts; however, research on its molecular regulatory mechanism remains deficient. Circular RNAs (circRNAs) and microRNAs (miRNAs) are involved in various biological processes, including reproduction. In this study, circRNAs and miRNAs involved in IGF3-induced ovarian maturation were evaluated in spotted scat (Scatophagus argus). In ovarian tissues, we identified 176 differentially expressed (DE) circRNAs and 52 DE miRNAs between IGF3 treatment and control groups. Gene Ontology (GO) enrichment analyses showed that host genes of DE circRNAs and target genes of DE miRNAs were enriched for various processes with a high degree of overlap, including cellular process, reproduction, reproductive process, biological adhesion, growth, extracellular region, cell junction, catalytic activity, and transcription factor activity. Enriched Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways included cell adhesion molecules, ECM–receptor interaction, regulation of actin cytoskeleton, focal adhesion, cell cycle, Hedgehog signaling pathway, phosphatidylinositol signaling system, PI3K-Akt signaling pathway, Apelin signaling pathway, Notch signaling pathway, insulin signaling pathway, and Rap1 signaling pathway. A circRNA–miRNA–mRNA regulatory network was constructed, including DE genes involved in reproduction (e.g., oocyte maturation, oocyte meiosis, and ECM remodeling), such as ccnd2, hecw2, dnm2, irs1, adam12, and cdh13. According to the regulatory network and tissue distribution, we identified one circRNA (Lachesis_group5:6245955|6270787) and three miRNAs (novel_miR_622, novel_miR_980, and novel_miR_64) that may exert regulatory effects in IGF3-induced ovarian maturation in S. argus. Taken together, this study provides a novel insight into the molecular mechanisms by which IGF3 functions in ovaries and highlights the effects of circRNAs and miRNAs in reproduction in S. argus.

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“…187 Other IRS molecules may have a negative feedback role in regulating IGF action. 187 Other IRS molecules may have a negative feedback role in regulating IGF action.…”

Section: Igf Receptorsmentioning

confidence: 99%

Disorders of Growth Hormone/Insulin-like Growth Factor Secretion and Action

Rosenfeld¹,

Cohen²

2008

Pediatric Endocrinology

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Insulin Resistance and Growth Retardation in Mice Lacking Insulin Receptor Substrate‐1 and Identification of Insulin Receptor Substrate‐2

Cited by 26 publications

References 7 publications

Overcoming Insulin Insufficiency by Forced Follistatin Expression in β -cells of db/db Mice

Overcoming Insulin Insufficiency by Forced Follistatin Expression in β -cells of db/db Mice

Analysis of circRNA and miRNA expression profiles in IGF3-induced ovarian maturation in spotted scat (Scatophagus argus)

Disorders of Growth Hormone/Insulin-like Growth Factor Secretion and Action

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