Gender differences in the gene expression profile of adipose tissue in an insulin resistant mouse model (irs2-/-)
Başlık çevirisi mevcut değil.
- Tez No: 912462
- Danışmanlar: Belirtilmemiş.
- Tez Türü: Yüksek Lisans
- Konular: Belirtilmemiş.
- Anahtar Kelimeler: adipose tissue, diabetes, gender, gene expression, irs2
- Yıl: 2019
- Dil: İngilizce
- Üniversite: Universitat de València
- Enstitü: Yurtdışı Enstitü
- Ana Bilim Dalı: Belirtilmemiş.
- Bilim Dalı: Belirtilmemiş.
- Sayfa Sayısı: 60
Özet
Insulin is an essential anabolic hormone involved in cell growth, proliferation, and development. Defects in this hormone production and function lead to diabetes. The insulin receptor substrate-2 (Irs2) coordinates insulin action in pancreatic cell function and peripheral tissues, including as a main target adipose tissue metabolism. Irs2 knockout (Irs2- /-) mouse model has shown to develop type 2 diabetes, thus we decided to investigate adipose tissue of this mouse model at the gene expression level including insulin signaling pathway (Irs1, Irs2, InsR, Igf1, Igf1R) and other signaling pathways that could be affected by Irs2 gene ko including FGF signaling (Fgf7, Fgf21), inflammation and obesity (IL-6, Tgfβ, Opn, Pparγ, Lep, LepR), and the mitochondrial gene Ucp2. Since biological differences between males and females cause changes in body metabolism, especially in the adipose tissue, we decided to include this gender variant, as well as the putative differences between fed and fasting state. In order to conduct a proper gene expression analysis, we selected from four putative genes (Hprt, 18s, Gapdh, and Ubc) the one that better adjusted to a housekeeping reference gene, selecting for further analysis the candidate Hprt. Gene expression studies have revealed a differential profile for male and females in fed conditions in which males were overexpressing Irs2, Igf1R, Lep, Fgf21, and Opn when compared to females, and females were overpressing Irs1, Fgf7, Il6, and LepR when compared to males, in normal condition. When insulin resistance was induced (Irs2-/- ko model), males compensated the absence of Irs2 by overexpressing other ins signaling pathways like Irs1, InsR or Igf1, while females decreased Irs1, Igf1R and Fgf7, Ucp2 and LepR expression, while increased Lep signal. Further, significant differences were observed between fed and fasting state (Irs1, Il6, Lep, LepR). Overall, our results highlight the importance of gender in gene expression analysis, especially in a situation of insulin resistance in order to look for proper markers that could be involved in the diagnosis, clinic, and treatment of type 2 diabetes in the future.
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