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Deletion of hypoxia-inducible factor-1α in adipocytes enhances glucagon-like peptide-1 secretion and reduces adipose tissue inflammation

Yoshitaka Kihira ; Mariko Miyake ; Manami Hirata ; Yoji Hoshina ; Kana Kato ; Hitoshi Shirakawa ; Hiroshi Sakaue ; Noriko Yamano ; Yuki Izawa-Ishizawa ; Keisuke Ishizawa ; Yasumasa Ikeda ; Koichiro Tsuchiya ; Toshiaki Tamaki ; Shuhei Tomita

PloS one, 01 January 2014, Vol.9(4), p.e93856 [Tạp chí có phản biện]

E-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0093856

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  • Nhan đề:
    Deletion of hypoxia-inducible factor-1α in adipocytes enhances glucagon-like peptide-1 secretion and reduces adipose tissue inflammation
  • Tác giả: Yoshitaka Kihira ; Mariko Miyake ; Manami Hirata ; Yoji Hoshina ; Kana Kato ; Hitoshi Shirakawa ; Hiroshi Sakaue ; Noriko Yamano ; Yuki Izawa-Ishizawa ; Keisuke Ishizawa ; Yasumasa Ikeda ; Koichiro Tsuchiya ; Toshiaki Tamaki ; Shuhei Tomita
  • Chủ đề: Sciences (General)
  • Là 1 phần của: PloS one, 01 January 2014, Vol.9(4), p.e93856
  • Mô tả: It is known that obese adipose tissues are hypoxic and express hypoxia-inducible factor (HIF)-1α. Although some studies have shown that the expression of HIF-1α in adipocytes induces glucose intolerance, the mechanisms are still not clear. In this study, we examined its effects on the development of type 2 diabetes by using adipocyte-specific HIF-1α knockout (ahKO) mice. ahKO mice showed improved glucose tolerance compared with wild type (WT) mice. Macrophage infiltration and mRNA levels of monocyte chemotactic protein-1 (MCP-1) and tumor necrosis factor α (TNFα) were decreased in the epididymal adipose tissues of high fat diet induced obese ahKO mice. The results indicated that the obesity-induced adipose tissue inflammation was suppressed in ahKO mice. In addition, in the ahKO mice, serum insulin levels were increased under the free-feeding but not the fasting condition, indicating that postprandial insulin secretion was enhanced. Serum glucagon-like peptide-1 (GLP-1) levels...
  • Ngôn ngữ: English
  • Số nhận dạng: E-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0093856

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