Blog
About

6
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Possible involvement of endoplasmic reticulum stress in obesity associated with leptin resistance.

      The journal of medical investigation : JMI

      Animals, physiology, Stress, Physiological, Signal Transduction, STAT3 Transcription Factor, physiopathology, Obesity, Models, Animal, Leptin, Janus Kinase 2, Humans, Endoplasmic Reticulum

      Read this article at

      ScienceOpenPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Leptin is a hormone, which plays a central role in inhibiting food intake and body weight gain. Leptin is secreted from exocrine as well as endocrine cells. Circulating leptin activates JAK-STAT tyrosine kinases through Ob-Rb leptin receptor in the hypothalamus and brain stem. In recent years, "leptin resistance" has been considered to be one of the main causes of obesity. However, the detailed mechanisms of leptin resistance are not well understood. Recently, we hypothesized possibility that endoplasmic reticulum (ER) stress is involved in leptin resistance. In the present manuscript, we would like to mention possible mechanisms of ER stress-induced leptin resistance and possible implication in obesity. In addition, pathophysiological role of leptin's action in regulating endocrine as well as exocrine functions at the state of ER stress are discussed.

          Related collections

          Author and article information

          Journal
          20224207

          Comments

          Comment on this article