Possible involvement of endoplasmic reticulum stress in obesity associated with leptin resistance.
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.
Department of Pharmacotherapy, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, Japan.
Toru
T
Hosoi
Koichiro
K
Ozawa
D000818:Animals; D004721:Endoplasmic Reticulum / Q000502:physiology*; D006801:Humans; D053614:Janus Kinase 2 / Q000502:physiology; D020738:Leptin / Q000502:physiology*; D023421:Models, Animal; D009765:Obesity / Q000503:physiopathology*; D050796:STAT3 Transcription Factor / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology; D013312:Stress, Physiological / Q000502:physiology*
D020738:Leptin; D050796:STAT3 Transcription Factor; D053614:Janus Kinase 2