Adiponectin receptor-mediated signaling ameliorates cerebral cell damage and regulates the neurogenesis of neural stem cells at high glucose concentrations: an in vivo and in vitro study

Song, Jeong Sup; Kang, Seung-Gul; Kim, E.; Kim, C. H.; Song, Ho Taek; Lee, Jong Eun

doi:10.1038/cddis.2015.220

Cited by 44 publications

(34 citation statements)

References 136 publications

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“…As expected, AdipoR1 absence followed by APN treatment did not rescue HCT116 cells, suggesting that this interaction is important for promoting IEC survival. These data are in agreement with other cellular stress systems where Adi-poR1 is necessary to reduce cellular damage and apoptosis (34,35). Importantly, it has been recently demonstrated that intracolonic injection of AdipoR1 siRNA worsens colitis in mice, thus reinforcing our observations (36).…”

Section: Discussionsupporting

confidence: 92%

Adiponectin confers protection from acute colitis and restricts a B cell immune response

Obeid

Wankell

Charrez

et al. 2017

Journal of Biological Chemistry

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Adiponectin demonstrates beneficial effects in various metabolic diseases, including diabetes, and in bowel cancer. Recent data also suggest a protective role in colitis. However, the precise molecular mechanisms by which adiponectin and its receptors modulate colitis and the nature of the adaptive immune response in murine models are yet to be elucidated. Adiponectin knock-out mice were orally administered dextran sulfate sodium for 7 days and were compared with wild-type mice. The severity of disease was analyzed histopathologically and through cytokine profiling. HCT116 colonic epithelial cells were employed to analyze the effects of adiponectin and AdipoR1 interactions in colonic injury following dextran sulfate sodium treatment. Adiponectin knock-out mice receiving dextran sulfate sodium exhibited severe colitis, had greater inflammatory cell infiltration, and an increased presence of activated B cells compared with controls. This was accompanied by an exaggerated proinflammatory cytokine profile and increased STAT3 signaling. Adiponectin knock-out mouse colons had markedly reduced proliferation and increased epithelial apoptosis and cellular stress., adiponectin reduced apoptotic, anti-proliferative, and stress signals and restored STAT3 signaling. Following the abrogation of AdipoR1 , these protective effects of adiponectin were abolished. In summary, adiponectin maintains intestinal homeostasis and protects against murine colitis through interactions with its receptor AdipoR1 and by modulating adaptive immunity.

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Section: Discussionsupporting

confidence: 92%

Adiponectin confers protection from acute colitis and restricts a B cell immune response

Obeid

Wankell

Charrez

et al. 2017

Journal of Biological Chemistry

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“…Adiponectin enters the brain from circulation and directly targets neurons (Ng and Chan 2017; Thundyil et al 2012; D. Zhang et al 2016; Zhang et al 2017; Song et al 2015). Its receptors are widely expressed in the dentate gyrus of hippocampus (D.…”

Section: Discussionmentioning

confidence: 99%

“…Given this broad distribution of adiponectin receptors in different brain regions, adiponectin’s role may be broader than the regulation of metabolic homeostasis and could plan an important role in the ‘adipocyte-brain cross-talk’ (Thundyil et al 2012). Adiponectin is involved in neurogenesis, dendritic spine remodeling, hippocampal neural stem cell proliferation and dentate gyrus neuronal excitability (Zhang et al 2017; Ng and Chan 2017; Song et al 2015; D. Zhang et al 2016).…”

Section: Discussionmentioning

confidence: 99%

Cord and Early Childhood Plasma Adiponectin Levels and Autism Risk: A Prospective Birth Cohort Study

Raghavan

Fallin

Hong

et al. 2018

J Autism Dev Disord

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Emerging research suggests that adiponectin, a cytokine produced by adipose tissue, may be implicated in ASD. In this prospective birth cohort study (n = 847), we assessed the association between cord, early childhood plasma adiponectin and the risk of developing ASD. ASD was defined based on ICD codes of physician diagnosis. Cord adiponectin levels were inversely associated with ASD risk (aOR 0.50; 95% CI 0.33, 0.77), independent of preterm birth, early childhood adiponectin and other known ASD risk factors. Early childhood adiponectin, assessed prior to ASD diagnosis, was associated with lower risk of ASD, which attenuated after adjusting for cord adiponectin, indicating the relative importance of cord adiponectin in ASD risk. Further research is warranted to confirm our findings and elucidate biological mechanisms.

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“…Adiponectin also exerts insulin-sensitizing effects in the CNS and, as noted above, adiponectin in the CNS promotes adaptive neuroplasticity. 20 We now know that adiponectin originating in plasma and transported to the cerebrospinal fluid exerts CNS effects, 21 and that adiponectin is also produced locally in the CNS. 6,22 A previous study found that adiponectin levels were reduced around the clock in patients with major depressive disorder (MDD), 23 and pre-clinical data also positively link adiponectin levels to depression.…”

Section: Introductionmentioning

confidence: 99%

The role of adipokines in the rapid antidepressant effects of ketamine

et al. 2016

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We previously found that body mass index (BMI) strongly predicted response to ketamine. Adipokines have a key role in metabolism (including BMI). They directly regulate inflammation and neuroplasticity pathways and also influence insulin sensitivity, bone metabolism and sympathetic outflow; all of these have been implicated in mood disorders. Here, we sought to examine the role of three key adipokines—adiponectin, resistin and leptin—as potential predictors of response to ketamine or as possible transducers of its therapeutic effects. Eighty treatment-resistant subjects who met DSM-IV criteria for either major depressive disorder (MDD) or bipolar disorder I/II and who were currently experiencing a major depressive episode received a single ketamine infusion (0.5 mg kg −1 for 40 min). Plasma adipokine levels were measured at three time points (pre-infusion baseline, 230 min post infusion and day 1 post infusion). Overall improvement and response were assessed using percent change from baseline on the Montgomery–Asberg Depression Rating Scale and the Hamilton Depression Rating Scale. Lower baseline levels of adiponectin significantly predicted ketamine’s antidepressant efficacy, suggesting an adverse metabolic state. Because adiponectin significantly improves insulin sensitivity and has potent anti-inflammatory effects, this finding suggests that specific systemic abnormalities might predict positive response to ketamine. A ketamine-induced decrease in resistin was also observed; because resistin is a potent pro-inflammatory compound, this decrease suggests that ketamine’s anti-inflammatory effects may be transduced, in part, by its impact on resistin. Overall, the findings suggest that adipokines may either predict response to ketamine or have a role in its possible therapeutic effects.

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Adiponectin receptor-mediated signaling ameliorates cerebral cell damage and regulates the neurogenesis of neural stem cells at high glucose concentrations: an in vivo and in vitro study

Cited by 44 publications

References 136 publications

Adiponectin confers protection from acute colitis and restricts a B cell immune response

Adiponectin confers protection from acute colitis and restricts a B cell immune response

Cord and Early Childhood Plasma Adiponectin Levels and Autism Risk: A Prospective Birth Cohort Study

The role of adipokines in the rapid antidepressant effects of ketamine

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