Identification of the promoter region required for human adiponectin gene transcription: Association with CCAAT/enhancer binding protein-β and tumor necrosis factor-α

Kita, Atsushi; Yamasaki, Hironori; Kuwahara, Hironaga; Moriuchi, Akira; Fukushima, Keiko; Kobayashi, Masakazu; Fukushima, Tetsuya; Takahashi, Ryoko; Abiru, Norio; Uotani, Shigeo; Kawasaki, Eiji; Eguchi, Katsumi

doi:10.1016/j.bbrc.2005.03.205

Cited by 64 publications

(45 citation statements)

References 30 publications

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“…Furthermore, adiponectin has been shown to suppress cytokine expression as well as cytokine signaling in vitro in both immune and nonimmune cells (52). Conversely, other studies, in addition to ours, show that cytokines inhibit adiponectin transcription and translation (53,54). Importantly, a single high fat meal has been shown to enhance systemic IL-18 and inhibit adiponectin levels in humans (55), and a prolonged high fat diet appears to reduce systemic adiponectin levels and increases pro-inflammatory cytokine levels in mice (56).…”

Section: Il-18 Suppresses Adiponectin Via Nfatc4 Phosphorylationmentioning

confidence: 81%

Interleukin-18 Suppresses Adiponectin Expression in 3T3-L1 Adipocytes via a Novel Signal Transduction Pathway Involving ERK1/2-dependent NFATc4 Phosphorylation

Chandrasekar

Patel

Mummidi

et al. 2008

Journal of Biological Chemistry

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An inverse correlation between the pro-inflammatory cytokine interleukin-18 and the anti-atherogenic adipokine adiponectin has been reported in the chronic pathological conditions obesity, insulin resistance, coronary artery disease, and metabolic syndrome. We investigated whether this relationship is coincidental or has a causal basis. Here we show that interleukin-18 (IL-18) suppresses adiponectin transcription, mRNA expression, and secretion by 3T3-L1 adipocytes. IL-18 suppresses adiponectin promoter-reporter activity, an effect reversed by deletion or mutation of the NFATc4 core DNAbinding site. IL-18 induces NFATc4 phosphorylation (Ser 676 ), nuclear translocation, and in vivo DNA binding. IL-18 induces ERK1/2 phosphorylation and enzyme activity, and pretreatment with the MEK inhibitor U0126, ERK1/2 inhibitor PD98059, or small interference RNA targeted to ERK1/2 attenuates ERK1/2 activation and NFATc4 phosphorylation. Finally, inhibition of ERK1/2 or NFATc4 knockdown reverses IL-18-mediated adiponectin suppression. In contrast to its inhibitory effects on adiponectin expression, IL-18 potently stimulates PAI-1 secretion. These data demonstrate for the first time that IL-18 selectively suppresses adiponectin expression via ERK1/2-dependent NFATc4 activation and suggest that the inverse relationship observed between IL-18 and adiponectin in various chronic pathological conditions is causally related. Thus, targeting IL-18 expression may enhance adiponectin expression and mitigate disease progression.

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Section: Il-18 Suppresses Adiponectin Via Nfatc4 Phosphorylationmentioning

confidence: 81%

Interleukin-18 Suppresses Adiponectin Expression in 3T3-L1 Adipocytes via a Novel Signal Transduction Pathway Involving ERK1/2-dependent NFATc4 Phosphorylation

Chandrasekar

Patel

Mummidi

et al. 2008

Journal of Biological Chemistry

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“…In obese individuals, both circulating levels of adiponectin and its mRNA expression in adipose tissue are markedly decreased compared with healthy subjects (42,43), possibly because hypoxia and inflammatory cytokines suppress adiponectin gene expression in enlarged adipocytes (44). Physical exercise has been shown to enhance adiponectin production by reducing fat mass and inflammation in obese/diabetic patients (12).…”

Section: Discussionmentioning

confidence: 99%

Physical exercise-induced hippocampal neurogenesis and antidepressant effects are mediated by the adipocyte hormone adiponectin

Yau

Li²,

Hoo

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

251

239

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Adiponectin (ADN) is an adipocyte-secreted protein with insulinsensitizing, antidiabetic, antiinflammatory, and antiatherogenic properties. Evidence is also accumulating that ADN has neuroprotective activities, yet the underlying mechanism remains elusive. Here we show that ADN could pass through the bloodbrain barrier, and elevating its levels in the brain increased cell proliferation and decreased depression-like behaviors. ADN deficiency did not reduce the basal hippocampal neurogenesis or neuronal differentiation but diminished the effectiveness of exercise in increasing hippocampal neurogenesis. Furthermore, exerciseinduced reduction in depression-like behaviors was abrogated in ADN-deficient mice, and this impairment in ADN-deficient mice was accompanied by defective running-induced phosphorylation of AMP-activated protein kinase (AMPK) in the hippocampal tissue. In vitro analyses indicated that ADN itself could increase cell proliferation of both hippocampal progenitor cells and Neuro2a neuroblastoma cells. The neurogenic effects of ADN were mediated by the ADN receptor 1 (ADNR1), because siRNA targeting ADNR1, but not ADNR2, inhibited the capacity of ADN to enhance cell proliferation. These data suggest that adiponectin may play a significant role in mediating the effects of exercise on hippocampal neurogenesis and depression, possibly by activation of the ADNR1/AMPK signaling pathways, and also raise the possibility that adiponectin and its agonists may represent a promising therapeutic treatment for depression.adiponectin | adiponectin receptor | physical exercise | hippocampal neurogenesis | depression-like behavior

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“…Deletion of the region where the K11391GOA SNP is located increases the ADIPOQ transcriptional activity, suggesting that the G allele negatively modulates ADIPOQ transcription (40). Additionally, one in vitro transcriptional assay suggested that the rare K11391A allele may directly increase ADIPOQ transcriptional activity (20).…”

Section: Discussionmentioning

confidence: 99%

Adiponectin: serum levels, promoter polymorphism, and associations with birth size and cardiometabolic outcome in young adults born large for gestational age

Bueno

Espineira²,

Fernandes-Rosa³

et al. 2010

European Journal of Endocrinology

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Objective: To assess whether the K11391GOA polymorphism in the regulatory region of the adiponectin gene (ADIPOQ) is associated with birth size, postnatal growth, adiponectinemia, and cardiometabolic risk in adult life. Design: Case-control study nested within a prospective cohort of 2063 community subjects born in 1978/1979 and followed since birth to date. Methods: ADIPOQ K11391GOA genotype-phenotype associations were evaluated in 116 subjects born large for gestational age (LGA) and 392 gender-matched controls at birth (birth size), at 8-10 years (catch-down growth), and at 23-25 years of age (cardiometabolic profile). Results: The K11391A variant allele frequency was higher in LGA subjects (PZ0.04). AA genotype was associated with augmented probability of being born LGA (odds ratioZ4.14; 95% confidence interval: 1.16-16.7; PZ0.03). This polymorphism was associated neither with body composition nor with postnatal growth pattern. At the age of 23-25 years, the K11391A variant allele was associated with higher serum adiponectin levels (GG: 10.7G6.2 versus GA: 12.2G6.5 versus AA: 14.2 G6.8 mg/ml; P!0.01). Subjects born LGA presented higher body mass index (BMI; PZ0.01), abdominal circumference (PZ0.04), blood pressure (PZ0.04), and homeostasis assessment model for insulin resistance (PZ0.01) than adequate for gestational age. Symmetry at birth did not influence these variables. The occurrence of catch-down of weight was associated with lower BMI and abdominal circumference (P!0.001) at 23-25 years. Conclusions: The K11391A ADIPOQ gene variant was associated with increased chance of being born LGA and with higher adiponectin levels in early adult life.

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Identification of the promoter region required for human adiponectin gene transcription: Association with CCAAT/enhancer binding protein-β and tumor necrosis factor-α

Cited by 64 publications

References 30 publications

Interleukin-18 Suppresses Adiponectin Expression in 3T3-L1 Adipocytes via a Novel Signal Transduction Pathway Involving ERK1/2-dependent NFATc4 Phosphorylation

Interleukin-18 Suppresses Adiponectin Expression in 3T3-L1 Adipocytes via a Novel Signal Transduction Pathway Involving ERK1/2-dependent NFATc4 Phosphorylation

Physical exercise-induced hippocampal neurogenesis and antidepressant effects are mediated by the adipocyte hormone adiponectin

Adiponectin: serum levels, promoter polymorphism, and associations with birth size and cardiometabolic outcome in young adults born large for gestational age

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