IGF-I downregulates resistin gene expression and protein secretion

Chen, Yen Hang; Hung, Pei Fang; Kao, Ying-Jer

doi:10.1152/ajpendo.00325.2004

Cited by 35 publications

(38 citation statements)

References 52 publications

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“…It has been shown that insulin upgrades leptin expression (Barr et al 1997) and downgrades resistin expression (Haugen et al 2001, Shojima et al 2002, Chen et al 2005. But the acute effects we observed are likely resulting from facilitation of regulated vesicular secretion of pre-stored adipokines instead of increased protein synthesis.…”

Section: Discussionmentioning

confidence: 69%

Vesicular storage, vesicle trafficking, and secretion of leptin and resistin: the similarities, differences, and interplays

Ye¹,

Than²,

Zhao³

et al. 2010

Journal of Endocrinology

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Adipose tissue is a highly active endocrine organ secreting a variety of signaling molecules called adipokines. Leptin and resistin are two adipokines critically involved in metabolic homeostasis. Nevertheless, the secretory pathways of these adipokines and their interplays are poorly elucidated. In this work, we have comparatively studied several key aspects of leptin and resistin secretion from 3T3-L1 adipocytes. It was found that leptin and resistin molecules are compartmentalized into different secretory vesicles. The trafficking of leptin and resistin vesicles, and the secretion of leptin and resistin are oppositely regulated by insulin/glycolytic substrates and cAMP/protein kinase A. Interestingly, these two adipokines adversely influence each other on secretion and vesicle trafficking. Finally, we demonstrated that both leptin and resistin secretion are Ca 2C dependent.

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Section: Discussionmentioning

confidence: 69%

Vesicular storage, vesicle trafficking, and secretion of leptin and resistin: the similarities, differences, and interplays

Ye¹,

Than²,

Zhao³

et al. 2010

Journal of Endocrinology

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“…The medium was then changed to DMEM containing 10% FBS for an additional 6 -10 days (replaced every other day). With this protocol, Ͼ90% adipocyte differentiation was achieved, as indicated by phenotypic appearance and triglyceride accumulation (10). Differentiated adipocytes expressed more Rstn mRNA than did preadipocytes or differentiating preadipocytes (10,44).…”

Section: Methodsmentioning

confidence: 99%

“…Acti-D (5 g/ml) and CHX (5 g/ml) were used to block transcriptional and translational activities, respectively (10,22). In experiments, 3T3-L1 adipocytes were pretreated with and without either Acti-D for 30 min or CHX for 90 min.…”

Section: Methodsmentioning

confidence: 99%

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Inhibitory effect of green tea (−)-epigallocatechin gallate on resistin gene expression in 3T3-L1 adipocytes depends on the ERK pathway

Liu

Chen

Hung

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

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is known as an adipocyte-specific secretory hormone that can cause insulin resistance and decrease adipocyte differentiation. By contrast, green tea catechins, especially (Ϫ)-epigallocatechin gallate (EGCG), have been reported as body weight and diabetes chemopreventatives. Whether EGCG regulates production of Rstn is unknown. Using 3T3-L1 adipocytes, we found that EGCG at 20 and 100 M suppressed Rstn mRNA levels by ϳ35 and 50%, respectively, after 3 h. The basal half-life of Rstn mRNA induced by actinomycin D was Ͼ12 h but shifted to 3 h in the presence of EGCG. This suggests that EGCG regulates the stability of Rstn mRNA. Treatment with cycloheximide did not prevent EGCGsuppressed Rstn mRNA levels, which suggests that the effect of EGCG does not require new protein synthesis. Intracellular Rstn protein significantly decreased in the presence of 100 M EGCG 3 h after treatment, whereas the release of the Rstn protein did not significantly change. This suggests that EGCG may modulate the distribution of Rstn protein between the intracellular and extracellular compartments. EGCG did not affect the amounts of extracellular signal-related kinase-1/2 (ERK1/2), phospho-JNK, phospho-p38, and phospho-Akt proteins but reduced the amounts of phospho-ERK1/2 proteins. Overexpression with MEK1 blocked EGCG-inhibited Rstn mRNA expression. These data suggest that EGCG downregulates Rstn expression via a pathway that is dependent on the ERK pathway.genistein; mitogen-activated protein kinase; extracellular signal-related kinase RESISTIN (RSTN) IS A CYSTEINE-RICH POLYPEPTIDE HORMONE (20,38) that, depending on the species, contains 4 -5 exons, 3-4 introns, 575-1217 bp of mRNA, and 108 -114 amino acids of protein (10 -12.5 kDa) (16,23,44,45). Rstn is first isolated from adipose tissues and found to link obesity to type 2 diabetes (44). In particular, Rstn mRNA expression in adipose tissues of obese humans is higher than that in normal subjects (12). In addition, a single nucleotide polymorphism in the Rstn gene promoter is associated with obesity (14) and diabetes (35), and the plasma Rstn levels are elevated in patients with obesity (12) and type 2 diabetes (59). Moreover, the dominant negative form of Rstn enhances adipogenesis and improves insulin sensitivity (24). Ever since its discovery, Rstn also has been found to possess numerous other actions. For example, Rstn regulates fasted blood glucose (6), causes dyslipidemia (39), suppresses insulin-stimulated glucose uptake in adipocytes (44) and muscle cells (30), inhibits dopamine and norepinephrine release in the hypothalamus (8), and promotes endothelial cell activation (50) and smooth muscle proliferation (9). To our knowledge, the expression of Rstn gene can be regulated by nutritional, endocrine, genetic, pharmacological, and developmental factors (5), and the mechanisms of action of Rstn are emerging. For example, Rstn promotes smooth muscle cell proliferation through the activation of extracellular signalregulated kinase (ERK1/2) and phosphatidylinositol 3-kinase (PI3K) ...

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“…In addition, treatment with resistin causes glucose intolerance (10). Resistin is regulated by cytokines, including endothelin, insulin, insulin-like growth factors and peroxisome proliferator-activated receptor γ (11,12). In rodents, resistin is located within adipocytes, while human resistin is primarily expressed in macrophages and neutrophils (13)(14)(15).…”

Section: Introductionmentioning

confidence: 99%

Resistin-induced cardiomyocyte hypertrophy is inhibited by apelin through the inactivation of extracellular signal-regulated kinase signaling pathway in H9c2 embryonic rat cardiomyocytes

et al. 2016

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Abstract. It has been reported that resistin induces, whereas apelin inhibits cardiac hypertrophy. However, the underlying molecular mechanisms of apelin inhibiting resistin-induced cardiac hypertrophy remain unclear. The aim of the current study is to investigate the effects of apelin on resistin-induced cardiomyocyte hypertrophy and elucidate the underlying molecular mechanism. H9c2 cells were used in the present study, and cell surface area and protein synthesis were evaluated. Reverse transcription-quantitative polymerase chain reaction was performed to analyze the expression levels of hypertrophic markers, brain natriuretic peptide (BNP) and β-myosin heavy chain (β-MHC). In addition, western blotting was conducted to examine phosphorylation of extracellular signal-regulated kinase (ERK)1/2. Following treatment of H9c2 cells with resistin, cell surface area, protein synthesis, and BNP and β-MHC mRNA expression levels were increased. Subsequent to co-treatment of H9c2 cells with apelin and resistin, lead to the inhibition of resistin-induced hypertrophic effects by apelin. In addition, treatment with resistin increased phosphorylation of ERK1/2, whereas pretreatment with apelin decreased phosphorylation of ERK1/2, which was increased by resistin. These results indicate that resistin-induced cardiac hypertrophy is inhibited by apelin via inactivation of ERK1/2 cell signaling.

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IGF-I downregulates resistin gene expression and protein secretion

Abstract: Chen, Yen-Hang, Pei-Fang Hung, and Yung-Hsi Kao. IGF-I downregulates resistin gene expression and protein secretion.

Cited by 35 publications

References 52 publications

Vesicular storage, vesicle trafficking, and secretion of leptin and resistin: the similarities, differences, and interplays

Vesicular storage, vesicle trafficking, and secretion of leptin and resistin: the similarities, differences, and interplays

Inhibitory effect of green tea (−)-epigallocatechin gallate on resistin gene expression in 3T3-L1 adipocytes depends on the ERK pathway

Resistin-induced cardiomyocyte hypertrophy is inhibited by apelin through the inactivation of extracellular signal-regulated kinase signaling pathway in H9c2 embryonic rat cardiomyocytes

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