Exendin-4, a GLP-1 receptor agonist, directly induces adiponectin expression through protein kinase A pathway and prevents inflammatory adipokine expression

Chung, Le Thi Kim; Hosaka, Toshio; Yoshida, Masaki; Harada, Nagakatsu; Sakaue, Hiroshi; Sakai, Tohru; Nakaya, Yutaka

doi:10.1016/j.bbrc.2009.10.015

Cited by 129 publications

(95 citation statements)

References 38 publications

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“…Furthermore, this study showed that BPA caused a decrease in plasma adiponectin and increase in plasma leptin, while exendin-4 maintained these hormones at similar levels to control. This finding is in agreement with previous findings, which showed exendin-4 through direct effect on GLP-1 receptors and protein kinase A (PKA) pathway, increased adiponectin level (24,25). The current experiment was consistent with that of Shabani et al (2015), which revealed that reduced leptin is associated with decrease in blood glucose (26).…”

Section: Discussionsupporting

confidence: 94%

Alteration Effect of Exendin-4 on Oxidative Stress and Metabolic Disorders Induced by Bisphenol A in Adult Male Mice

Ahangarpour

Afshari

Mard

et al. 2016

Jentashapir J Health Res

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Section: Discussionsupporting

confidence: 94%

Alteration Effect of Exendin-4 on Oxidative Stress and Metabolic Disorders Induced by Bisphenol A in Adult Male Mice

Ahangarpour

Afshari

Mard

et al. 2016

Jentashapir J Health Res

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“…To explore the effect of exendin-4 on inflammatory adipokines, the expression of IL-6 in 3T3-L1 adipocytes was examined by quantitative real-time RT-PCR. The results illustrated that exendin-4 decreased the level of IL-6 mRNA in 3T3-L1 adipocytes [64] . The levels of the pro-inflammatory cytokines IL-6 (P < 0.01), IL-12p70 (P < 0.01), and IL-1β (P < 0.05) were reduced in the brains of animals treated with liraglutide for 30 d [65] .…”

Section: Effects Of Glp-1ras On Fibrosis and Cell Deathmentioning

confidence: 78%

“…GLP-1 infusion in patients with T2DM was associated with a significant reduction in circulating IL-6 at 120 min and at 180 min (P = 0.0001 and P = 0.001) [63] . Ex-4 decreased the mRNA levels of inflammatory adipokines [64] . Chen [59] treated female SD rats with exendin-4 for 9 wk, and the results revealed that the expression level of IL-6 mRNA was reduced in the liver of the mice.…”

Section: Effects Of Glp-1ras On Fibrosis and Cell Deathmentioning

confidence: 94%

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Effects of glucagon-like peptide-1 receptor agonists on non-alcoholic fatty liver disease and inflammation

Wang¹

2014

WJG

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Glucagon-like peptide1 (GLP-1) is secreted from Langerhans cells in response to oral nutrient intake. Glucagon-like peptide-1 receptor agonists (GLP-1RAs) are a new class of incretin-based anti-diabetic drugs. They function to stimulate insulin secretion while suppressing glucagon secretion. GLP-1-based therapies are now well established in the management of type 2 diabetes mellitus (T2DM), and recent literature has suggested potential applications of these drugs in the treatment of obesity and for protection against cardiovascular and neurological diseases. As we know, along with change in lifestyles, the prevalence of non-alcoholic fatty liver disease (NAFLD) in China is rising more than that of viral hepatitis and alcoholic fatty liver disease, and NAFLD has become the most common chronic liver disease in recent years. Recent studies further suggest that GLP1RAs can reduce transaminase levels to improve NAFLD by improving blood lipid levels, cutting down the fat REVIEW 14821October 28, 2014|Volume 20|Issue 40| WJG|www.wjgnet.com content to promote fat redistribution, directly decreasing fatty degeneration of the liver, reducing the degree of liver fibrosis and improving inflammation. This review shows the NAFLD-associated effects of GLP-1RAs in animal models and in patients with T2DM or obesity who are participants in clinical trials.

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“…Further studies on mechanisms by which GLP-1 improves insulin sensitivity have shown that treatment of 3T3-L1 adipocytes with exendin-4, a GLP-1 receptor agonist, increases insulin-stimulated glucose uptake [13] and amplifies insulin signalling by upregulating basal insulin receptor, IRS-1 and GLUT4 abundance [14]. It has also been reported that exendin-4 increases adiponectin levels and prevents inflammatory adipokine production in 3T3-L1 adipocytes [15]. However, it is not known whether GLP-1 plays any role in adipose tissue inflammation, including ATM.…”

Section: Introductionmentioning

confidence: 99%

Glucagon-like peptide-1 inhibits adipose tissue macrophage infiltration and inflammation in an obese mouse model of diabetes

et al. 2012

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Aims/hypothesis Obesity and insulin resistance are associated with low-grade chronic inflammation. Glucagon-like peptide-1 (GLP-1) is known to reduce insulin resistance. We investigated whether GLP-1 has anti-inflammatory effects on adipose tissue, including adipocytes and adipose tissue macrophages (ATM). Methods We administered a recombinant adenovirus (rAd) producing GLP-1 (rAd-GLP-1) to an ob/ob mouse model of diabetes. We examined insulin sensitivity, body fat mass, the infiltration of ATM and metabolic profiles. We analysed the mRNA expression of inflammatory cytokines, lipogenic genes, and M1 and M2 macrophage-specific genes in adipose tissue by real-time quantitative PCR. We also examined the activation of nuclear factor κB (NF-κB), extracellular signalregulated kinase 1/2 and Jun N-terminal kinase (JNK) in vivo and in vitro. Results Fat mass, adipocyte size and mRNA expression of lipogenic genes were significantly reduced in adipose tissue of rAd-GLP-1-treated ob/ob mice. Macrophage populations (F4/80 + and F4/80 + CD11b + CD11c + cells), as well as the expression and production of IL-6, TNF-α and monocyte chemoattractant protein-1, were significantly reduced in adipose tissue of rAd-GLP-1-treated ob/ob mice. Expression of M1-specific mRNAs was significantly reduced, but that of M2-specific mRNAs was unchanged in rAd-GLP-1-treated ob/ob mice. NF-κB and JNK activation was significantly reduced in adipose tissue of rAd-GLP-1-treated ob/ob mice. Lipopolysaccharide-induced inflammation was reduced by the GLP-1 receptor agonist, exendin-4, in 3T3-L1 adipocytes and ATM. Conclusions/interpretation We suggest that GLP-1 reduces macrophage infiltration and directly inhibits inflammatory pathways in adipocytes and ATM, possibly contributing to the improvement of insulin sensitivity.

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Exendin-4, a GLP-1 receptor agonist, directly induces adiponectin expression through protein kinase A pathway and prevents inflammatory adipokine expression

Cited by 129 publications

References 38 publications

Alteration Effect of Exendin-4 on Oxidative Stress and Metabolic Disorders Induced by Bisphenol A in Adult Male Mice

Alteration Effect of Exendin-4 on Oxidative Stress and Metabolic Disorders Induced by Bisphenol A in Adult Male Mice

Effects of glucagon-like peptide-1 receptor agonists on non-alcoholic fatty liver disease and inflammation

Glucagon-like peptide-1 inhibits adipose tissue macrophage infiltration and inflammation in an obese mouse model of diabetes

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