Palmitate-induced IL6 expression ameliorated by chicoric acid through AMPK and SIRT1-mediated pathway in the PBMCs of newly diagnosed type 2 diabetes patients and healthy subjects

Sadeghabadi, Zahra Arab; Ziamajidi, Nasrin; Abbasalipourkabir, Roghayeh; Mohseni, Roohollah; Borzouei, Shiva

doi:10.1016/j.cyto.2018.12.012

Cited by 20 publications

(9 citation statements)

References 39 publications

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“…AICAR, a pharmacological AMPK activator, increases cellular NAD + levels and SIRT1 activity, whereas SIRT1 deacetylates LKB1, an AMPK kinase, resulting in AMPK phosphorylation . Notably, chicoric acid attenuated palmitate‐induced IL‐6 expression via AMPK and SIRT1‐dependent pathways in peripheral blood mononuclear cells of diabetic subjects . Herein, these data indicate that treatment of hepatocytes with PDX increased SIRT1 expression in a dose‐dependent manner.…”

Section: Discussionmentioning

confidence: 72%

Protectin DX ameliorates palmitate‐induced hepatic insulin resistance through AMPK/SIRT1‐mediated modulation of fetuin‐A and SeP expression

Jung

Ahn

Shin

et al. 2019

Clin Exp Pharma Physio

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The role as well as the molecular mechanisms of protectin DX (PDX) in the prevention of hepatic insulin resistance, a hallmark of type 2 diabetes, remains unknown. Therefore, the present study was designed to explore the direct impact of PDX on insulin resistance and to investigate the expression of fetuin-A and selenoprotein P (SeP), hepatokines that are involved in insulin signalling, in hepatocytes. Human serum levels of PDX as well as fetuin-A and SeP were determined by high-performance liquid chromatography (HPLC). Human primary hepatocytes were treated with palmitate and PDX. NF-κB phosphorylation as well as expression of insulin signalling associated genes and hepatokines were determined by Western blotting analysis.FOXO1 binding levels were measured by quantitative real-time PCR. Selected genes from candidate pathways were evaluated by small interfering (si) RNA-mediated gene suppression. Serum PDX levels were significantly (P < 0.05) downregulated, whereas serum fetuin-A and SeP levels were increased (P < 0.05) in obese subjects compared with healthy subjects. In in vitro experiments, PDX treatment increased AMP-activated protein kinase (AMPK) phosphorylation and SIRT1 expression and attenuated palmitate-induced fetuin-A and SeP expression and insulin resistance in hepatocytes.AMPK or SIRT1 siRNA mitigated the suppressive effects of PDX on palmitate-induced fetuin-A through NF-κB and SeP expression linked to FOXO1 and insulin resistance.Recombinant fetuin-A and SeP reversed the suppressive effects of fetuin-A and SeP expression on palmitate-mediated impairment of insulin signalling. The current finding provides novel insight into the underlying mechanism linking hepatokines to the pathogenesis of hepatic insulin resistance. K E Y W O R D SAMPK, fetuin-A, hepatocytes, protectin DX, selenoprotein P, SIRT1 | 899 JUNG et al.

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Section: Discussionmentioning

confidence: 72%

Protectin DX ameliorates palmitate‐induced hepatic insulin resistance through AMPK/SIRT1‐mediated modulation of fetuin‐A and SeP expression

Jung

Ahn

Shin

et al. 2019

Clin Exp Pharma Physio

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“…The nuclear factor‐κB (NF‐κB) signaling pathway is the major pathway involved in the activation of the inflammation process 44 . NF‐κB is a key transcription factor that is required for induction of a wide array of inflammatory factor genes expression including IL‐6, TNF‐α, and IL‐1β 4,43,45 . A growing body of literature reported that activation of AMPK alleviates NF‐κB activation.…”

Section: Ampk and Inflammationmentioning

confidence: 99%

“…There are many factors related to obesity, for example, AMP‐activated protein kinase (AMPK), silent information regulators (SIRTs), inflammatory mediators, oxidative stress parameters, gastrointestinal hormones, adipokines, angiopoietin‐like proteins (ANGPTLs), and microRNAs (miRNAs) (Figure 1). 4 Changes in obesity‐associated factors during obesity illustrated in Table 1. AMPK has emerged as a key regulator of energy metabolic homeostasis.…”

Section: Introductionmentioning

confidence: 99%

AMP‐activated protein kinase is a key regulator of obesity‐associated factors

Mohseni

Teimouri

Safaei

et al. 2022

Cell Biochemistry & Function

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An imbalance between caloric intake and energy expenditure leads to obesity.Obesity is an important risk factor for the development of several metabolic diseases including insulin resistance, metabolic syndrome, type 2 diabetes mellitus, and cardiovascular disease. So, controlling obesity could be effective in the improvement of obesity-related diseases. Various factors are involved in obesity, such as AMP-activated protein kinases (AMPK), silent information regulators, inflammatory mediators, oxidative stress parameters, gastrointestinal hormones, adipokines, angiopoietin-like proteins, and microRNAs. These factors play an important role in obesity by controlling fat metabolism, energy homeostasis, food intake, and insulin sensitivity. AMPK is a heterotrimeric serine/threonine protein kinase known as a fuel-sensing enzyme. The central role of AMPK in obesity makes it an attractive molecule to target obesity and related metabolic diseases. In this review, the critical

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“…Interestingly, previous studies have shown that SIRT1 played a vital role in influencing immune responses (31), and SIRT1 can regulate immune responses directly through deacetylation of some key transcriptional factors or indirectly through metabolic pathways (32). A recent study found that diabetic patients and obese subjects had higher serum IL-6 but lower SIRT1 levels compared to healthy subjects (33). Further evidence from another recent study also showed SIRT1 agonist resveratrol could significantly inhibit the immune inflammation of the body and improve the dysfunction of glycolipid metabolism (32,34).…”

Section: Introductionmentioning

confidence: 99%

Association Between SIRT1, Cytokines, and Metabolic Syndrome in Schizophrenia Patients With Olanzapine or Clozapine Monotherapy

Fang

Wang

et al. 2020

Front. Psychiatry

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Objective: Previous studies consistently showed the interaction between Sirtuin 1 (SIRT1) and immune inflammation is significantly related to metabolic abnormalities, but their role in the pathogenesis of metabolic syndrome caused by second-generation antipsychotics (SGAs) in schizophrenia patients largely remains unknown. Hence, the present study aimed to fill this gap.Methods: A total of 54 schizophrenia patients with olanzapine or clozapine monotherapy [metabolic syndrome (MetS)/non-MetS patients, 27/27] and 67 healthy subjects were recruited in the present study. The Positive and Negative Syndrome Scale was used, and the plasma levels of SIRT1, interleukin 6 (IL-6), IL-8, IL-10, and tumor necrosis factor α (TNF-α) were measured.Results: The results showed that schizophrenia patients treated with olanzapine or clozapine (both MetS and non-MetS groups) had significantly higher plasma levels of IL-6, IL-10, and TNF-α compared to normal controls (all P < 0.05). Moreover, the MetS patients exhibited markedly lower plasma levels of SIRT1 and higher plasma levels of IL-6 than non-MetS patients and normal controls (all P < 0.05). However, there were no significant differences in IL-8 levels between groups. Our correlation analysis showed that SIRT1 was significantly correlated with diastolic blood pressure, triglyceride, and high-density lipoprotein cholesterol in schizophrenia patients. The stepwise logistic regression analysis further identified the IL-6 × SIRT1 (β = −0.463, t = 10.040, P = 0.002) as the influencing factor for the MetS in the patients.Conclusion: Our preliminary findings suggest that SIRT1 interacted with inflammatory cytokines associated with MetS in schizophrenia patients treated with SGA monotherapy.

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Palmitate-induced IL6 expression ameliorated by chicoric acid through AMPK and SIRT1-mediated pathway in the PBMCs of newly diagnosed type 2 diabetes patients and healthy subjects

Cited by 20 publications

References 39 publications

Protectin DX ameliorates palmitate‐induced hepatic insulin resistance through AMPK/SIRT1‐mediated modulation of fetuin‐A and SeP expression

Protectin DX ameliorates palmitate‐induced hepatic insulin resistance through AMPK/SIRT1‐mediated modulation of fetuin‐A and SeP expression

AMP‐activated protein kinase is a key regulator of obesity‐associated factors

Association Between SIRT1, Cytokines, and Metabolic Syndrome in Schizophrenia Patients With Olanzapine or Clozapine Monotherapy

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