Adiponectin, the past two decades

Wang, Zhao V.; Scherer, Philipp E.

doi:10.1093/jmcb/mjw011

Cited by 481 publications

(461 citation statements)

References 53 publications

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“…One such strategy is to identify pharmacological approaches to increase adiponectin production [283]. In the current report we have investigated the hypothesis that chronic induction of HO-1 will modulate differentiation of human preadipocytes in a manner that results in increased adiponectin production [217,230,239].…”

Section: Discussionmentioning

confidence: 99%

“…The exception to this comes from a study which employed an atypical delivery approach involving intracardial injection of a lentiviral construct (aP2-HO-1) to drive adipocyte-specific overexpression of HO-1 [209]. Notably, this approach resulted in a significant decrease in weight gain with a concomitant reduction in white adipose tissue mass and inflammation [209], factors that are sufficient to increase adiponectin levels [252,283]. It is also worth noting that these observations resemble a scenario of caloric restriction, where adiponectin production from the bone marrow is increased [304].…”

Section: Discussionmentioning

confidence: 99%

“…Adiponectin is an important adipocyte derived hormone or 'adipokine' that exhibits a range of beneficial properties that include anti-inflammatory, cardioprotective and insulin-sensitizing effects to reduce cardiometabolic disease [252,283]. In contrast to most other adipokines circulating levels of adiponectin are reduced in obesity, type 2 diabetes and associated conditions [252,283].…”

Section: Introductionmentioning

confidence: 99%

“…In contrast to most other adipokines circulating levels of adiponectin are reduced in obesity, type 2 diabetes and associated conditions [252,283].…”

Section: Introductionmentioning

confidence: 99%

“…In addition, adiponectin knockout mice or humans with polymorphisms that decrease adiponectin production typically develop cardiometabolic dysfunction and or type 2 diabetes [252,283]. For these reasons, therapeutic strategies to increase the circulating levels of adiponectin are considered attractive.…”

Section: Introductionmentioning

confidence: 99%

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Characterisation of the relationship between Heme-oxygenase-1 and adiponectin

Yang¹

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The prevalence of obesity is growing at an alarming rate worldwide, and current therapies have limited benefits. Therefore, it is essential to increase our understanding of the underlying mechanisms so that new strategies can be developed to reduce the incidence of obesity related diseases. Adiponectin is an adipocyte-derived hormone that regulates glucose and lipid metabolism via direct and indirect mechanisms and has anti-inflammatory, anti-diabetic, anti-atherogenic and cardioprotective properties. Hypoadiponectinemia is implicated in the aetiology of obesity-related diseases making strategies to increase circulating adiponectin levels therapeutically attractive.Emerging evidence, predominantly from preclinical studies, suggests induction of heme-oxygenase-1 (HO-1) increases adiponectin production concomitant with decreased inflammatory tone prompting the proposal of a "HO-1 -adiponectin axis." However, the underlying mechanisms of increased adiponectin production via HO-1 induction are poorly defined; indeed a direct relationship has not been demonstrated. Thus, the overarching aim of this thesis is to investigate the effects of HO-1 induction on adiponectin production as well as adipocyte and adipose tissue remodelling and metabolic parameters using cellular and mouse models.Initial studies were designed to characterize the direct effect of HO-1 induction on adiponectin production. We found that treatment with the widely used HO-1 inducer cobalt protoporphyrin (CoPP) or hemin for 24-48 h increased HO-1 expression and activity without affecting adiponectin expression and secretion, in human mature adipocyte under a variety of experimental scenarios.Treatment of adipocytes with TNFα reduced adiponectin production and induced pro-inflammatory cytokines production. HO-1 induction failed to reverse these effects. These results do not support a direct HO-1 -adiponectin axis.However, literature suggests that chronic induction of HO-1 via CoPP administration throughout differentiation, promotes adiponectin secretion, albeit in the context of reduced adipogenesis. While our previous findings argued against the existence of a direct "HO-1 -adiponectin axis," they did not address the potential effects of chronic induction of HO-1 on adiponectin production. Thus, we extended our study to characterise the effects of chronic HO-1 induction throughout differentiation of human preadipocytes. In this study we demonstrate that chronic induction of HO-1 with CoPP or hemin throughout differentiation results in dose-dependent inhibition of adipogenesis and adiponectin production as well as induction of additional NRF2 target genes. Co-treatment with SnMP (HO-1 activity inhibitor) and HO-1 siRNA did not prevent these effects. These findings suggest that the chronic treatment with CoPP or hemin inhibits adipogenesis and adiponectin production potentially by a HO-1-independent mechanism that may be downstream of NRF2.iii However, our results contradict the majority of reports in the literature. One possibility is that the ...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…In contrast to most other adipokines circulating levels of adiponectin are reduced in obesity, type 2 diabetes and associated conditions [252,283].…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Characterisation of the relationship between Heme-oxygenase-1 and adiponectin

Yang¹

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Leveraging Genetics to Address the Role of GALNT2 on Atherogenic Dyslipidemia

et al. 2023

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Several studies have shown that downregulation of GALNT2 (Polypeptide N‐Acetylgalactosaminyltransferase 2), encoding polypeptide N‐acetylgalactosaminyltransferase 2, decreases high‐density lipoprotein cholesterol (HDL‐C) and increases triglycerides levels by glycosylating key enzymes of lipid metabolism, such as angiopoietin like 3, apolipoprotein C‐III, and phospholipid transfer protein. GALNT2 is also a positive modulator of insulin signaling and action, associated with in vivo insulin sensitivity and during adipogenesis strongly upregulates adiponectin. Thus, the hypothesis that GALNT2 affects HDL‐C and triglycerides levels also through insulin sensitivity and/or circulating adiponectin, is tested. In 881 normoglycemic individuals the G allele of rs4846914 SNP at the GALNT2 locus, known to associate with GALNT2 downregulation, is associated with low HDL‐C and high values of triglycerides, triglycerides/HDL‐C ratio, and theHomeostatic Model Assessment of insulin resistance HOMAIR (p‐values = 0.01, 0.027, 0.002, and 0.016, respectively). Conversely, no association is observed with serum adiponectin levels (p = 0.091). Importantly, HOMAIR significantly mediates a proportion of the genetic association with HDL‐C (21%, 95% CI: 7–35%, p = 0.004) and triglyceride levels (32%, 95% CI: 4–59%, p = 0.023). The results are compatible with the hypothesis that, besides the effect on key lipid metabolism enzymes, GALNT2 alters HDL‐C and triglyceride levels also indirectly through a positive effect on insulin sensitivity.

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The relationship between body mass index and postoperative delirium

et al. 2022

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Purpose:We aimed to investigate the relevance of body mass index (BMI) to postoperative delirium (POD), and to test whether the influences of BMI on POD were mediated by cerebrospinal fluid (CSF) biomarkers.Patients and methods: Our study recruited 682 and 761 cognitively intact individuals from the perioperative neurocognitive disorder risk factor and prognosis (PNDRFAP) study and the perioperative neurocognitive disorder and biomarker lifestyle (PND-ABLE) study, respectively. The incidence of POD was evaluated by using Confusion Assessment Method (CAM), and POD severity was measured by using the Memorial Delirium Assessment Scale (MDAS). Logistic regression was used to analyze the relationship between BMI and POD. The levels of Aβ40, Aβ42, T-tau, and P-tau in preoperative CSF were measured by enzyme-linked immune-sorbent assay (ELISA) in the PND-ABLE study. Mediation analysis with 5000 bootstrapped iterations was used to explore the mediation effects. Results:In the PNDRFAP study, the incidence of POD was 16.3%, with logistic regression analysis showing that BMI (odds ratio [OR] = 0.900, 95% confidence interval [CI] 0.823-0.985, p = .022) is a protective factor of POD. In the PNDABLE study, the incidence of POD was 18.7%, and regression analysis confirmed that BMI (OR = 0.832, 95% CI 0.761-0.910, p < .001) is a protective factor of POD, while T-tau (OR = 1.005, 95% CI 1.003-1.006, p < .001) and P-tau (OR = 1.037, 95% CI 1.024-1.050, p < .001) were risk factors of POD. Mediation analyses revealed that the association between BMI and POD was partially mediated by T-tau (proportion: 36%) and P-tau (proportion: 24%). Conclusion:Higher BMI mediated protective effects on POD through CSF biomarkers (T-tau and P-tau).

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Adiponectin, the past two decades

Cited by 481 publications

References 53 publications

Characterisation of the relationship between Heme-oxygenase-1 and adiponectin

Characterisation of the relationship between Heme-oxygenase-1 and adiponectin

Leveraging Genetics to Address the Role of GALNT2 on Atherogenic Dyslipidemia

The relationship between body mass index and postoperative delirium

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