The Roles and Associated Mechanisms of Adipokines in Development of Metabolic Syndrome

Kim, Ji Eun; Kim, Jin-Sun; Jo, Min-Jee; Cho, Eun Jung; Ahn, S.T.; Kwon, Youngjoo; Ko, Gang Jee

doi:10.3390/molecules27020334

Cited by 85 publications

(70 citation statements)

References 173 publications

(182 reference statements)

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“…Conventional CV risk factors appear to be the major contributors to the higher carotid IMT and lower FMD in our SpA sample. The association between conventional CV risk factors and subclinical atherosclerosis in SpA could be linked through adipokines, which take part in both metabolic syndrome 51 and accelerated atherosclerosis in SpA. 32 35 52 The role of adipokines, metabolic syndrome-related biomarkers and biomarkers of endothelial cell activation and inflammation was shown to be relevant in both SpA.…”

Section: Discussionmentioning

confidence: 99%

Endothelial dysfunction and increased carotid intima–media thickness in patients with spondyloarthritis without traditional cardiovascular risk factors

et al. 2022

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BackgroundThe aim of our study was to assess subclinical atherosclerosis in spondyloarthritis (SpA) by combining three ultrasound methods (flow-mediated dilation (FMD), carotid intima–media thickness (cIMT) and Ankle Brachial Index (ABI)) and to determine the predictive factors of theses parameters.MethodsThis was a case control study conducted over 12 months including 47 patients with SpA-free-cardiovascular (CV) disease in comparison with age and sex matched 47 healthy controls. Sociodemographic, clinical and biological features as well as therapeutic modalities were recorded in our patients. All subjects had Doppler ultrasound with measurement of cIMT, FMD and ABI. Ultrasound measurements were compared between patients and controls. Linear regression was performed and assessed by machine learning to determine the predictive models of markers of subclinical atherosclerosis.ResultsWe found higher cIMT (p<0.0001), lower FMD (p=0.008) and higher left ABI (0.048) in patients with SpA compared with controls. cIMT was positively correlated to patient-related parameters (age, systolic blood pressure) and disease parameters (age at onset of SpA, disease duration and renal involvement). Biologically, cIMT was positively correlated with creatinine, blood-glocose, total cholesterol (CT) and CT/cholesterol-high density lipoprotein ratio. FMD was negatively correlated with male gender, age, systolic blood pressure, creatinine, blood glucose and Left Lequesne Index. ABI was significantly associated with diastolic blood pressure. Multiple regression analysis identified age, CT and creatinine as independents predictive factors for increased cIMT. Regarding endothelial dysfunction, blood glucose and Left Lequesne Index were the independents predictive factors of decreased FMD.ConclusionOur study supported the accelerated subclinical atherosclerosis in patients with SpA. This subclinical atherosclerosis was mainly mediated by traditional CV risk factors.

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Section: Discussionmentioning

confidence: 99%

Endothelial dysfunction and increased carotid intima–media thickness in patients with spondyloarthritis without traditional cardiovascular risk factors

et al. 2022

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“…Although numerous animal studies considering neuregulin-4 (NRG4) have been performed, there are limited data in humans. NRG4 is known to serve as a one of the factors improving insulin sensitivity [ 135 ], protecting the liver from fatty liver disease (FLD) [ 131 ] and its low circulating level may potentially serve as a risk factor for gestational diabetes mellitus [ 136 ]; however, the NRG4–PCOS relationship is poorly represented in the literature.…”

Section: Neuregulin-4mentioning

confidence: 99%

Review of Novel Potential Insulin Resistance Biomarkers in PCOS Patients—The Debate Is Still Open

Kruszewska

Laudy-Wiaderny²,

Kunicki

2022

IJERPH

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Research on proteins and peptides that play roles in metabolic regulation, which may be considered potential insulin resistance markers in some medical conditions, such as diabetes mellitus, obesity and polycystic ovarian syndrome (PCOS), has recently gained in interest. PCOS is a common endocrine disorder associated with hyperandrogenemia and failure of ovulation, which is often accompanied by metabolic abnormalities, including obesity, dyslipidemia, hyperinsulinemia, and insulin resistance. In this review, we focus on less commonly known peptides/proteins and investigate their role as potential biomarkers for insulin resistance in females affected by PCOS. We summarize studies comparing the serum fasting concentration of particular agents in PCOS individuals and healthy controls. Based on our analysis, we propose that, in the majority of studies, the levels of nesfastin-1, myonectin, omentin, neudesin were decreased in PCOS patients, while the levels of the other considered agents (e.g., preptin, gremlin-1, neuregulin-4, xenopsin-related peptide, xenin-25, and galectin-3) were increased. However, there also exist studies presenting contrary results; in particular, most data existing for lipocalin-2 are inconsistent. Therefore, further research is required to confirm those hypotheses, as well as to elucidate the involvement of these factors in PCOS-related metabolic complications.

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“…Adipose tissue is now recognized as a highly metabolic organ involved in the regulation of vital physiological functions [54,55]. AT dysfunction has been implicated in systemic metabolic disorders both as a cause and a consequence.…”

Section: Adipose Tissue: An Endocrine Organ Involved In Mo-offspring'...mentioning

confidence: 99%

“…AT dysfunction has been implicated in systemic metabolic disorders both as a cause and a consequence. However, fat distribution is a more powerful indicator of obesity risk and associated comorbidities than whole-adiposity [54].…”

Section: Adipose Tissue: An Endocrine Organ Involved In Mo-offspring'...mentioning

confidence: 99%

The Endocrine–Metabolic Axis Regulation in Offspring Exposed to Maternal Obesity—Cause or Consequence in Metabolic Disease Programming?

et al. 2022

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Obesity incidence is rising worldwide, including women of reproductive age, contributing to increased gestations in which Maternal Obesity (MO) occurs. Offspring born to obese mothers present an increased predisposition to develop metabolic (e.g., obesity, diabetes) and cardiovascular disease (CVD). The developmental programming of the metabolic dysfunction in MO offspring can initiate in utero. The different availability of metabolic substrates, namely glucose, can modulate cellular growth, proliferation, and differentiation, resulting in different levels of tissue maturation and function. We defined the remodelling of these early processes as the first hit of metabolic disease programming. Among these, adipocyte early differentiation and gut dysbiosis are initial repercussions occurring in MO offspring, contributing to -tissue-specific dysfunction. The second hit of disease programming can be related to the endocrine–metabolic axis dysregulation. The endocrine–metabolic axis consists of multi-organ communication through the release of factors that are able to regulate the metabolic fate of cells of organs involved in physiological metabolic homeostasis. Upon adipose tissue and gut early dysregulation, these organs’ endocrine function can be programmed to the disrupted release of multiple factors (e.g., adiponectin, leptin, glucagon-like peptide). This can be perceived as a natural mechanism to overcome metabolic frailty in an attempt to prevent or postpone organ-specific disease. However, the action of these hormones on other tissues may potentiate metabolic dysfunction or even trigger disease in organs (liver, pancreas, heart) that were also programmed in utero for early disease. A second phase of the endocrine–metabolic dysregulation happens when the affected organs (e.g., liver and pancreas) self-produce an endocrine response, affecting all of the involved tissues and resulting in a new balance of the endocrine–metabolic axis. Altogether, the second hit exacerbates the organ-specific susceptibility to disease due to the new metabolic environment. The developmental programming of the endocrine–metabolic axis can start a vicious cycle of metabolic adaptations due to the release of factors, leading to an endocrine response that can jeopardize the organism’s function. Diseases programmed by MO can be boosted by endocrine dysregulation, namely Non-Alcoholic Fatty Liver Disease, Non-Alcoholic Fatty Pancreas Disease, and the aggravation of the adipose tissue and gut dysfunction. Chronic metabolic dysregulation can also predispose MO offspring to CVD through the modulation of the endocrine environment and/or the metabolic status. To cease the vicious cycle of MO disease transmission among generations and-provide preventive and specialized prenatal and postnatal care to MO offspring, it is necessary to understand the molecular mechanisms underlying the MO-related disease development. In this review, we summarize most of the developmental programming molecular events of the endocrine–metabolic axis described on the offspring exposed to MO, providing a brief overview of the potential mechanisms that predispose MO offspring to metabolic disease, and discuss the programming of the endocrine–metabolic axis as a plausible mechanism for metabolic disease predisposition in MO offspring.

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The Roles and Associated Mechanisms of Adipokines in Development of Metabolic Syndrome

Cited by 85 publications

References 173 publications

Endothelial dysfunction and increased carotid intima–media thickness in patients with spondyloarthritis without traditional cardiovascular risk factors

Endothelial dysfunction and increased carotid intima–media thickness in patients with spondyloarthritis without traditional cardiovascular risk factors

Review of Novel Potential Insulin Resistance Biomarkers in PCOS Patients—The Debate Is Still Open

The Endocrine–Metabolic Axis Regulation in Offspring Exposed to Maternal Obesity—Cause or Consequence in Metabolic Disease Programming?

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