Adipokines and Obesity. Potential Link to Metabolic Disorders and Chronic Complications

Zorena, Katarzyna; Jachimowicz-Duda, Olga; Ślęzak, Daniel; Robakowska, Marlena; Mrugacz, Małgorzata

doi:10.3390/ijms21103570

Cited by 275 publications

(252 citation statements)

References 117 publications

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“…In addition to the raise in cytokine production, obesity is characterized by increased adhesion molecule levels, which, along with the mentioned cytokines, stimulate tissue-specific macrophage recruitment. Such local inflammation eventually induces IR [ 40 ]. Based on the analytical changes in the chemokine, adipokine and cytokine profiles of obese children, Rivera et al developed a diagnostic tool for IR, rendering a sensitivity and specificity of 93.2%, including levels of leptin, triglyceride:HDL-col ratio, insulin-like growth factor-I (IGF-I), TNFα, monocyte chemoattract protein 1 (MCP1) and pro-fibrotic platelet-derived growth factor (PDGF-BB) [ 41 ].…”

Section: Obesity Inflammation and Oxidative Stressmentioning

confidence: 99%

Iron Metabolism in Obesity and Metabolic Syndrome

González-Domínguez

Visiedo-Garcia

Domínguez-Riscart

et al. 2020

IJMS

128

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Obesity is an excessive adipose tissue accumulation that may have detrimental effects on health. Particularly, childhood obesity has become one of the main public health problems in the 21st century, since its prevalence has widely increased in recent years. Childhood obesity is intimately related to the development of several comorbidities such as nonalcoholic fatty liver disease, dyslipidemia, type 2 diabetes mellitus, non-congenital cardiovascular disease, chronic inflammation and anemia, among others. Within this tangled interplay between these comorbidities and associated pathological conditions, obesity has been closely linked to important perturbations in iron metabolism. Iron is the second most abundant metal on Earth, but its bioavailability is hampered by its ability to form highly insoluble oxides, with iron deficiency being the most common nutritional disorder. Although every living organism requires iron, it may also cause toxic oxygen damage by generating oxygen free radicals through the Fenton reaction. Thus, iron homeostasis and metabolism must be tightly regulated in humans at every level (i.e., absorption, storage, transport, recycling). Dysregulation of any step involved in iron metabolism may lead to iron deficiencies and, eventually, to the anemic state related to obesity. In this review article, we summarize the existent evidence on the role of the most recently described components of iron metabolism and their alterations in obesity.

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Section: Obesity Inflammation and Oxidative Stressmentioning

confidence: 99%

Iron Metabolism in Obesity and Metabolic Syndrome

González-Domínguez

Visiedo-Garcia

Domínguez-Riscart

et al. 2020

IJMS

128

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“…Adipose tissue (AT), in addition to its storage functions, is an endocrine tissue that secretes several adipokines and chemokines [ 74 ]. AT also participates in the development of insulin resistance when it is in a state of inflammation known as “low-grade” [ 75 ].…”

Section: S1p Metabolism and Insulin Action: Muscle Liver And Adimentioning

confidence: 99%

Sphingosine-1-Phosphate Metabolism in the Regulation of Obesity/Type 2 Diabetes

Guitton

Bandet

Mariko

et al. 2020

Cells

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Obesity is a pathophysiological condition where excess free fatty acids (FFA) target and promote the dysfunctioning of insulin sensitive tissues and of pancreatic β cells. This leads to the dysregulation of glucose homeostasis, which culminates in the onset of type 2 diabetes (T2D). FFA, which accumulate in these tissues, are metabolized as lipid derivatives such as ceramide, and the ectopic accumulation of the latter has been shown to lead to lipotoxicity. Ceramide is an active lipid that inhibits the insulin signaling pathway as well as inducing pancreatic β cell death. In mammals, ceramide is a key lipid intermediate for sphingolipid metabolism as is sphingosine-1-phosphate (S1P). S1P levels have also been associated with the development of obesity and T2D. In this review, the current knowledge on S1P metabolism in regulating insulin signaling in pancreatic β cell fate and in the regulation of feeding by the hypothalamus in the context of obesity and T2D is summarized. It demonstrates that S1P can display opposite effects on insulin sensitive tissues and pancreatic β cells, which depends on its origin or its degradation pathway.

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“…In a recent study, our group showed an increase in body fat composition after six weeks of therapy using second-generation antipsychotics (SGAs) with a magnitude that depended upon the presence of MetS [ 5 ]. The endocrine functions of adipose tissue are widely known for their ability to produce bioactive peptides and cytokines, or so-called “adipokines,” which regulate metabolism and inflammation and may decrease the insulin sensitivity of tissues [ 6 , 7 , 8 , 9 ]. Chronic, low-grade inflammation during obesity has been established to represent a risk factor for psychiatric disorders [ 10 , 11 ].…”

Section: Introductionmentioning

confidence: 99%

Adipocytokines and Metabolic Syndrome in Patients with Schizophrenia

et al. 2020

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The adipokines leptin, adiponectin, tumor necrosis factor-alpha (TNF-α), and interleukin 6 (IL-6) might be associated with metabolic syndrome (MetS) in patients with schizophrenia. In the present study, we attempted to confirm the results of previous reports and assessed their MetS-related correlation with body fat composition and biochemical parameters. We measured in 46 patients with schizophrenia and MetS serum levels of adiponectin insulin, leptin, TNF-α and IL-6 and compared these levels to those of patients with schizophrenia without MetS. The MetS patients had significantly increased leptin levels and leptin/adiponectin ratios, as well as decreased adiponectin levels. Leptin levels correlated with several metabolic parameters, both in patients with and without MetS, including body fat percentage, total fat fold, and body mass index (BMI). Patients without abnormal MetS components had lower levels of leptin and leptin/adiponectin ratios compared with patients who had one or two MetS components. Leptin/adiponectin ratios were higher in patients who had four rather than three MetS components. Multiple regression analysis revealed multiple associations for leptin but only one for adiponectin, TNF-α, and IL-6. Our results support an important pathophysiological role for leptin more than adiponectin in patients with schizophrenia with MetS.

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Adipokines and Obesity. Potential Link to Metabolic Disorders and Chronic Complications

Cited by 275 publications

References 117 publications

Iron Metabolism in Obesity and Metabolic Syndrome

Iron Metabolism in Obesity and Metabolic Syndrome

Sphingosine-1-Phosphate Metabolism in the Regulation of Obesity/Type 2 Diabetes

Adipocytokines and Metabolic Syndrome in Patients with Schizophrenia

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