Existing epidemiologic and clinical studies have demonstrated that obesity is associated with the risk of a variety of cancers. In recent years, an increasing number of experimental and clinical studies have unraveled the complex relationship between obesity and cancer risk and the underlying mechanisms. Obesity-induced abnormalities in immunity and biochemical metabolism, including chronic inflammation, hormonal disorders, dysregulation of adipokines, and microbial dysbiosis, may be important contributors to cancer development and progression. These contributors play different roles in cancer development and progression at different sites. Lifestyle changes, weight loss medications, and bariatric surgery are key approaches for weight-centered, obesity-related cancer prevention. Treatment of obesity-related inflammation and hormonal or metabolic dysregulation with medications has also shown promise in preventing obesity-related cancers. In this review, we summarize the mechanisms through which obesity affects the risk of cancer at different sites and explore intervention strategies for the prevention of obesity-associated cancers, concluding with unresolved questions and future directions regarding the link between obesity and cancer. The aim is to provide valuable theoretical foundations and insights for the in-depth exploration of the complex relationship between obesity and cancer risk and its clinical applications.
Humans ; Adipokines/metabolism* ; Bariatric Surgery ; Inflammation/therapy* ; Neoplasms/prevention & control* ; Obesity/therapy* ; Risk Factors

Sarcopenia is an age-related disease that mainly involves decreases in muscle mass, muscle strength and muscle function. At the same time, the body fat content increases with aging, especially the visceral fat content. Adipose tissue is an endocrine organ that secretes biologically active factors called adipokines, which act on local and distant tissues. Studies have revealed that some adipokines exert regulatory effects on muscle, such as higher serum leptin levels causing a decrease in muscle function and adiponectin inhibits the transcriptional activity of Forkhead box O3 (FoxO3) by activating peroxisome proliferators-activated receptor-γ coactivator -1α (PGC-1α) and sensitizing cells to insulin, thereby repressing atrophy-related genes (atrogin-1 and muscle RING finger 1 [MuRF1]) to prevent the loss of muscle mass. Here, we describe the effects on muscle of adipokines produced by adipose tissue, such as leptin, adiponectin, resistin, mucin and lipocalin-2, and discuss the importance of these adipokines for understanding the development of sarcopenia.
Humans ; Adipokines ; Leptin ; Adiponectin ; Sarcopenia ; Muscles

OBJECTIVE: To investigate the correlation between expression levels of adipokine and clinicopathological features and prognosis of patients with upper tract urothelial carcinoma (UTUC) based on immunohistochemical staining and bioinformatics analysis. METHODS: The 8 adipokines in this study included adiponectin (AdipoQ), leptin (LEP), interleukin (IL)-6, IL-10 and their receptors (AdipoR1, AdipoR2, LEPR, IL-6R, IL-10RA, IL-10RB). Tissue samples of patients with UTUC who underwent surgical treatment in Peking University People's Hospital from January 2014 to April 2021 were selected for immunohistochemical staining. Their quantitative gene expression data were calculated by H-Score, and relevant clinical and follow-up data were collected retrospectively. Transcription group sequencing data of UTUC patients in Gene Expression Omnibus database (GSE134292 dataset) were downloaded for comparison. Chi-square test or t-test was used to compare the expression level of adipokine between non-muscle invasive group and muscle invasive group. Univariate and multivariate Cox regression analysis and Kaplan-Meier survival curve were utilized to analyze independent predictors of overall survival (OS), disease-free survival (DFS), intravesical recurrence-free survival (IVRFS) in the both cohorts. The P < 0.05 was considered statistically significant. RESULTS: In the study, 63 tissue samples of the patients with UTUC who underwent surgical treatment in Peking University People's Hospital and 57 UTUC patients in GSE134292 dataset were selected. In immunohistochemical cohort, the expressions of AdipoQ (P=0.003 6), AdipoR1 (P=0.006 5), LEP (P=0.007 7), IL-10 (P=0.006 9), and IL-10RA (P=0.008 9) were statistically higher in muscle invasive group. In GSE134292 cohort, the expressions of AdipoR1 (P=0.000 4), AdipoR2 (P=0.000 4), IL-6 (P=0.005 0), IL-10 (P=0.001 7), and IL-10RA (P=0.008 1) were statistically higher in muscle invasive group. Kaplan-Meier survival curve and multivariate Cox regression analysis showed that high IL-10RA expression was an independent predictive factor of IVRFS (P=0.044, HR=0.996, 95%CI: 0.992-0.998) in immunohistochemical cohort, which was confirmed in GSE134292 cohort (P=0.014, HR=0.515, 95%CI: 0.304-0.873). CONCLUSION The expression levels of AdipoQ, AdipoR1, IL-10, and IL-10RA were correlated with tumor stage, suggesting that these adipokines played important roles in tumor progression. IL-10RA was an independent predictor of IVRFS, suggesting that IL-10 and its receptor played a critical role in tumor recurrence.
Adipokines ; Carcinoma, Transitional Cell/surgery* ; Humans ; Interleukin-10 ; Neoplasm Recurrence, Local ; Prognosis ; Retrospective Studies ; Urinary Bladder Neoplasms/surgery* ; Urologic Neoplasms/pathology*

Adipokines,the bioactive polypeptides secreted by adipose tissue,are related to the occurrence and development of obesity,metabolic syndrome,renal insufficiency,cardiovascular disease,diabetes mellitus and other diseases.They may be the disease intervention targets and a breakthrough in the study of disease pathogenesis.In this paper,we summarize the latest research progress of the adipokines omentin,chemerin and nesfatin.
Adipokines ; Adipose Tissue ; Chemokines ; Cytokines ; Humans ; Kidney Diseases ; Metabolic Syndrome ; Obesity

OBJECTIVES: To study the expression of adipokines in children with primary nephrotic syndrome (PNS) before and after treatment and its correlation with blood lipids, as well as the role of adipokines in PNS children with hyperlipidemia. METHODS: A total of 90 children who were diagnosed with incipient PNS or recurrence of PNS after corticosteroid withdrawal for more than 6 months were enrolled as subjects. Thirty children who underwent physical examination were enrolled as the control group. Venous blood samples were collected from the children in the control group and the children with PNS before corticosteroid therapy (active stage) and after urinary protein clearance following 4 weeks of corticosteroid therapy (remission stage). ELISA was used to measure the levels of adipokines. An automatic biochemical analyzer was used to measure blood lipid levels. RESULTS: Compared with the control group, the children with PNS had a significantly lower level of omentin-1 in both active and remission stages, and their level of omentin-1 in the active stage was significantly lower than that in the remission stage ( CONCLUSIONS Omentin-1 may be associated with disease activity, dyslipidemia, and proteinuria in children with PNS. Blood lipid ratios may be more effective than traditional blood lipid parameters in monitoring early cardiovascular risk in children with PNS.
Adipokines ; Chemokines ; Child ; Cytokines/metabolism* ; GPI-Linked Proteins/metabolism* ; Humans ; Hyperlipidemias ; Lectins/metabolism* ; Lipids ; Nephrotic Syndrome/drug therapy* ; Proteinuria

OBJECTIVE: To study the changes in the serum levels of Chemerin and Omentin-1 in children with Kawasaki disease (KD) in the acute stage after intravenous immunoglobulin (IVIG) treatment and related clinical significance. METHODS: A total of 60 children who were diagnosed with KD from January 2015 to April 2019 were enrolled as subjects. Forty healthy children and 40 children with acute infectious diseases were enrolled as the healthy control group and the infection control group respectively. According to the sensitivity to IVIG treatment, the children with KD were divided into an IVIG sensitive group with 51 children and a non-IVIG sensitive group with 9 children. According to the presence or absence of coronary artery lesion, the children with KD were divided into a CAL group with 13 children and a non-CAL group with 47 children. ELISA was used to measure the serum levels of Omentin-1 and Chemerin before and after the treatment. RESULTS: The children with KD had significantly higher serum levels of Chemerin and Omentin-1 than the healthy control and infection control groups before treatment (P<0.05). After 48 hours of treatment, the IVIG sensitive group had a significant reduction in the serum level of Chemerin (P<0.05), while there was no significant change in the serum level of Omentin-1 after treatment (P>0.05). Before treatment, the non-IVIG sensitive group had a significantly higher serum level of Chemerin than the IVIG sensitive group (P<0.05), and the CAL group had a significantly higher serum level of Chemerin than the non-CAL group, while there was no significant difference in the serum level of Omentin-1 between the IVIG sensitive and non-IVIG sensitive groups, as well as between the CAL and non-CAL groups (P>0.05). CONCLUSIONS High serum levels of Chemerin and Omentin-1 may play an important role in the development and progression of KD. Chemerin may be involved in the development of CAL in children with KD. The serum level of Chemerin may be used as a new index for predicting the sensitivity to IVIG treatment.
Adipokines ; Chemokines ; Child ; Coronary Artery Disease ; Humans ; Immunoglobulins, Intravenous ; Mucocutaneous Lymph Node Syndrome

OBJECTIVE: To study the effects of high-fat (HF) diet and exercise on the expressions of asprosin and CTRP6 in adipose tissues in different regions of rats during mid-gestation. METHODS: Pregnant SD rats were fed on a standard chow diet or a high-fat (60% fat content) diet for 14 days starting on gestation day (GD) 1. Starting from GD3, the rats fed either on normal or high-fat diet in the exercise groups (CH-RW and HF-RW groups) were allowed access to the running wheels for voluntary running, and those in sedentary groups (CH-SD and HF-SD groups) remained sedentary. At the end of the 14 days, adipose tissues were sampled from different regions of the rats for detecting the mRNA and protein expressions of asprosin and CTRP6 using RT-qPCR and Western blotting. RESULTS: The mRNA expression of asprosin in retroperitoneal adipose tissues was significantly higher in HF-RW group than in the other 3 groups ( CONCLUSIONS High-fat diet and exercise during mid-gedtation can affect the expression levels of asprosin and CTRP6 in adipose tissues of rats in a site-specific manner.
Adipokines ; Animals ; Blood Glucose ; Diet, High-Fat/adverse effects* ; Female ; Intra-Abdominal Fat ; Pregnancy ; Rats ; Rats, Sprague-Dawley

It is now recognized that the heart can behave as a true endocrine organ, which can modulate the function of other tissues. Emerging evidence has shown that visceral fat is one such distant organ the heart communicates with. In fact, it appears that bi-directional crosstalk between adipose tissue and the myocardium is crucial to maintenance of normal function in both organs. In particular, factors secreted from the heart are now known to influence the metabolic activity of adipose tissue and other organs, as well as modulate the release of metabolic substrates and signaling molecules from the periphery. This review summarizes current knowledge regarding primary cardiokines and adipokines involved in heart-fat crosstalk, as well as implications of their dysregulation for cardiovascular health.
Adipocytes ; Adipokines ; Adipose Tissue ; Heart ; Intra-Abdominal Fat ; Myocardium ; Myocytes, Cardiac

Adipokines/blood* ; Adult ; Biomarkers/blood* ; Humans ; Male ; Middle Aged ; Semen/chemistry* ; Young Adult

Obesity causes inflammation and impairs thermogenic functions in brown adipose tissue (BAT). The adipokine lipocalin 2 (LCN2) has been implicated in inflammation and obesity. Herein, we investigated the protective effects of caloric restriction (CR) on LCN2-mediated inflammation and oxidative stress in the BAT of high-fat diet (HFD)-fed mice. Mice were fed a HFD for 20 weeks and then either continued on the HFD or subjected to CR for the next 12 weeks. CR led to the browning of the white fat-like phenotype in HFD-fed mice. Increased expressions of LCN2 and its receptor in the BAT of HFD-fed mice were significantly attenuated by CR. Additionally, HFD+CR-fed mice had fewer neutrophils and macrophages expressing LCN2 and iron-positive cells than HFD-fed mice. Further, oxidative stress and mitochondrial fission induced by a HFD were also significantly attenuated by CR. Our findings indicate that the protective effects of CR on inflammation and oxidative stress in the BAT of obese mice may be associated with regulation of LCN2.
Adipokines ; Adipose Tissue, Brown ; Animals ; Caloric Restriction ; Diet, High-Fat ; Inflammation ; Lipocalins ; Macrophages ; Mice ; Mice, Obese ; Mitochondrial Dynamics ; Neutrophils ; Obesity ; Oxidative Stress ; Phenotype