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PloS One 2024Body mass index (BMI) is inversely proportional with adiponectin levels among adults, while insulin, C-reactive protein (CRP), interleukin 6 (IL-6), resistin and tumor...
BACKGROUND AND OBJECTIVES
Body mass index (BMI) is inversely proportional with adiponectin levels among adults, while insulin, C-reactive protein (CRP), interleukin 6 (IL-6), resistin and tumor necrosis factor-alpha (TNF-α) have been linked with elevated BMI. The role and relation of these biomarkers with BMI among a Hispanic pediatric population are less known. Thus, the objective of this study was to examine the association of inflammatory markers with the odds of overweight/obesity while controlling for several sociodemographic factors among a Hispanic youth population in Northeast Tennessee.
METHODS
Height, weight, demographic information, and blood samples were collected from 107 Hispanic children aged 2 to 10 years recruited at a large community health center in 2015-2016 in Northeast Tennessee. Data for this research were accessed and analyzed in 2022. Multivariable logistic regression was conducted to assess the relations between adiponectin, insulin, resistin, CRP, TNF-α, and IL-6, and overweight/obesity vs. having a healthy (normal) weight.
RESULTS
Adiponectin levels were significantly lower among overweight/obese Hispanic children (p = 0.0144) compared to healthy weight children. The odds of overweight/obesity decreased by 4% for every one-unit increase in serum adiponectin. Insulin levels were significantly higher among overweight/obese Hispanic children compared to healthy weight children (p = 0.0048). The odds of overweight/obesity increased by 7% for every one-unit increase in serum insulin. Resistin, IL-6, TNF-α, and CRP were not significantly associated with overweight/obesity in this population.
CONCLUSION
Adiponectin behaves similarly in Hispanic youth as it does in other pediatric populations, possibly making it a valuable marker when examining metabolic health status in this population.
Topics: Humans; Child; Body Mass Index; Male; Female; Hispanic or Latino; Child, Preschool; Biomarkers; Adiponectin; C-Reactive Protein; Interleukin-6; Resistin; Insulin; Tumor Necrosis Factor-alpha; Inflammation; Pediatric Obesity; Overweight; Tennessee
PubMed: 38941300
DOI: 10.1371/journal.pone.0289523 -
International Journal of Oncology Aug 2024Obesity is a chronic disease caused by the accumulation of excessive adipose tissue. This disorder is characterized by chronic low‑grade inflammation, which promotes... (Review)
Review
Obesity is a chronic disease caused by the accumulation of excessive adipose tissue. This disorder is characterized by chronic low‑grade inflammation, which promotes the release of proinflammatory mediators, including cytokines, chemokines and leptin. Simultaneously, chronic inflammation can predispose to cancer development, progression and metastasis. Proinflammatory molecules are involved in the recruitment of specific cell populations in the tumor microenvironment. These cell populations include myeloid‑derived suppressor cells (MDSCs), a heterogeneous, immature myeloid population with immunosuppressive abilities. Obesity‑associated MDSCs have been linked with tumor dissemination, progression and poor clinical outcomes. A comprehensive literature review was conducted to assess the impact of obesity‑associated MDSCs on cancer in both preclinical models and oncological patients with obesity. A secondary objective was to examine the key role that leptin, the most important proinflammatory mediator released by adipocytes, plays in MDSC‑driven immunosuppression Finally, an overview is provided of the different therapeutic approaches available to target MDSCs in the context of obesity‑related cancer.
Topics: Humans; Myeloid-Derived Suppressor Cells; Obesity; Neoplasms; Tumor Microenvironment; Disease Progression; Animals; Leptin; Inflammation
PubMed: 38940351
DOI: 10.3892/ijo.2024.5667 -
Frontiers in Bioscience (Landmark... Jun 2024This study aimed to elucidate the molecular mechanism through which C1q/tumor necrosis factor (TNF)-related protein 9 (CTRP9) acts in the formation and differentiation...
BACKGROUND
This study aimed to elucidate the molecular mechanism through which C1q/tumor necrosis factor (TNF)-related protein 9 (CTRP9) acts in the formation and differentiation of brown adipose tissue (BAT).
METHODS
Adenovirus particles encoding CTRP9 and green fluorescent protein were inoculated into the scapula of C57BL/6J mice and fed a high-fat diet for 8 weeks; the body weight, lipid droplet morphology, glucose tolerance, insulin tolerance, and protein expression levels were analyzed. In addition, CTRP9 adenovirus was transfected into brown preadipocytes, and differentiation was induced to identify the effect of CTRP9 overexpression on adipocyte differentiation.
RESULTS
CTRP9 overexpression significantly increased the weight gain of mice. Additionally, the CTRP9 overexpression group exhibited significantly increased adipose tissue weight and glucose clearance rates and decreased insulin sensitivity and serum triglyceride levels compared to the control group. Furthermore, CTRP9 overexpression significantly upregulated the adipose triglyceride lipase (ATGL) and perilipin 1 protein expression levels in BAT. The cell experiment results confirmed that CTRP9 overexpression significantly inhibited the adipogenesis of brown adipocytes as evidenced by the downregulation of uncoupling protein 1, beta-3 adrenergic receptor, ATGL, and hormone-sensitive lipase mRNA levels and the significant suppression of uncoupling protein 1, ATGL, and perilipin 1 protein levels in brown adipocytes.
CONCLUSIONS
The finding of this study demonstrated that CTRP9 promotes lipolysis by upregulating ATGL expression and inhibits the differentiation of brown preadipocytes .
Topics: Animals; Lipolysis; Diet, High-Fat; Adipose Tissue, Brown; Mice, Inbred C57BL; Male; Mice; Adiponectin; Insulin Resistance; Lipase; Cell Differentiation; Adipogenesis; Perilipin-1; Acyltransferases; Glycoproteins
PubMed: 38940054
DOI: 10.31083/j.fbl2906236 -
Frontiers in Bioscience (Landmark... May 2024Polycystic ovary syndrome (PCOS) is a prevalent reproductive, endocrine, and metabolic disease that affects 5-18% of women worldwide, with a rising incidence.... (Review)
Review
Polycystic ovary syndrome (PCOS) is a prevalent reproductive, endocrine, and metabolic disease that affects 5-18% of women worldwide, with a rising incidence. Hyperandrogenemia and insulin resistance are two key pathophysiological factors that contribute to PCOS, both of which contribute to a variety of health issues such as menstrual irregularities, obesity, dysfunctional glucose and lipid homeostasis, infertility, mental disorders, and cardiovascular and cerebrovascular diseases. Despite ongoing studies, the origin and pathogenesis of PCOS remain elusive; there is also a clinical need for simpler, more effective, longer lasting, and more comprehensive treatments for women with PCOS. The gut-fat axis, a critical regulatory route for metabolism, endocrine function, and immune response, has received considerable interest in recent years in the research of the etiology and treatment of metabolic illnesses such as type 2 diabetes mellitus and non-alcoholic fatty liver disease. The latest research in PCOS has revealed significant alterations in the homogeneity and phylogenetic diversity of the gut microbiota. Animal research using fecal microbiota transplantation has confirmed the importance of gut microbiota in regulating insulin sensitivity and sex hormone balance in PCOS. Furthermore, studies have shown a decrease in the volume and/or activity of brown adipose tissue (BAT) in PCOS patients, a change that alters adipokine release, leading to insulin resistance and hyperandrogenemia, aggravating PCOS progression. Given the function of BAT in increasing energy expenditure and alleviating metabolic parameters, efforts to activate BAT or induce browning of white adipose tissue have emerged as possible treatments for PCOS. Recent research has suggested that the gut microbiota can influence BAT creation and activity via metabolites such as short-chain fatty acids and bile acids, as well as the gut-brain axis. Cold exposure, healthy dieting, metformin, bariatric surgery, glucagon-like peptide 1 receptor agonists and melatonin have all been shown in basic and clinical studies to modulate BAT activity by influencing the gut microbiota, demonstrating significant clinical potential. However, more studies into the regulation mechanisms of the gut-BAT axis are required to produce more effective, comfortable, and safe tailored therapeutics for PCOS.
Topics: Polycystic Ovary Syndrome; Humans; Female; Gastrointestinal Microbiome; Adipose Tissue, Brown; Animals; Insulin Resistance; Fecal Microbiota Transplantation; Obesity
PubMed: 38940030
DOI: 10.31083/j.fbl2906208 -
Sheng Li Xue Bao : [Acta Physiologica... Jun 2024As a multifunctional adipokine, chemerin plays a crucial role in various pathophysiological processes through endocrine and paracrine manner. It can bind to three known... (Review)
Review
As a multifunctional adipokine, chemerin plays a crucial role in various pathophysiological processes through endocrine and paracrine manner. It can bind to three known receptors (ChemR23, GPR1 and CCRL2) and participate in energy metabolism, glucose and lipid metabolism, and inflammation, especially in metabolic diseases. Polycystic ovary syndrome (PCOS) is one of the most common endocrine diseases, which seriously affects the normal life of women of childbearing age. Patients with PCOS have significantly increased serum levels of chemerin and high expression of chemerin in their ovaries. More and more studies have shown that chemerin is involved in the occurrence and development of PCOS by affecting obesity, insulin resistance, hyperandrogenism, oxidative stress and inflammatory response. This article mainly reviews the production, subtypes, function and receptors of chemerin protein, summarizes and discusses the research status of chemerin protein in PCOS from the perspectives of metabolism, reproduction and inflammation, and provides theoretical basis and reference for the clinical diagnosis and treatment of PCOS.
Topics: Polycystic Ovary Syndrome; Humans; Chemokines; Female; Intercellular Signaling Peptides and Proteins; Receptors, Chemokine; Insulin Resistance; Animals; Receptors, G-Protein-Coupled; Chemotactic Factors
PubMed: 38939937
DOI: No ID Found -
Scientific Reports Jun 2024A rise in bone turnover markers (BTM) after bariatric surgery predicts poor bone health years later. This study explored factors associated with BTM and changes in BTM...
A rise in bone turnover markers (BTM) after bariatric surgery predicts poor bone health years later. This study explored factors associated with BTM and changes in BTM after bariatric surgery. Inclusion criteria were subjects 18 to 65 years of age with morbid obesity undergoing bariatric surgery. All data were measured before and 6 and 12 months after surgery. The study included 104 subjects: women/men: 83/21; mean age 43.1 (SD 8.4) years; BMI: 38.8 kg/m (SD 3.8). Surgery with Roux-en-Y gastric bypass (RYGB) and sleeve gastrectomy (SG) was performed in 84 (81%) and 20 (19%) subjects, respectively. From before to 6-12 months after surgery, procollagen type 1 N-terminal propeptid (P1NP) increased by 45.6 µg/L (95% CI 41.5-50.0, p < 0.001), and alkaline phosphatase (ALP) by 10 U/L (95% CI 7-14, p < 0.001). The increases were significantly larger after RYGB than after SG. The APOE- Ɛ3 allele was associated with low levels of BTM and high levels of leptin. There was an unfavourable increase in BTM after bariatric surgery. SG compared to RYGB and the presence of the APOE-Ɛ3 allele were associated with less unfavourable effects. The study emphasises the importance of optimal prophylactic interventions after bariatric surgery to prevent osteoporosis.
Topics: Humans; Female; Male; Adult; Middle Aged; Bone Remodeling; Biomarkers; Bariatric Surgery; Obesity, Morbid; Peptide Fragments; Procollagen; Gastrectomy; Gastric Bypass; Alkaline Phosphatase; Leptin; Aged; Adolescent
PubMed: 38937532
DOI: 10.1038/s41598-024-65952-y -
Life Sciences Jun 2024Chronic kidney disease (CKD) represents a significant and escalating global health challenge, with morbidity and mortality rates rising steadily. Evidence increasingly... (Review)
Review
Chronic kidney disease (CKD) represents a significant and escalating global health challenge, with morbidity and mortality rates rising steadily. Evidence increasingly implicates perirenal adipose tissue (PRAT) deposition as a contributing factor in the pathogenesis of CKD. This review explores how PRAT deposition may exert deleterious effects on renal structure and function. The anatomical proximity of PRAT to the kidneys not only potentially causes mechanical compression but also leads to the dysregulated secretion of adipokines and inflammatory mediators, such as adiponectin, leptin, visfatin, tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and exosomes. Additionally, PRAT deposition may contribute to renal lipotoxicity through elevated levels of free fatty acids (FFA), triglycerides (TAG), diacylglycerol (DAG), and ceramides (Cer). PRAT deposition is also linked to the hyperactivation of the renin-angiotensin-aldosterone system (RAAS), which further exacerbates CKD progression. Recognizing PRAT deposition as an independent risk factor for CKD underscores the potential of targeting PRAT as a novel strategy for the prevention and management of CKD. This review further discusses interventions that could include measuring PRAT thickness to establish a baseline, managing metabolic risk factors that promote its deposition, and inhibiting key PRAT-induced signaling pathways.
PubMed: 38936605
DOI: 10.1016/j.lfs.2024.122866 -
Endocrinology May 2024
Correction to: "Liver-Specific GH Receptor Gene-Disrupted (LiGHRKO) Mice Have Decreased Endocrine IGF-I, Increased Local IGF-I, and Altered Body Size, Body Composition, and Adipokine Profiles".
Topics: Animals; Mice; Insulin-Like Growth Factor I; Liver; Adipokines; Body Composition; Mice, Knockout; Receptors, Somatotropin; Body Size
PubMed: 38935339
DOI: 10.1210/endocr/bqae065 -
Frontiers in Nutrition 2024Intermittent fasting (IF) and exercise training (Exe) have been evaluated in several studies for improving cardiometabolic biomarkers related to weight loss. However,...
Effects of intermittent fasting combined with exercise on serum leptin and adiponectin in adults with or without obesity: a systematic review and meta-analysis of randomized clinical trials.
CONTEXT
Intermittent fasting (IF) and exercise training (Exe) have been evaluated in several studies for improving cardiometabolic biomarkers related to weight loss. However, further investigation is required to understand the potential effects on leptin and adiponectin concentrations. IF protocols have been shown to be efficient in improving adipokines, but further research is required to determine whether or not IF regimens combined with Exe are superior to Exe alone.
OBJECTIVE
The aim of this study was to determine whether or not interventions combining IF plus Exe are more effective than Exe only for improving serum leptin and adiponectin in adults with and without obesity.
DATA EXTRACTION
A systematic review and meta-analysis was performed by searching PubMed, Scopus, and Web of Science databases up to August 2023 for randomized clinical trials that determined the effects of IF plus Exe vs. Exe alone (control) on body weight, serum leptin, and serum adiponectin. Analyses were conducted for IF plus Exe vs. Exe alone to calculate weighted mean differences (WMD) and standardized mean differences (SMD).
ANALYSIS
The current meta-analysis included 6 studies with a total sample of 153 participants, with intervention durations ranging from three days to 52 weeks. IF plus Exe elicited significantly larger decreases in leptin levels [SMD = -0.47, = 0.03], which were accompanied by weight loss [WMD = -1.25 kg, = 0.05], as compared with exercise-only interventions, but adiponectin did not differ between the two [SMD = 0.02, = 0.9].
CONCLUSION
IF combined with Exe reduced leptin significantly, but did not change adiponectin levels, when compared to exercise only. Perhaps these reductions in leptin levels may have been associated with weight loss; however, due to the small number of included studies and the high heterogeneity in the weight loss outcomes, this result is uncertain.
SYSTEMATIC REVIEW REGISTRATION
https://www.crd.york.ac.uk/prospero/, identifier CRD42023460735.
PubMed: 38933888
DOI: 10.3389/fnut.2024.1362731 -
Frontiers in Immunology 2024Air pollution is an urgent concern linked to numerous health problems in low- and middle-income countries, where 92% of air pollution-related deaths occur. Particulate... (Review)
Review
Air pollution is an urgent concern linked to numerous health problems in low- and middle-income countries, where 92% of air pollution-related deaths occur. Particulate matter 2.5 (PM) is the most harmful component of air pollutants, increasing inflammation and changing gut microbiota, favoring obesity, type 2 diabetes, and Alzheimer's Disease (AD). PM contains lipopolysaccharides (LPS), which can activate the Toll-like receptor 4 (TLR4) signaling pathway. This pathway can lead to the release of pro-inflammatory markers, including interleukins, and suppressor of cytokine signaling-3 (SOCS3), which inhibits leptin action, a hormone that keeps the energy homeostasis. Leptin plays a role in preventing amyloid plaque deposition and hyperphosphorylation of tau-protein (p-tau), mechanisms involved in the neurodegeneration in AD. Approximately 50 million people worldwide are affected by dementia, with a significant proportion living in low-and middle-income countries. This number is expected to triple by 2050. This mini-review focuses on the potential impact of PM exposure on the TLR4 signaling pathway, its contribution to leptin resistance, and dysbiosis that exacerbates the link between obesity and AD.
Topics: Humans; Alzheimer Disease; Obesity; Leptin; Air Pollution; Particulate Matter; Toll-Like Receptor 4; Inflammation; Animals; Signal Transduction; Air Pollutants
PubMed: 38933275
DOI: 10.3389/fimmu.2024.1401800