Search Results (24)

Metabolic Syndrome (MetS) is a complex, multifactorial condition characterized by risk factors such as abdominal obesity, insulin resistance, dyslipidemia and hypertension, which significantly contribute to the development of cardiovascular disease (CVD), the leading cause of death worldwide. Early identification and effective monitoring of MetS is crucial for preventing serious cardiovascular complications. This article provides a comprehensive overview of various biomarkers associated with MetS, including lipid profile markers (triglyceride/high-density lipoprotein cholesterol (TG/HDL-C) ratio and apolipoprotein B/apolipoprotein A1 (ApoB/ApoA1) ratio), inflammatory markers (interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α), plasminogen activator inhibitor type 1 (PAI-1), C-reactive protein (CRP), leptin/adiponectin ratio, omentin and fetuin-A/adiponectin ratio), oxidative stress markers (lipid peroxides, protein and nucleic acid oxidation, gamma-glutamyl transferase (GGT), uric acid) and microRNAs (miRNAs) such as miR-15a-5p, miR5-17-5p and miR-24-3p. Additionally, this review highlights the importance of biomarkers in MetS and the need for advancements in their identification and use for improving prevention and treatment. Seaweed therapy is also discussed as a significant intervention for MetS due to its rich content of fiber, antioxidants, minerals and bioactive compounds, which help improve cardiovascular health, reduce inflammation, increase insulin sensitivity and promote weight loss, making it a promising nutritional strategy for managing metabolic and cardiovascular health. Full article

Background: Cardiometabolic heart failure with preserved ejection fraction (HFpEF) is largely driven by obesity-related factors, including adipokines and bioactive peptides primarily secreted by the adipose tissue, such as leptin, adiponectin, and resistin. These molecules link metabolic dysregulation to cardiovascular dysfunction, influencing HFpEF progression and patient outcomes Methods: A comprehensive literature search was conducted in PubMed up to 20 November 2024, using keywords and MeSH terms, such as “HFpEF”, “adipokines”, “leptin”, “adiponectin”, and “resistin”, yielding 723 results. Boolean operators refined the search, and reference lists of key studies were reviewed. After screening for duplicates and irrelevant studies, 103 articles were included, providing data on adipokines’ roles in HFpEF pathophysiology, biomarkers, and therapeutic implications. Results: Both preclinical and clinical studies have demonstrated that adipokines play a role in modulating cardiovascular function, thereby contributing to the development of cardiometabolic HFpEF. Leptin promotes myocardial hypertrophy, fibrosis, endothelial dysfunction, and inflammation, though contradictory evidence suggests potential cardioprotective roles in subgroups like obese African American women. Adiponectin generally offers protective effects but presents a paradox, where elevated levels may correlate with worse outcomes, which may reflect either a compensatory response to cardiac dysfunction or a maladaptive state characterized by adiponectin resistance. Resistin is associated with increased cardiovascular risk through pro-inflammatory and pro-fibrotic effects, though its role in HFpEF requires further clarification. Other adipokines, like retinol-binding protein 4 and omentin-1, have emerged as potential contributors. Despite growing insights, clinical translation remains limited, underscoring a significant gap between experimental evidence and therapeutic application. Conclusions: Future research should focus on targeted interventions that modulate adipokine pathways to potentially improve HFpEF outcomes. Innovative treatment strategies addressing underlying metabolic disturbances and adipokine dysregulation are essential for advancing the management of this challenging condition. Full article

Objectives: The aim of this research was to evaluate changes in body composition, adipokine levels, and dyslipidemia parameters in males with abdominal obesity following two distinct interventions: exercise alone and exercise combined with an ad libitum diet. Methods: This study included 44 males with abdominal obesity (mean age 34.7 ± 5.5 years, waist circumference [WC] 110.3 ± 8.5, BMI 32.0 ± 3.9), who were randomly assigned to three groups: an experimental group engaging in aerobic-resistance exercise (II, n = 16), an experimental group engaging in aerobic-resistance exercise combined with an ad libitum high-protein, low-glycemic index carbohydrate diet (III, n = 16), both interventions lasting 6 weeks, and a control group without interventions (I, n = 12). Body composition metrics (body mass index [BMI], waist circumference [WC], body fat [BF], abdominal fat [ABD]) and fat-free mass [FFM], along with biochemical blood analyses (irisin [IR], omentin [OMEN], glucose [GLU], insulin [INS], LDL- and HDL-cholesterol), were measured at baseline and after the 6-week intervention. The effects of the interventions on the analyzed variables across groups were assessed using mixed ANOVA tests with post-hoc comparisons. Effect size (ES) was also calculated using partial eta squared (ηp²). Results: The intervention in group III resulted in a significant decrease in IR (p < 0.01, ηp² = 0.03) by 41% and LDL-C (p < 0.01, ηp² = 0.02) by 14%. These effects were associated with a reduction in BF (p < 0.01, ηp² = 0.02) by 14%, ABD (p < 0.01, ηp² = 0.03) by 31%, and WC (p < 0.01, ηp² = 0.01) by 3%. In group II, decreases after 6 weeks of intervention were noted only in WC (p = 0.02, ηp² = 0.01) by 1% and in INS (p < 0.01, ηp² = 0.04) by 47%. No differences were found between groups. The use of low-glycemic index carbohydrates (p < 0.01, ηp² = 0.06) and increased protein intake (p < 0.01, ηp² = 0.30) led to changes in the fiber-to-energy value of the diet ratio (p < 0.01, ηp² = 0.18) and a reduction in dietary energy value (p < 0.01, ηp² = 0.13) by 23%, resulting in a greater energy deficit than in the II group. Conclusions: These findings highlight the effect of combining dietary and exercise interventions to achieve significant changes in body composition and metabolic parameters, even over a short period of intervention. Full article

Approximately 50% of all global blindness is caused by cataract in adults aged ≥50 years. The mechanisms of the disease are most arguably related to a redox imbalance and inflammation; therefore, the aim of the study was to evaluate the processes associated with inflammation in cataract patients. Twenty-four patients aged 22–60 years (62.5% females) participated in the study, with 33 controls aged 28–60 years (66.7% females). Venous blood serum of the subjects was examined for alpha 1-antitrypsin, as well as selected lysosomal enzymes and adipokines. The activities of lysosomal enzymes, as well as the activity of alpha 1-antitrypsin and the concentrations of c-reactive protein and leptin, were similar in the patients versus the controls. The concentrations of interleukin 6 and resistin were lower, in turn, whereas omentin-1 and adiponectin were higher. Moreover, the study revealed the existence of many linear relationships between the parameters, including multiple linear regression, especially gender-wise. No systemic inflammation was probably noted in the cataract patients tested; nevertheless, the deregulation of adiponectin, omentin-1 and resistin secretion was observed. Full article

Adipose tissue serves as an energy store and is also an active endocrine organ, exerting activity that influences obesity-related processes through the production of regulatory proteins called adipokines or adipocytokines. Adipokines play important direct and indirect roles in the pathogenesis of insulin resistance, the regulation of local and systemic inflammatory processes, and related metabolic complications. There have been an increasing number of studies showing the relationship between some adipokines and carcinogenesis. This work reviews the current literature concerning the effects of omentin-1 on carcinogenesis. Full article

Leptin (LEP) and omentin (OMEN) are proteins whose concentrations change with the development of the metabolic syndrome (MetS). There are few intervention studies using various forms of physical activity in people with MetS that aim to determine the impact of physical exercise on the fluctuations of the presented hormones, and their results are contradictory. The present study aimed to examine the effect of two types of exercise intervention on LEP and OMEN concentrations and indicators of lipid and carbohydrate metabolism in males with MetS. The study included 62 males with MetS (age 36.6 ± 6.9 years, body mass 110.31 ± 17.37 kg), randomly allocated to EG1, the examined group with aerobic training (n = 21); EG2, the examined group with combined aerobic and resistance training (n = 21), both for 12 weeks, and the control group (CG) without interventions (n = 20). Anthropometric measurements, body composition (body fat [BF], android body fat [ANDR]), as well as a biochemical blood analysis (omentin [OMEN], leptin [LEP], quantitative insulin sensitivity check index [QUICKI], high-density lipoprotein cholesterol [HDL-C] and nonHDL-C) were performed at baseline, and at 6 and 12 weeks of interventions and after 4 weeks after ending intervention (follow-up). Intergroup and intragroup comparisons were performed. In the intervention groups EG1 and EG2, a decrease in BF was observed as well as an improvement in carbohydrate metabolism parameters. In the EG1 group, the level of ANDR was reduced. In EG2 a decrease in LEP concentration between measurements was confirmed. However, no significant changes were found in the concentration of OMEN in any groups. Combined aerobic and resistance exercises led to a higher reduction of LEP concentration than applying only aerobic training in males with MetS. Full article

Non-alcoholic fatty liver disease (NAFLD) shows liver fat depots without alcohol consumption. NAFLD does not have specific drug therapies, with a healthy lifestyle and weight loss being the main approaches to prevent and treat NAFLD. The aim was to assess the antioxidant and pro-inflammatory state in patients with NAFLD after 12-month-lifestyle intervention depending on the change in adherence to a Mediterranean diet (AMD). Antioxidant and inflammatory biomarkers were measured in 67 adults (aged 40–60 years old) diagnosed with NAFLD. Anthropometric parameters and dietary intake were measured by a validated semi-quantitative 143-item food frequency questionnaire. The nutritional intervention improved anthropometric and biochemical parameters after a 12-month follow-up. However, decreases in alanine aminotransferase (ALT) and C reactive protein (CRP) were higher in participants with high AMD, which also showed higher improvement in physical fitness (Chester step test) and intrahepatic fat contents. The intervention reduced plasma levels of malondialdehyde, myeloperoxidase, zonulin, and omentin, and increased resolvin D1 (RvD1), whereas the decrease in leptin, ectodysplasin-A (EDA), cytokeratin-18 (CK-18), interleukin-1ra (IL-1ra) and endotoxin was only significant in participants with higher AMD. The current study showed that a one-year nutritional intervention improved main NAFLD features such as body mass index, IFC, liver enzymes, and prooxidant and proinflammatory status. There was also a decrease in the concentration of plasmatic endotoxin, suggesting an improvement in intestinal permeability. These health benefits were more evident in participants that improved AMD to a greater extent. The trial was registered at ClinicalTrials.gov with registry number NCT04442620. Full article

(1) Background: Non-communicable diseases (NCD) are an important concern for public health because of their high rates of morbidity and mortality. A prevalent lifestyle-linked NCD is type 2 diabetes mellitus (T2D). Recently, molecular biomarkers secreted by adipocytes, called adipokines, have been linked with T2D and muscle function disturbances. However, the effects of resistance training (RT) interventions on adipokine levels in patients with T2D have not been systematically studied. (2) Methods: The PRISMA guidelines were followed. Searches for the studies were performed in the PubMed/MEDLINE and Web of Science electronic databases. Eligibility criteria included: (i) participants with T2D; (ii) RT interventions; (iii) randomized controlled trials; and (iv) measurement of serum adipokines. The PEDro scale was used to assess the methodological quality of the selected studies. Significant differences (p ≤ 0.05) and effect size were screened for each variable. (3) Results: Of the initial 2166 records, database search extraction yielded 14 studies to be included. The methodological quality of the included data was high (median PEDro score of 6.5). Analyzed adipokines in the included studies were leptin, adiponectin, visfatin, apelin, resistin, retinol-binding protein 4 (RBP4), vaspin, chemerin, and omentin. RT interventions (6–52 weeks; minimal effective duration >12 weeks) exert a meaningful effect on serum adipokine, (e.g., leptin) levels in T2D patients. (4) Conclusions: RT may be an alternative, but not an optimal, option in adipokine disruptions in T2D. Combined (i.e., aerobic and RT) long-term training may be considered the optimal intervention for treating adipokine level disturbances. Full article

Background and objective: Obstructive sleep apnea (OSA) can be related to changes in the levels of adipokines and neuropeptides, which in turn may affect the energy balance components of neuronal cells. Herein, a systematic review and meta-analysis checked the changes in serum/plasma levels of omentin-1 (OM-1: an adipokine) and orexin-A (OXA: a neuropeptide) in adults (age > 18 years old) with OSA (aOSA) compared to controls. Materials and methods: Four databases (Cochrane Library, PubMed, Web of Science, and Scopus) were systematically searched until 14 November 2022, without any restrictions. The Joanna Briggs Institute (JBI) critical appraisal checklist adapted for case–control studies was used to assess the quality of the papers. The effect sizes were extracted using the Review Manager 5.3 software for the blood levels of OM-1 and OXA in aOSA compared with controls. Results: Thirteen articles, with six studies for OM-1 levels and eight for OXA levels, were included. The pooled standardized mean differences were −0.85 (95% confidence interval (CI): −2.19, 0.48; p = 0.21; I² = 98%) and −0.20 (95%CI: −1.16, 0.76; p = 0.68; I² = 96%) for OM-1 and OXA levels, respectively. Among the studies reporting OM-1, five were high and one was moderate quality. Among the studies reporting OXA, six were moderate, one was high, and one was low quality. Based on the trial sequential analysis, more participants are needed to confirm the pooled results of the analyses of blood levels of OM-1 and OXA. In addition, the radial plot showed outliers as significant factors for high heterogeneity. Conclusions: The main findings indicated a lack of association between the blood levels of OM-1 and OXA and OSA risk. Therefore, OM-1 and OXA did not appear to be suitable biomarkers for the diagnosis and development of OSA. Full article

The autophagy gene ATG7 has been shown to be essential for the induction of autophagy, a process that used to be suppressed in nonalcoholic fatty liver disease (NAFLD). However, the specific role of ATG7 in NAFLD remains unclear. The aim of this study was to analyze hepatic ATG7 mRNA and ATG7 protein expression regarding obesity-associated NAFLD. Patients included women classified into normal weight (NW, n = 6) and morbid obesity (MO, n = 72). The second group was subclassified into normal liver (NL, n = 11), simple steatosis (SS, n= 29), and nonalcoholic steatohepatitis (NASH, n = 32). mRNA expression was analyzed by RT–qPCR and protein expression was evaluated by Western blotting. Our results showed that NASH patients presented higher ATG7 mRNA and ATG7 protein levels. ATG7 mRNA expression was increased in NASH compared with SS, while ATG7 protein abundance was enhanced in NASH compared with NL. ATG7 mRNA correlated negatively with the expression of some hepatic lipid metabolism-related genes and positively with endocannabinoid receptors, adiponectin hepatic expression, and omentin levels. These results suggest that ATG7-mediated autophagy may play an important role in the pathogenesis of NAFLD, especially in NASH, perhaps playing a possible protective role. However, this is a preliminary study that needs to be further studied. Full article

Idiopathic pulmonary fibrosis (IPF) is a fatal age-related chronic lung disease, characterized by progressive scarring of the lungs by activated fibroblasts. The effect of omentin-1 against pulmonary fibrosis and fibroblast activation has not been investigated. The purpose of this experiment is to investigate the role of omentin-1 in bleomycin (BLM)-induced lung fibrosis and its mechanism. Our results showed that the loss of omentin-1 exaggerated lung fibrosis induced by BLM. On the contrary, adenoviral-overexpression of omentin-1 significantly alleviated BLM-induced lung fibrosis both in preventive and therapeutic regimens. Moreover, omentin-1 prevented fibroblast activation determined by a decreased number of S100A4⁺ (fibroblasts marker) α-SMA⁺ cells in vivo, and a decreased level of α-SMA expression both in mice primary fibroblasts and human primary fibroblasts induced by TGF-β in vitro. Furthermore, the phosphorylation of AMP-activated protein kinase (p-AMPK) was significantly lower in the fibrotic foci induced by BLM, and the adenoviral-overexpression of omentin-1 significantly increased the p-AMPK level in vivo. Importantly, Compound C, the inhibitor of AMPK, significantly attenuated the protective effect of omentin-1 on BLM-induced lung fibrosis and reversed the effect of omentin-1 on fibroblast activation by TGF-β. Omentin-1 can be a promising therapeutic agent for the prevention and treatment of lung fibrosis. Full article

The study aimed to assess effects of high-intensity interval training (HIIT) on plasma adipokines and cardiometabolic markers in normal and excess weight youth. Eighteen healthy young males (18.2 ± 1.06 yrs.) were divided in normal-weight group (NWG; body mass index (BMI), 20.5 ± 1.51 kg/m²; n = 9) and excess-weight group (EWG; BMI, 30.8 ± 4.56 kg/m²; n = 9). Participants performed an eight-week HIIT program without caloric restriction. Body composition, plasma leptin, adiponectin, chemerin, omentin-1, lipids, C-reactive protein (CRP), and the homeostasis model assessment index for insulin resistance (HOMA-IR) were assessed before and after the HIIT program. The program resulted in significant increases in omentin levels (p < 0.01) in EWG (27%) and NWG (22%), but no changes in leptin, adiponectin, and chemerin in both groups. BMI (−1.62%; p = 0.015), body fat (−1.59%; p = 0.021), total cholesterol (−11.8%; p = 0.026), triglycerides (−21.3%; p = 0.023), and HOMA-IR (−31.5%; p = 0.043) decreased in EWG only. Repeated measures detected significant interaction “Time x Group” for body mass and BMI only. Eight-week HIIT program improved body composition, lipid profile, and insulin sensitivity in excess-weight individuals. It resulted in an increase in omentin levels in both normal- and excess-weight groups, but no changes in leptin, adiponectin, and chemerin. Body composition has not influenced the response of the four adipokines to HIIT. Full article

Gestational diabetes mellitus (GDM) has become a major public health problem and one of the most discussed issues in modern obstetrics. GDM is associated with serious adverse perinatal outcomes and long-term health consequences for both the mother and child. Currently, the importance and purposefulness of finding a biopredictor that will enable the identification of women with an increased risk of developing GDM as early as the beginning of pregnancy are highly emphasized. Both “older” molecules, such as adiponectin and leptin, and “newer” adipokines, including fatty acid-binding protein 4 (FABP4), have proven to be of pathophysiological importance in GDM. Therefore, in our previous review, we presented 13 novel biomolecules, i.e., galectins, growth differentiation factor-15, chemerin, omentin-1, osteocalcin, resistin, visfatin, vaspin, irisin, apelin, FABP4, fibroblast growth factor 21, and lipocalin-2. The purpose of this review is to present the potential and importance of another nine lesser known molecules in the pathogenesis of GDM, i.e., 3-carboxy-4-methyl-5-propyl-2-furanpropanoic acid (CMPF), angiopoietin-like protein-8 (ANGPTL-8), nesfatin-1, afamin, adropin, fetuin-A, zonulin, secreted frizzled-related proteins (SFRPs), and amylin. It seems that two of them, fetuin-A and zonulin in high serum levels, may be applied as biopredictors of GDM. Full article

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. Full article

The global burden of obesity has multiplied owing to its rapidly growing prevalence and obesity-related morbidity and mortality. In addition to the classic role of depositing extra energy, adipose tissue actively interferes with the metabolic balance by means of secreting bioactive compounds called adipokines. While most adipokines give rise to inflammatory conditions, the others with anti-inflammatory properties have been the novel focus of attention for the amelioration of cardiometabolic complications. This review compiles the current evidence on the roles of anti-inflammatory adipokines, namely, adiponectin, vaspin, the C1q/TNF-related protein (CTRP) family, secreted frizzled-related protein 5 (SFRP5), and omentin-1 on cardiometabolic health. Further investigations on the mechanism of action and prospective human trials may pave the way to their clinical application as innovative biomarkers and therapeutic targets for cardiovascular and metabolic disorders. Full article