Role of epicardial adipose tissue in cardiac remodeling.

Epicardial adipose tissue, or epicardial fat, is a type of visceral fat located between the heart and the pericardium. Due to its anatomical proximity to the heart, EAT plays a significant role in both cardiac physiology and pathologies, including cardiac remodeling and cardiovascular diseases (CVD). However, our understanding of how EAT pathology is influenced by risk factors such as obesity and type 2 diabetes mellitus and how altered EAT can drive cardiac remodeling and CVD, remains limited. Herein, we aimed to summarize and discuss the latest findings on EAT and its role in cardiac remodeling, highlighting the outcomes of clinical and observational studies, provide mechanistic insights, and finally introduce emerging therapeutic agents and nutritional guidelines aimed at preventing these conditions.

Long-Term Prognostic Value of Adipocytokines in Patients with Acute Coronary Syndrome: An 8-Year Clinical Prospective Cohort Study.

Purpose: To elucidate the predictive values of adipocytokines in patients with acute coronary syndrome (ACS). Patients and Methods: Overall, 297 patients with ACS were consecutively enrolled in this prospective cohort study between June 2015 and July 2017 and completed follow-up with a median follow-up time of 6.5 years. For consistency, the last visit date was June 20, 2023. Serum levels of retinol-binding protein-4 (RBP4), interleukin-1ß (IL-1ß), monocyte chemoattractant protein 1(MCP-1), adrenomedullin (ADM), netrin 1 (NTN 1), and omentin were measured using enzyme-linked immunosorbent assay. Follow-up data were collected during clinical visits or through telephone interviews at 1, 3, 6, 12 months, and annually. The primary endpoint was defined as major adverse cardiovascular events (MACEs), including all-cause mortality, rehospitalization for percutaneous coronary intervention, and severe angina requiring rehospitalization. Results: All biomarkers displayed a good diagnostic ability of MACEs. The Kaplan-Meier curve showed that the cumulative survival rates of high level of RBP4, IL-1ß, and MCP-1 and low level of the ADM, NTN1, and omentin had lower cumulative survival rates (Log rank tests: all p<0.05). After adjustment in the Cox hazard proportional model, the results were RBP4 ≥ 6.87 ng/mL, hazard ratio (HR)=2.512, p=0.003; IL-1ß≥ 58.95 pg/mL, HR=3.809, p<0.001; MCP-1 ≥ 401.75 pg/mL, HR=4.047, p<0.001; ADM≤120.01 ng/mL, HR=3.930, p=0.008; NTN1 ≤63.7 pg/mL, HR=3.345, p=0.007; omentin ≤ 4.54 ng/mL, HR=2.830, p=0.004. P-values for interaction were > 0.05 in the sex, age, and dyslipidemia subgroups. Conclusion: Pro-inflammation adipocytokines RBP4, IL-1ß, and MCP-1 increased and anti-inflammation biomarkers ADM, NTN1, and omentin decreased were independently associated with a higher risk of MACEs in patients with ACS.

New Insights into the Link Between Melanoma and Obesity.

The significant increase in the incidence of obesity represents a global health crisis. Obesity is actually a multi-organ disease affecting the entire organism; hence, skin is no exception. As the functional alterations in the adipose tissue are contributing factors to many diseases, including cancer, recently, the link between the development of melanoma skin cancer and obesity gains increased attention. Besides several other factors, the increase of adipose stromal/stem cells (ASCs) impacts cancer progression. Moreover, increased production of cytokines and growth factors done by ASCs induces tumorigenesis and metastasis. The chronic inflammatory state that is sustained by this metabolic imbalance favors skin malignancies, melanoma included. Cutaneous melanoma, as an aggressive skin cancer, has both intrinsic and extrinsic risk factors where sun exposure and lifestyles are the main environmental factors inducing this skin cancer. With the advent of recent targeted and immune-based therapies in melanoma, the link between obesity and the efficacy of these therapies in melanoma remains controversial. A recent molecular relationship between the melanocortin pathway appending to both melanin synthesis and obesity was established. The biology of adipokines, molecules secreted by the adipose tissue, is linked to inflammation, and their molecular pathways can be involved in angiogenesis, migration, invasion, and proliferation of melanoma cells. In melanoma cells, among the most noticeable metabolic reprogramming characteristics is an increased rate of lipid synthesis. Lipid mediators impact classical oncogenic pathways, affecting melanoma progression. The chapter will tackle also the practical implications for melanoma prevention and treatment, namely, how metabolic manipulation can be exploited to overcome immunosuppression and support immune checkpoint blockade efficacy.

Milk protein concentrate supplementation improved appetite, metabolic parameters, adipocytokines, and body composition in dieting women with obesity: a randomized controlled trial.

BACKGROUND: Dairy consumption is associated with many health benefits. However, to our knowledge, no clinical trials examined the effects of milk protein concentrate (MPC) on metabolic health in overweight and obese adults. This study investigated the effect of supplementation with MPC on glycaemic status, lipid profile, biomarkers of inflammation, and anthropometric measurements in women with obesity under a weight loss diet. METHODS: This is a single-blind, open-labelled, parallel-group, randomized trial. Forty-four healthy women with obesity were randomized into a control (n = 22) or MPC (n = 22) group. Participants in the MPC group were supplemented with 30 g of MPC per day for 8 weeks. Both groups were on a calorie-restricted diet plan with 800 Kcal lower intakes than their needs. Blood samples, dietary intake, and body composition were assessed before and after the intervention. RESULTS: MPC group had a significantly lower body mass index (P = 0.009), waist circumference (P = 0.013), fat mass (P = 0.021), appetite score (P = 0.002), fasting blood sugar (P < 0.001), insulin (P = 0.027), low-density lipoprotein cholesterol (P = 0.025), and leptin (P = 0.014) levels and higher high-density lipoprotein cholesterol (P = 0.001) and adiponectin (P = 0.032) compared to the control group after supplementation. Lean body mass, total cholesterol, and triglyceride did not differ significantly (P > 0.05). CONCLUSION: Daily intake of 30 g of MPC for 8 weeks may improve several anthropometric and metabolic markers in women with obesity under a hypocaloric diet.

Non-alcoholic fatty liver disease in obese subjects as related to increasing insulin resistance and deteriorating glucose control: Three years of follow-up from a longitudinal survey.

Purpose: This observational trial was performed to evaluate liver parameters in overweight or obese subjects in the context of insulin resistance and glucose control over time. Subjects/Methods: Insulin resistance, glucose control and several parameters for liver integrity were monitored in 177 overweight (BMI > 28 kg/m2) subjects over a mean of 30 months. Volunteers were categorized according to insulin resistance (HOMAIR score) and glucose control in subjects with normal glucose control (NGT), impaired glucose control (IGT), or diabetes mellitus type 2 (T2DM). Liver fat and fibrosis were evaluated by sonographic elastography (FibroScan®) and clinical scores, such as the AST/ALT ratio, fatty liver index (FLI), and NAFLD fibrosis score (NFS). Results: Liver fat fraction as estimated by the controlled attenuation parameter (CAP), and the FLI were significantly higher in subjects with T2DM compared to IGT and NGT. While fasting insulin levels and the HOMAIR score continuously increased over time, no change in CAP or FLI occurred during follow up. CAP was correlated with FLI (r = 0.50; p < 0.0001) and the HOMAIR score (r = 0.32; p < 0.0001). An inverse correlation was observed between serum adiponectin levels and FLI (r = -0.37; p < 0.0001), the HOMAIR score (r = -0.19; p < 0.001, and CAP (r = -0.15; p < 0.01). Conclusions: In subjects with a BMI ≥ 28 kg/m2, liver fat fraction is significantly elevated in those with T2DM compared to IGT or NGT. Liver fat fraction is associated with deteriorating insulin sensitivity and loss of glucose control. Despite a continuous increase in insulin resistance, no change in liver fat content or stiffness occurred over 30 months.

Comparison of UVA vs UVB Photoaging Rat Models in Short-term Exposure.

Background: Prolonged exposure to sunlight is known to induce photoaging of the skin, leading to various skin changes and disorders, such as dryness, wrinkles, irregular pigmentation, and even cancer. Ultraviolet A (UVA) and ultraviolet B (UVB) radiation are particularly responsible for causing photoaging. Objective: This study aims to identify and compare photoaging rat models exposed to UVA and UVB. Methods: This research method compared macroscopic (scoring degree of wrinkling) and microscopic (histology) signs and symptoms on skin samples of rat exposed to UVA and UVB for 4 weeks at a radiation dose of 840mJ/cm2. Results: The results of this study indicated that the degree of wrinkling was highest in rat skin exposed to UVB rays by 51% (p<0.05). UVB histological results showed that the epidermis layer (40 µm, p<0.05) was thickened and the dermis layer (283 µm, p<0.05) was thinned in the skin of mice exposed to UVB light. The UVB group, showed the density of collagen in the dermis with a mean value of 55% (p<0.05). Conclusion: Our results suggest that short-term exposure to UVB radiation (in the acute, subacute or subchronic phase) induces more rapid and pronounced damage to rat skin when compared to UVA radiation exposure.

Impact of obesity on airway remodeling in asthma: pathophysiological insights and clinical implications.

The prevalence of obesity among asthma patients has surged in recent years, posing a significant risk factor for uncontrolled asthma. Beyond its impact on asthma severity and patients' quality of life, obesity is associated with reduced lung function, increased asthma exacerbations, hospitalizations, heightened airway hyperresponsiveness, and elevated asthma-related mortality. Obesity may lead to metabolic dysfunction and immune dysregulation, fostering chronic inflammation characterized by increased pro-inflammatory mediators and adipocytokines, elevated reactive oxygen species, and reduced antioxidant activity. This chronic inflammation holds the potential to induce airway remodeling in individuals with asthma and obesity. Airway remodeling encompasses structural and pathological changes, involving alterations in the airway's epithelial and subepithelial layers, hyperplasia and hypertrophy of airway smooth muscle, and changes in airway vascularity. In individuals with asthma and obesity, airway remodeling may underlie heightened airway hyperresponsiveness and increased asthma severity, ultimately contributing to the development of persistent airflow limitation, declining lung function, and a potential increase in asthma-related mortality. Despite efforts to address the impact of obesity on asthma outcomes, the intricate mechanisms linking obesity to asthma pathophysiology, particularly concerning airway remodeling, remain incompletely understood. This comprehensive review discusses current research investigating the influence of obesity on airway remodeling, to enhance our understanding of obesity's role in the context of asthma airway remodeling.

The Mesentery's Pivotal Role in the Brain-Gut-Liver Axis.

Background: Prior to 2012, the mesentery was perceived as a fragmented structure, lacking distinct functional and anatomical characteristics, and was merely considered part of other digestive organs. Dr. J. Calvin Coffey's in 2012 in his study redefined the mesentery as a distinct organ with a clearly defined anatomical and histological structure, although its specific function remains under investigation. The continuous structure and unique tissue properties of the mesentery classify it as the 78th independent organ in the human body. Insights into mesenteric adipose tissue have enhanced our understanding of normal metabolic processes and disease etiology, impacting health significantly. Experimental and clinical research highlights the vital roles of visceral adipose tissue, influencing neighboring organ function. The interaction within the brain-gut-liver axis is illuminated by the newfound functions of mesenteric adipose tissue, emphasizing its independent organ status. Objective: This study aims to evaluate the latest findings on the structure and function of the mesentery, focusing on visceral-mesenteric adipose tissue, and assess its role as a new organ in the brain-gut-liver axis. Methods: A comprehensive analysis of clinical and experimental studies on the mesentery's structure and function was conducted, focusing on recent discoveries regarding mesenteric adipose tissue and its role in the brain-gut-liver axis. Results and Discussion: Recent research has revealed the mesentery's unique functions, particularly in mesenteric adipose tissue. Mesenteric adipose tissue plays a crucial role in metabolic functions and influences disease onset. It acts as a vital link in the brain-gut-liver axis, directly influencing hepatic metabolism and disorders such as metabolic syndrome. Conclusion: Scientific evidence confirms the mesentery's anatomical and functional specificities, solidifying its status as the 78th independent organ in the human body. It serves as a crucial link in the brain-mesentery-small intestine-liver axis, impacting health and disease. Ongoing research holds promise for advancing our understanding of pathophysiological mechanisms and treatment approaches for metabolic syndrome and other chronic diseases.

Circulating Adipocytokines and Insulin Like-Growth Factors and Their Modulation in Obesity-Associated Endometrial Cancer.

The rising global incidence of uterine cancer is linked to the escalating prevalence of obesity. Obesity results in alterations in adipocytokines and IGFs, driving cancer progression via inflammation, increased cell proliferation, and apoptosis inhibition, although the precise mechanisms are still unclear. This study examined a set of six markers, namely, adiponectin, leptin, IL6, TNFα, IGF1, and IGF2 and compared them between fifty age-matched endometrial cancer patients (study group) and non-cancer patients with benign gynaecological conditions (control group). We also assessed the relationship of these markers with obesity and explored the correlation between these markers and various tumour characteristics. In the cancer population, these markers were also assessed 24 h and 6 months post-surgery. Remarkably, low adiponectin levels were associated with a 35.8% increase in endometrial cancer risk. Interestingly, compared to control subjects where IGF levels decreased after menopause, post-menopausal women in the study group showed elevated IGF1 and IGF2 levels, suggesting a potential influence of endometrial cancer on the IGF system, particularly after menopause. Lastly, it is noteworthy that a discernible inverse relationship trend was observed in the levels of adipocytokines and IGFs 6 months post-surgery. This indicates that treatment for endometrial cancer may have a differential impact on adipocytokines and IGFs, potentially holding clinical significance that merits further investigation.

Spirulina Supplementation with High-Intensity Interval Training Decreases Adipokines Levels and Cardiovascular Risk Factors in Men with Obesity.

Adiposity, a state characterized by excessive accumulation of body fat, is closely linked to metabolic complications and the secretion of specific adipokines. This study explores the potential of exercise and Spirulina supplementation to mitigate these complications and modulate adipokine release associated with obesity. The primary objective of this investigation was to examine the impact of a 12-week regimen of high-intensity training combined with Spirulina supplementation on adipokine concentrations and lipid profiles in male individuals with obesity (N = 44). The participants were randomly distributed into four groups, each consisting of 11 participants: a control group (CG), a supplement group (SG), a training group (TG), and a training plus supplement group (TSG). The intervention comprised a 12-week treatment involving Spirulina supplementation (6 g capsule daily), a 12-week high-intensity interval training (HIIT) protocol with three sessions per week, or a combined approach. Following the interventions, metabolic parameters, anthropometric measurements, cardiorespiratory indices, and circulating adipokines [CRP, Sema3C, TNF-α, IL-6, MCP1, IL-8] were assessed within 48 h of the before and final training session. Statistical analyses revealed significant differences across all measures among the groups (p < 0.05). Notably, post hoc analyses indicated substantial disparities between the CG and the three interventional groups regarding body weight (p < 0.05). The combined training and supplementation approach led to noteworthy reductions in low-density lipoprotein (LDL), total cholesterol (TC), and triglyceride (TGL) levels (all p < 0.0001), coupled with an elevation in high-density lipoprotein-cholesterol (HDL-C) levels (p = 0.0001). Furthermore, adipokine levels significantly declined in the three intervention groups relative to the CG (p < 0.05). The findings from this 12-week study demonstrate that Spirulina supplementation in conjunction with high-intensity interval training reduced adipokine levels, improved body weight and BMI, and enhanced lipid profiles. This investigation underscores the potential of Spirulina supplementation and high-intensity interval training as a synergistic strategy to ameliorate obesity-related complications and enhance overall cardiometabolic well-being in obese males.

Adipose Tissue, Non-Communicable Diseases, and Physical Exercise: An Imperfect Triangle.

The study of adipose tissue has received considerable attention due to its importance not just in maintaining body energy homeostasis but also in playing a role in a number of other physiological processes. Beyond storing energy, adipose tissue is important in endocrine, immunological, and neuromodulatory functions, secreting hormones that participate in the regulation of energy homeostasis. An imbalance of these functions will generate structural and functional changes in the adipose tissue, favoring the secretion of deleterious adipocytokines that induce a pro-inflammatory state, allowing the development of metabolic and cardiovascular diseases and even some types of cancer. A common theme worldwide has been the development of professional guidelines for the control and treatment of obesity, with emphasis on hypocaloric diets and exercise. The aim of this review is to examine the pathophysiological mechanisms of obesity, considering the relationship among adipose tissue and two aspects that contribute positively or negatively to keeping a healthy body homeostasis, namely, exercise and noninfectious diseases. We conclude that the relationship of these aspects does not have homogeneous effects among individuals. Nevertheless, it is possible to establish some common mechanisms, like a decrease in pro-inflammatory markers in the case of exercise, and an increase in chronic inflammation in non-communicable diseases. An accurate diagnosis might consider the particular variables of a patient, namely their molecular profile and how it affects its metabolism, routines, and lifestyle; their underling health conditions; and probably even the constitution of their microbiome. We foresee that the development and accessibility of omics approaches and precision medicine will greatly improve the diagnosis, treatment, and successful outcomes for obese patients.

Associations of Adipocytokines with The Development of Cardiovascular Events in Young People.

The research was aimed to study the associations of adipocytokines with the risk of cardiovascular events and to determine the threshold values of adipocytes for the prognosis of cardiovascular events in a young population. MATERIALS AND METHODS: The study is an epidemiological cohort study. The analysis included 1240 people aged 25-44 years. The endpoint was combined and included: death from cardiovascular disease, myocardial infarction, probable myocardial infarction, acute cerebrovascular accident, hospitalization for cardiovascular disease, and revascularization. Adipocytokines were determined with a MILLIPLEX panel. RESULTS: In the examined population, 1.7% of cases of cardiovascular events were detected during cohort observation, of which 28.6% were fatal events. In men, cardiovascular endpoints were recorded 4.3 times more often than in women (17 (81%) vs. 4 (19%), p = 0.003). In individuals with cardiovascular events, arterial hypertension (2.6 times), diabetes mellitus (8.6 times), and overweight/obesity (1.5 times) were more often recorded compared to individuals without cardiovascular events. For tumor necrosis factor-alpha (TNFa), the threshold value was 2.5 pg/mL, with sensitivity assessment (Se) at 85.7% and specificity (Sp) at 83.3%. For amylin, the threshold value was 10.5 pg/mL, with Se at 73.7% and Sp at 67.0%. For pancreatic polypeptide (PP), the threshold value was 43.7 pg/mL, with Se at 85.7% and Sp at 56.7%. CONCLUSION: A method for assessing the risk of cardiovascular events in young people includes determining the levels of amylin, PP, and TNFa in blood serum. The cut-off points for predicting cardiovascular events were levels of amylin above 10.5 pg/mL, PP above 43.7 pg/mL, or a decrease in TNFa below 3.8 pg/mL.

Association between adipocytokines and diabetic retinopathy: a systematic review and meta-analysis.

Background: Diabetic retinopathy (DR) is a common complication of diabetes. The adipocytokines are closely associated with the occurrence and development of diabetes and its related complications. Literature confirms that the level of adiponectin in patients with DR is significantly higher; however, the relationship between other adipocytokines (leptin, chemerin, apelin, and omentin-1) and DR remains unclear. Aim: This study aimed to systematically evaluate the association between adipocytokines (leptin, chemerin, apelin, and omentin-1) and DR. Methods: The PubMed, Web of Science, Embase, EBSCO and Willy databases were used to search for potential studies with keywords such as "diabetic retinopathy" or "DR" in combination with the terms "leptin," "chemerin", "apelin" or "omentin-1" in the search titles or abstracts. Standardized mean differences (SMD) with corresponding 95% confidence intervals (CIs) were determined as the results of the meta-analysis. Results: After screening, 18 articles were included in the meta-analysis including 750 DR cases and 993 controls. Leptin and chemerin levels in patients with DR were significantly higher than those in the control group (SMD: 0.68, 95% CI [0.1, 1.26]; SMD: 0.79, 95% CI [0.35, 1.23]). The omentin-1 levels in patients with DR were significantly lower than those in the controls (SMD: -0.85, 95% CI [-1.08, -0.62]). Conclusions: To the best of our knowledge, this is the first meta-analysis to evaluate the leptin, chemerin, apelin, and omentin-1 levels in patients with DR. Further high-quality studies are warranted to support the association between these adipocytokines and DR. Systematic review registration: https://www.crd.york.ac.uk/PROSPERO/display_record.php?RecordID=443770, identifier CRD42023443770.

Adipocyte dysfunction promotes lung inflammation and aberrant repair: a potential target of COPD.

Background: Obesity and chronic obstructive pulmonary disease (COPD) are prevailing worldwide, bringing a heavy medical burden. Clinical and pathophysiological relationship between obesity and COPD is paradoxical and elusive. We aim to explore their inherent associations from clinical, genetic, and animal levels. Methods: We performed literature review and cohort analysis of patients with COPD to compare lung function, symptom, and prognosis among different weight groups. After retrieving datasets of obesity and COPD in Gene Expression Omnibus (GEO) database, we carried out differentially expressed gene analysis, functional enrichment, protein-protein interactions network, and weighted gene co-expression network analysis. Then, we acquired paraffin-embedded lung tissues of fatty acid-binding protein 4-Cre-BMPR2fl/fl conditional knockout (CKO) mice that were characterized by adipocyte-specific knockout of bone morphogenetic protein receptor 2 (BMPR2) for staining and analysis. Results: Our cohort study reports the effect of obesity on COPD is inconsistent with previous clinical studies. Lung function of overweight group was statistically superior to that of other groups. We also found that the inflammatory factors were significantly increased hub genes, and cytokine-associated pathways were enriched in white adipose tissue of patients with obesity. Similarly, injury repair-associated genes and pathways were further enhanced in the small airways of patients with COPD. CKO mice spontaneously developed lung injury, emphysema, and pulmonary vascular remodeling, along with increased infiltration of macrophages. BMPR2-defiecient adipocytes had dysregulated expression of adipocytokines. Conclusion: Inflammation and abnormal repair might be potential mechanisms of the pathological association between obesity and COPD. BMPR2-associated adipocyte dysfunction promoted lung inflammation and aberrant repair, in which adipocytokines might play a role and thus could be a promising therapeutic target.

The role of perivascular adipose tissue-secreted adipocytokines in cardiovascular disease.

Perivascular adipose tissue and the vessel wall are connected through intricate bidirectional paracrine and vascular secretory signaling pathways. The secretion of inflammatory factors and oxidative products by the vessel wall in the diseased segment has the ability to influence the phenotype of perivascular adipocytes. Additionally, the secretion of adipokines by perivascular adipose tissue exacerbates the inflammatory response in the diseased vessel wall. Therefore, quantitative and qualitative studies of perivascular adipose tissue are of great value in the context of vascular inflammation and may provide a reference for the assessment of cardiovascular ischemic disease.

Effect of non-surgical periodontal treatment on cytokines/adipocytokines levels among periodontitis patients with or without obesity: a systematic review and meta-analysis.

BACKGROUND: The objective of this systematic review and meta-analysis was to evaluate the effects of non-surgical periodontal therapy (NSPT) on inflammatory-related cytokines/adipocytokines in periodontitis patients with or without obesity. METHODS: We followed the preferred reporting items for systematic reviews and meta-analyses statement and registered the study (CRD42022375331) in the Prospective International Register of Systematic Reviews. We screened randomized-controlled trials and controlled clinical trials from six databases up to December 2022. Quality assessment was performed with RoB-2 and ROBINS-I tools for randomized trials and non-randomized trials, respectively. Meta-analysis was carried out using a random-effect model. RESULTS: We included seventeen references in the systematic analysis, and sixteen in the meta-analysis. Baseline results of pro-inflammatory biomarkers, including serum interleukin (IL)-6, serum and gingival crevicular fluid (GCF), tumor necrosis factor (TNF)-a, serum C-reactive protein (CRP)/hs-CRP, and serum and GCF resistin, were higher in obesity subjects than in normal weight subjects. The effect of NSPT with respect to levels of cytokines/adipocytokines, including IL-6, TNF-a, CRP/hs-CRP, resistin, adiponectin, leptin and retinol binding protein 4 (RBP4), were then analyzed in the systematic and meta-analysis. After three months of NSPT, serum (MD = -0.54, CI = -0.62 - -0.46), and GCF (MD = -2.70, CI = -4.77 - -0.63) levels of IL-6, along with the serum RBP4 (MD = -0.39, CI = -0.68-0.10) decreased in periodontitis individuals with obesity. NSPT also improved GCF adiponectin levels after three months (MD = 2.37, CI = 0.29 - 4.45) in periodontitis individuals without obesity. CONCLUSIONS: Obese status altered the baseline levels of cytokines/adipocytokines (serum IL-6, serum and GCF TNF-a, serum CRP/hs-CRP, and serum and GCF resistin). Then NSPT can shift the levels of specific pro-inflammatory mediators and anti-inflammatory mediators in biological fluids, both in obesity and non-obesity individuals. NSPT can reduce serum and GCF IL-6 levels together with serum RBP4 level in individuals with obesity after 3 months, besides, there is no sufficient evidence to prove that obese patients have a statistically significant decrease in the levels of other cytokines compared to patients with normal weight. NSPT can also increase GCF adiponectin level in normal weight individuals after 3 months. Our findings imply the potential ideal follow-up intervals and sensitive biomarkers for clinical bioanalysis in personalized decision-making of effect of NSPT due to patients' BMI value.

Exploring the Network between Adipocytokines and Inflammatory Response in SARS-CoV-2 Infection: A Scoping Review.

Adipose tissue is actually regarded as an endocrine organ, rather than as an organ that merely stores energy. During the COVID-19 pandemic, obesity has undoubtedly emerged as one of the most important risk factors for disease severity and poor outcomes related to SARS-CoV-2 infection. The aberrant production of cytokine-like hormones, called adipokines, may contribute to alterations in metabolism, dysfunction in vascular endothelium and the creation of a state of general chronic inflammation. Moreover, chronic, low-grade inflammation linked to obesity predisposes the host to immunosuppression and excessive cytokine activation. In this respect, understanding the mechanisms that link obesity with the severity of SARS-CoV-2 infection could represent a real game changer in the development of new therapeutic strategies. Our review therefore examines the pathogenic mechanisms of SARS-CoV-2, the implications with visceral adipose tissue and the influences of the adipose tissue and its adipokines on the clinical behavior of COVID-19.

Actinidia deliciosa Extract as a Promising Supplemental Agent for Hepatic and Renal Complication-Associated Type 2 Diabetes (In Vivo and In Silico-Based Studies).

Type 2 diabetes (T2D) is a chronic metabolic condition associated with obesity, oxidative stress-mediated inflammation, apoptosis, and impaired insulin signaling. The utilization of phytochemical therapy generated from plants has emerged as a promising approach for the treatment of diabetes and its complications. Kiwifruit is recognized for its substantial content of antioxidative phenolics. Therefore, this work aimed to examine the effect of Actinidia deliciosa (kiwi fruit) on hepatorenal damage in a high-fat diet (HFD) and streptozotocin (STZ)-induced T2D in rats using in vivo and in silico analyses. An increase in hepatic and renal lipid peroxidation was observed in diabetic rats accompanied by a decrease in antioxidant status. Furthermore, it is important to highlight that there were observable inflammatory and apoptotic responses in the hepatic and renal organs of rats with diabetes, along with a dysregulation of the phosphorylation levels of mammalian target of rapamycin (mTOR), protein kinase B (Akt), and phosphoinositide 3-kinase (PI3K) signaling proteins. However, the administration of kiwi extract to diabetic rats alleviated hepatorenal dysfunction, inflammatory processes, oxidative injury, and apoptotic events with activation of the insulin signaling pathway. Furthermore, molecular docking and dynamic simulation studies revealed quercetin, chlorogenic acid, and melezitose as components of kiwi extract that docked well with potential as effective natural products for activating the silent information regulator 1(SIRT-1) pathway. Furthermore, phenolic acids in kiwi extract, especially syringic acid, P-coumaric acid, caffeic acid, and ferulic acid, have the ability to inhibit the phosphatase and tensin homolog (PTEN) active site. In conclusion, it can be argued that kiwi extract may present a potentially beneficial adjunctive therapy approach for the treatment of diabetic hepatorenal complications.

Hormonal Determinants of Growth and Weight Gain in the Human Fetus and Preterm Infant.

The factors controlling linear growth and weight gain in the human fetus and newborn infant are poorly understood. We review here the changes in linear growth, weight gain, lean body mass, and fat mass during mid- and late gestation and the early postnatal period in the context of changes in the secretion and action of maternal, placental, fetal, and neonatal hormones, growth factors, and adipocytokines. We assess the effects of hormonal determinants on placental nutrient delivery and the impact of preterm delivery on hormone expression and postnatal growth and metabolic function. We then discuss the effects of various maternal disorders and nutritional and pharmacologic interventions on fetal and perinatal hormone and growth factor production, growth, and fat deposition and consider important unresolved questions in the field.

Pre-procedural high serum visfatin and tumor necrosis factor-α might predict recurrent atrial fibrillation after catheter ablation.

BACKGROUND: Many patients would require repeated ablation procedures owing to recurrent atrial fibrillation with its associated symptoms. Identifying those who are at risk of recurrent AF could assist us to develop preventive strategies and to properly select those who will benefit more from catheter ablation. Our aim is to study the role of preprocedural serum level of certain biomarkers in the prediction of AF recurrence after catheter ablation. RESULTS: The present study included 117 patients: 26 patients with persistent and 91 patients with paroxysmal AF. Blood samples for estimation of serum levels of studied cytokines were obtained prior to the procedure. Pulmonary vein isolation was performed in all patients through point-by point radiofrequency ablation guided by 3D electroanatomical mapping system. Patients were followed for 12 months for AF recurrence. Forty-one (35%) patients developed AF recurrence. Those patients were significantly older, had significantly higher BMI, lower ejection fraction, and wider maximal left atrial diameter (LAD). Serum hs-CRP, IL-6, TNF-α, visfatin, and adiponectin levels were significantly higher compared to those who did not develop AF recurrence. Correlation analysis showed positive correlations between the incidence of RAF and patients' age, BMI, and maximum LAD and elevated cytokine levels and maximal LAD showed significant correlations with the type of AF and elevated serum TNF-α, visfatin, and adiponectin. Statistical analyses defined elevated serum levels of TNF-α, visfatin, and adiponectin as positive predictors for RAF, and automatic linear modeling analysis showed that elevated serum visfatin, TNF-α, and adiponectin can predict RAF by accuracy rates of 50%, 34%, and 16%, respectively. CONCLUSIONS: RAF is most probably an outcome of the interplay between patients' clinical data, obesity, and inflammation. Pre-procedural estimation of serum levels of visfatin and TNF-α might determine patients with probability for RAF.