Investigation of serum Metrnl levels in pregnant women with gestational diabetes mellitus: a prospective non-interventional cohort study.

OBJECTIVE: The objective of this study was to investigate serum Metrnl levels in pregnant women with gestational diabetes mellitus and compare them with pregnant women without gestational diabetes mellitus. METHODS: The gestational diabetes mellitus group consisted of 87 pregnant women diagnosed with gestational diabetes mellitus, and the control group consisted of 93 healthy pregnant women without gestational diabetes mellitus. Serum Metrnl levels were determined by the enzyme-linked immunosorbent assay method. RESULTS: The two groups were similar in terms of demographic features. The median serum Metrnl level was found to be 1.16 ng/mL in the gestational diabetes mellitus group, while it was determined as 2.2 ng/mL in the control group (p=0.001). The two groups were divided into two subgroups based on participants' body mass index, normal weight and overweight. The lowest median Metrnl level was detected in the normal weight gestational diabetes mellitus group, followed by the overweight gestational diabetes mellitus group, normal weight control group, and overweight control group (1.1, 1.2, 2, and 2.4 ng/mL, respectively). Receiver operating curve analysis was performed to determine the value of the serum Metrnl level in terms of predicting gestational diabetes mellitus. The area under the curve analysis of serum Metrnl for gestational diabetes mellitus estimation was 0.768 (p=0.000, 95%CI 0.698-0.839). The optimal cutoff value for serum Metrnl level was determined as 1.53 ng/mL with 69% sensitivity and 70% specificity. CONCLUSION: Serum Metrnl levels in pregnant women with gestational diabetes mellitus were found to be significantly lower than in pregnant women without gestational diabetes mellitus. The mechanisms underlying the decrease in serum Metrnl levels in gestational diabetes mellitus remain unclear for now, and future studies will reveal the role of Metrnl in the pathophysiology of gestational diabetes mellitus.

Asprosin levels in patients with type 2 diabetes mellitus, metabolic syndrome and obesity: A systematic review and meta-analysis.

BACKGROUND & AIMS: Asprosin is a promising candidate for novel treatments for metabolic-endocrine disorders. The objective of this systematic review and meta-analysis was to consolidate the existing evidence regarding asprosin levels in patients diagnosed with type 2 diabetes (T2D), metabolic syndrome (MetS), and obesity. METHODS: Scopus, Embase, PubMed, Ovid/Medline, and Web of Science were systematically searched without restrictions. We only used the standardized mean differences (SMD) with their 95 % confidence intervals (95 % CI) as the effect measure. A random-effects model (DerSimonian and Laird method) was used for the meta-analysis. Risk of bias was assessed with the Newcastle-Ottawa Scale and Newcastle-Ottawa Scale for Cross-Sectional Studies. RESULTS: Twenty-six studies (n = 3,787) were included in the meta-analysis. Participants with T2D had higher asprosin values than those without T2D (SMD: 1.64; 95 % CI: 1.08-2.21; I2 = 97 %). Patients with MetS had higher asprosin levels compared to those without MetS (SMD: 0.99; 95 % CI: 0.34-1.64; I2 = 96 %). Patients with obesity had higher asprosin levels than participants without obesity (SMD: 1.49; 95 % CI: 0.23-2.76; I2 = 98 %). CONCLUSIONS: Asprosin is significantly higher in patients with either T2D, MetS, or obesity, compared with controls.

Total Gestational Weight Gain Is Explained by Leptin and Body Fat, Regardless of Pre-Pregnancy Body Mass Index and Other Adipokines, in Mexican Adolescents.

Pre-pregnancy body mass index (pBMI) is a predictor of gestational weight gain (GWG). However, other factors, such as adipokines and inflammation markers, may also be associated with GWG. The aim of the study was to determine the association of leptin, adiponectin, irisin, and C-reactive protein, with GWG in adolescents. A longitudinal study was conducted from 2018 to 2023 in adolescents with a clinically healthy pregnancy. The assessments included sociodemographic and clinical data, pBMI, percent of body fat, serum concentrations of leptin, adiponectin, irisin, and high-sensitivity C-reactive protein (hsCRP), and total GWG adequacy. Cox regression models were performed, the outcome variables were inadequate and excessive GWG. In 198 participants, being overweight/obesity was marginally associated with a protective effect against inadequate GWG (HR = 0.44, 95%CI = 0.18-1.06), regardless of maternal characteristics and adipokines. Leptin (HR = 1.014, 95%CI = 1.008-1.021), and body fat percent (HR = 1.11, 95%CI = 1.05-1.17) were associated with a higher risk of excessive GWG, independent of other maternal variables such as pBMI, while adiponectin was associated with a lower risk. These findings suggest that, in Mexican adolescents, adipose tissue and its adipokines during pregnancy may play a more significant role in the final GWG than body weight.

Comparative Effects of Gymnema sylvestre and Berberine on Adipokines, Body Composition, and Metabolic Parameters in Obese Patients: A Randomized Study.

Gymnema sylvestre (GS) and berberine (BBR) are natural products that have demonstrated therapeutic potential for the management of obesity and its comorbidities, as effective and safe alternatives to synthetic drugs. Although their anti-obesogenic and antidiabetic properties have been widely studied, comparative research on their impact on the gene expression of adipokines, such as resistin (Res), omentin (Ome), visfatin (Vis) and apelin (Ap), has not been reported. METHODOLOGY: We performed a comparative study in 50 adult Mexican patients with obesity treated with GS or BBR for 3 months. The baseline and final biochemical parameters, body composition, blood pressure, gene expression of Res, Ome, Vis, and Ap, and safety parameters were evaluated. RESULTS: BBR significantly decreased (p < 0.05) body weight, blood pressure and Vis and Ap gene expression and increased Ome, while GS decreased fasting glucose and Res gene expression (p < 0.05). A comparative analysis of the final measurements revealed a lower gene expression of Ap and Vis (p < 0.05) in patients treated with BBR than in those treated with GS. The most frequent adverse effects in both groups were gastrointestinal symptoms, which attenuated during the first month of treatment. CONCLUSION: In patients with obesity, BBR has a better effect on body composition, blood pressure, and the gene expression of adipokines related to metabolic risk, while GS has a better effect on fasting glucose and adipokines related to insulin resistance, with minimal side effects.

Associations of Abnormal Maternal Glucose Regulation in Pregnancy with Offspring Adiposity, Insulin Resistance, and Adipokine Markers During Childhood and Adolescence.

OBJECTIVE: To examine the associations of abnormal maternal glucose regulation in pregnancy with offspring adiposity, insulin resistance, adipokine, and inflammatory markers during childhood and adolescence. STUDY DESIGN: Project Viva is a prospective prebirth cohort (n = 2128 live births) initiated from 1999 through 2002 in Eastern Massachusetts, US. During the second trimester of pregnancy, clinicians used 2-step oral glucose challenge testing to screen for gestational diabetes mellitus. In the offspring, we measured anthropometry, insulin resistance, adipokines, lipids, and inflammatory markers in mid-childhood (n = 1107), early adolescence (n = 1027), and mid-adolescence (n = 693). We used multivariable linear regression models and generalized estimating equations adjusted for child age and sex, and for maternal age, race/ethnicity, education, parity, and smoking during pregnancy; we further adjusted for prepregnancy body mass index (BMI). RESULTS: In mid-adolescence (17.1 [0.8] years of age), offspring of mothers with gestational diabetes mellitus (n = 27) had a higher BMI z-score (ß; 95% Cl; 0.41 SD; 0.00, 0.82), sum of skinfolds (8.15 mm; 2.48, 13.82), homeostatic model assessment for insulin resistance (0.81 units; 0.13, 1.50), leptin z-score (0.40 SD; 0.01, 0.78), and leptin/adiponectin ratio z-score (0.51 SD; CI 0.09, 0.93) compared with offspring of mothers with normoglycemia (multivariable-adjusted models). The associations with BMI, homeostatic model assessment for insulin resistance, and adiponectin seemed stronger in mid-adolescence compared with earlier time points. The associations were attenuated toward the null after adjustment for maternal prepregnancy BMI. CONCLUSION: Exposure to gestational diabetes mellitus is associated with higher adiposity, insulin resistance, and altered adipokines in mid-adolescence. Our findings suggest that the peripubertal period could be a key time for the emergence of prenatally programmed metabolic abnormalities.

Underlying Mechanisms behind the Brain-Gut-Liver Axis and Metabolic-Associated Fatty Liver Disease (MAFLD): An Update.

Metabolic-associated fatty liver disease (MAFLD) includes several metabolic dysfunctions caused by dysregulation in the brain-gut-liver axis and, consequently, increases cardiovascular risks and fatty liver dysfunction. In MAFLD, type 2 diabetes mellitus, obesity, and metabolic syndrome are frequently present; these conditions are related to liver lipogenesis and systemic inflammation. This study aimed to review the connection between the brain-gut-liver axis and MAFLD. The inflammatory process, cellular alterations in hepatocytes and stellate cells, hypercaloric diet, and sedentarism aggravate the prognosis of patients with MAFLD. Thus, to understand the modulation of the physiopathology of MAFLD, it is necessary to include the organokines involved in this process (adipokines, myokines, osteokines, and hepatokines) and their clinical relevance to project future perspectives of this condition and bring to light new possibilities in therapeutic approaches. Adipokines are responsible for the activation of distinct cellular signaling in different tissues, such as insulin and pro-inflammatory cytokines, which is important for balancing substances to avoid MAFLD and its progression. Myokines improve the quantity and quality of adipose tissues, contributing to avoiding the development of MAFLD. Finally, hepatokines are decisive in improving or not improving the progression of this disease through the regulation of pro-inflammatory and anti-inflammatory organokines.

The role of adiposity, adipokines and polymorphisms of leptin and adiponectin in myelodysplastic syndromes.

The aim of the present study was to investigate the relationship between leptin and adiponectin gene polymorphisms, circulating levels of leptin and adiponectin, adiposity and clinical markers in patients with myelodysplastic syndrome (MDS). This cross-sectional study was conducted with 102 adults and elderly MDS patients and 102 age- and sex-matched controls. Clinical characteristics, co-morbidities, anthropometric data, laboratory evaluation and genetic analysis (polymorphisms -2548G > A/rs7799039 of the LEP gene and +276G > T/rs1501299 of the ADIPOQ gene) were investigated. Serum leptin was higher and adiponectin lower in MDS when compared with controls. There was a significant positive correlation between serum leptin levels and BMI (r = 0·264, P = 0·025), waist circumference (r = 0·235, P = 0·047), body fat percentage (BF %) (r = 0·373, P = 0·001) and the fat mass index (FMI) (r = 0·371, P < 0·001). A lower mean adiponectin was found among patients with high BF %, higher visceral adiposity index and metabolic syndrome. A significant association was found between the AA genotype (mutant) of the LEP polymorphism rs7799039 and male sex and blast excess (≥ 5 %). In addition, a significant association was observed between the TT genotype (mutant) of the ADIPOQ rs1501299 polymorphism and Fe overload. These results demonstrate the importance of a comprehensive and systematic evaluation in patients with MDS in order to identify and control negative factors not related to the disease at an early stage.

High glycemia and resistin normalized in children with double burden of malnutrition: a cross-sectional study.

The coexistence of stunting and excess weight in the same individual is defined as a double burden of malnutrition (DBM) and is associated with noncommunicable diseases. In this study, we evaluated the impact of DBM on adipokine concentrations and metabolic profiles in children compared with weight excess alone. Children were allocated to the weight excess group (n = 23) (height-for-age (HAZ) > 0.0 and < 2.0 Z-score and body mass index-for-age (BMI/A) > 1.0 Z-score) or DBM (n = 22) group (HAZ < -1.0 Z-score (including mild stunting) and BMI/A > 1.0 Z-score). Lipid, glycemic profile, resistin, plasminogen activator inhibitor-1, leptin, and adiponectin concentrations were analyzed. Glycemia was significantly higher in the DBM group compared to the weight excess group (5.05 (4.76-5.31) mmol/L vs. 4.57 (4.35-4.81) mmol/L), although no differences were found in insulin and homeostasis model assessment of insulin resistance (HOMA-IR). Adipokine concentrations did not differ between the groups. However, the DBM group showed higher resistin concentrations normalized by body fat mass than those of the weight excess group (1.44 (0.98-1.93) ng/mL vs. 0.76 (0.55-1.45) ng/mL). Insulin and HOMA-IR showed a negative correlation with adiponectin (r = -0.590 and -0.624, respectively, both p < 0.01). DBM was associated with increased glucose and resistin concentrations adjusted by fat mass compared to that associated with excess weight alone. Therefore, this association between mild stunting and weight excess has deleterious potential for long-term metabolic function, highlighting an additional precaution against weight gain in children, especially in those with stunting.

Adipokines and Inflammatory Markers in Acute Myocardial Infarction Patients with and without Obstructive Sleep Apnea: A Comparative Analysis.

An association has been suggested between acute myocardial infarction (AMI) and obstructive sleep apnea (OSA). Considering the role of adipose-tissue-derived inflammatory mediators (adipokines) and the shared risk factor of obesity in OSA and AMI, this study aimed to investigate the involvement of adipokines in AMI patients with and without OSA. Serum levels of adipokines and inflammatory mediators were quantified, and home respiratory polygraphy was conducted. A total of 30 AMI patients and 25 controls were included. Patients with AMI exhibited elevated levels of resistin (7.4 vs. 3.7 ng/mL), interleukin-6 (8.8 vs. 1.3 pg/mL), and endothelin-1 (3.31 vs. 1.8 pg/mL). Remarkably, AMI patients with concomitant OSA exhibited higher levels of resistin (7.1 vs. 3.7 ng/mL), interleukin-6 (8.9 vs. 1.3 pg/mL), endothelin-1 (3.2 vs. 1.8 pg/mL), creatin kinase (1430 vs. 377 U/L), creatine kinase-MB (64.6 vs. 9.7 ng/mL), and troponin T (2298 vs. 356 pg/mL) than their non-OSA counterparts. Leptin showed a correlation with OSA severity markers. OSA was associated with greater cardiac damage in AMI patients. Our findings underscore that adipokines alone are not sufficient to discriminate the risk of AMI in the presence of OSA. Further research is necessary to determine the potential mechanisms contributing to exacerbated cardiac damage in patients with both conditions.

Excessive Pregestational Weight and Maternal Obstetric Complications: The Role of Adipokines.

There is a high frequency of overweight and obesity in women of reproductive age. Women who start pregnancy with overweight or obesity have an increased risk of developing maternal obstetric complications such as gestational hypertension, pre-eclampsia, gestational diabetes mellitus, postpartum hemorrhage, and requiring C-section to resolve the pregnancy with a higher risk of C-section surgical site infection. Excessive weight in pregnancy is characterized by dysregulation of adipokines, the functions of which partly explain the predisposition of pregnant women with overweight or obesity to these maternal obstetric complications. This review compiles, organizes, and analyzes the most recent studies on adipokines in pregnant women with excess weight and the potential pathophysiological mechanisms favoring the development of maternal pregnancy complications.

Adipokines from adipose tissue and common variable immunodeficiency: Is there any association?

Adiponectin and leptin are adipokines, secreted by white adipose tissue (WAT), which play an important role in energy homeostasis. Some evidence has shown that adipokine-producing adipose cells present in the bone marrow (BM) appear to exert an influence on hematopoiesis and B cell development. Common variable immunodeficiency (CVID) is one of the most common inborn errors of immunity in humans. In CVID, numerical and/or functional defects of B cells and their precursors result in hypogammaglobulinemia, usually Immunoglobulin (Ig) A and IgG. Manifestations of CVID include immunodeficiency, autoimmunity, inflammation and lymphoproliferation, resulting in a wide range of phenotypes. How adipokines interact and influence the pathophysiology of CVID is still unclear. In this review, we seek to summarize the aspects known so far concerning the interface between adipokines, B cells and CVID. More research is needed to fully understand these interactions; this knowledge is a potential avenue for the discovery of useful biomarkers and may provide new therapeutic targets for the treatment of patients with CVID and related diseases.

Serum levels and gestational curve of adiponectin and leptin during adolescent pregnancy.

OBJECTIVE: This study aimed to develop a curve of weekly serum levels of adiponectin and leptin among pregnant adolescents. In addition, pregestational body mass index and weight gain were assessed and correlated with the serum concentration of these molecules. METHODS: This was a prospective cohort study, including only pregnant adolescents with eutrophic pre-gestational body mass index who were weekly followed during the evolution of gestation. The serum concentrations of adipokines were determined using commercial ELISA kits and were correlated to pre-gestational body mass index and pregnancy weight gain. A total of 157 pregnant women participated in this study. RESULTS: Adiponectin levels showed a significant decrease among the trimesters (p=0.0004). However, we did not observe significant differences among its levels when compared weekly, neither of which was between adiponectin concentration and pre-gestational body mass index or weight gain (p=0.36 and p=0.10, respectively). In contrast, we detected a significant increase in weekly serum leptin levels (p<0.0001), positively correlated to both pre-gestational body mass index and weight gain (p=0.003 and p=0.0007, respectively). CONCLUSION: These adipokines present a different profile throughout adolescent pregnancy.

Adiponectin and resistin modulate the progression of Alzheimer´s disease in a metabolic syndrome model.

Metabolic syndrome (MetS), a cluster of metabolic conditions that include obesity, hyperlipidemia, and insulin resistance, increases the risk of several aging-related brain diseases, including Alzheimer's disease (AD). However, the underlying mechanism explaining the link between MetS and brain function is poorly understood. Among the possible mediators are several adipose-derived secreted molecules called adipokines, including adiponectin (ApN) and resistin, which have been shown to regulate brain function by modulating several metabolic processes. To investigate the impact of adipokines on MetS, we employed a diet-induced model to induce the various complications associated with MetS. For this purpose, we administered a high-fat diet (HFD) to both WT and APP/PSN1 mice at a pre-symptomatic disease stage. Our data showed that MetS causes a fast decline in cognitive performance and stimulates Aß42 production in the brain. Interestingly, ApN treatment restored glucose metabolism and improved cognitive functions by 50% while decreasing the Aß42/40 ratio by approximately 65%. In contrast, resistin exacerbated Aß pathology, increased oxidative stress, and strongly reduced glucose metabolism. Together, our data demonstrate that ApN and resistin alterations could further contribute to AD pathology.

The role of sex in the relationship between fasting adipokines levels, maximal fat oxidation during exercise, and insulin resistance in young adults with excess adiposity.

AIM: Previous evidence suggest that a sexual dimorphism in exercise fat oxidation and adipokines levels may explain a lower risk of cardio-metabolic disorders in women. Therefore, we investigated the role of sex in the relationship between adipokines levels, maximal fat oxidation (MFO) during exercise and insulin resistance. METHODS: Fifty young adults with excess adiposity (31 women; body fat: 38.7 ± 5.3%) were included in this study. The fasting levels of leptin, adiponectin, glucose and insulin were determined from blood samples and the homeostatic model assessment of insulin resistance index (HOMA-IR) subsequently calculated. Body fat percentage and visceral adipose tissue (VAT) were assessed through dual-energy X-ray absorptiometry whereas MFO was estimated during an incremental-load exercise test after an overnight fasting through indirect calorimetry. RESULTS: Men had lower levels of body fat (d = 1.80), adiponectin (d = 1.35), leptin (d = 0.43) and MFO (d = 1.25) than women. Conversely, men showed higher VAT (d = 0.85) and fasting glucose levels (d = 0.89). No sex differences were observed in HOMA-IR (d = 0.34). Adipokines levels were not associated with MFO in both sexes (r < 0.30), whereas adiponectin levels were inversely related with HOMA-IR in both men (r = -0.58) and women (r = -0.50). Leptin concentration was associated to HOMA-IR only in men (r = 0.41), while no statistically significant relationships were observed between MFO and HOMA-IR in both sexes (r < 0.44). CONCLUSION: Insulin resistance was similar between sexes regardless of superior levels of adipokines and MFO during exercise in women. Therefore, adiponectin and leptin may regulate glucose homeostasis without altering whole body fat oxidation rate during exercise.

Serum levels of anti-inflammatory/proinflammatory adipocytokines, and copper levels in overweight and obese women in an adult Mexican population.

BACKGROUND: An imbalance between adipokines and micronutrient concentrations, such as those of copper (Cu), has been linked to dysregulation of energy homeostasis leading to weight gain and the development of other comorbidities; however, information on this issue remains limited. Our aim was to investigate the correlation between Cu status and serum adipokine levels and their relationship in normal-weight, overweight, and obese adult women. METHODS: Sixty patients were evaluated and classified according to their body mass index (BMI) and biochemical parameters; adipokines and Cu were measured at fasting. RESULTS: Leptin (Lep) and resistin (Res) levels were elevated, whereas adiponectin (Adpn) and ghrelin (Ghr) values were decreased in overweight and obese women (p = 0.001). The mean Adpn/Lep ratio was <0.5 in overweight and obese subjects, while the Lep/Ghr ratio increased significantly in relation to weight gain, suggesting an inverse link between the ratios of these hormones in the regulation of obesity. The analysis revealed a positive association between BMI and Cu levels in obese women. Moreover, a negative association between Cu and Res in normal-weight subjects was found. CONCLUSIONS: Circulating fasting Res levels are negatively associated with serum Cu concentration in normal-weight adult women. We also observed a close relationship between Adpn/Lep and Lep/Ghr ratios with obesity. However, more observational studies are required to confirm these results in future research.

Effect of obesity, lipids and adipokines on allergic rhinitis risk: a Mendelian randomization study.

OBJECTIVES: Observational studies suggested that obesity may promote the development of allergic rhinitis. The aim of this study was to explore the association of obesity, lipids and adipokines with this allergic disease at the genetic level using Mendelian randomization strategies. METHODS: Summary data for three obesity indicators (such as body mass index), eight lipid indicators (such as triglycerides) and six adipokines (such as interleukin-6 and adipocyte fatty acid-binding protein) were collected, and suitable instrumental variables were extracted from these summary data according to the three main assumptions of Mendelian randomization. Three Mendelian randomization methods (such as inverse variance weighted) were used to detect the casual effect of the above indicators on allergic rhinitis risk. Sensitivity analyses were performed to assess heterogeneity and horizontal pleiotropy. RESULTS: After Bonferroni correction, the inverse variance weighted reported that elevated levels of interleukin-6 and adipocyte fatty acid-binding protein were nominally associated with the decreased risk of allergic rhinitis (OR = 0.870, 95% CI 0.765-0.990, p = 0.035; OR = 0.732, 95% CI 0.551-0.973, p = 0.032). The other Mendelian randomization methods supported these results. Obesity, lipids and other adipokines were not related to this allergic disease. Sensitivity analyses found no heterogeneity and horizontal pleiotropy in the study. CONCLUSION: The study provided some interesting, but not sufficient, evidence to suggest that interleukin-6 and adipocyte fatty acid-binding protein might play a protective role in the development of allergic rhinitis at the genetic level. These findings should be validated by more research. LEVEL OF EVIDENCE: This was a Mendelian randomized study with a level of evidence second only to clinical randomized trials, and higher than cohort and case-control studies.

Marcadores bioquímicos propuestos para el estudio de la sarcopenia / Proposed biochemical markers for the study of sarcopenia

La sarcopenia asociada a la edad es una condición clínica caracterizada por una disminución en la fuerza, calidad y cantidad de masa muscular así como también en la función muscular. Un biomarcador se define como una característica que es medible objetivamente y evaluable como indicador de un proceso biológico normal, patológico o respuesta terapéutica a una intervención farmacológica. Los marcadores bioquímicos propuestos para el estudio de la sarcopenia pueden ser categorizados en dos grupos. El primero de ellos evalúa el estatus musculoesquelético; este panel de marcadores está formado por miostatina/folistatina, procolágeno aminoterminal tipo III e índice de sarcopenia. El segundo grupo de marcadores bioquímicos evalúa factores causales, para lo cual se sugiere medir el factor de crecimiento insulino-símil tipo 1 (IGF-1), dehidroepiandrosterona (DHEAS), cortisol, facto-res inflamatorios [proteína C reactiva (PCR), interleuquina 6 (IL-6) y factor de necrosis tu-moral (TNF-a)]. Las recomendaciones realiza-das están basadas en la evidencia científica disponible en la actualidad y la disponibilidad de la metodología apropiada para cada uno de los biomarcadores. (AU)

Sarcopenia is a progressive and generalized skeletal muscle disorder defined by decrease in the strength, quality and quantity of muscle mass as well as in muscle function. A biomarker is defined as a feature objectively measured and evaluated as an indicator of a normal biologic process, a pathogenic process or a pharmacologic response to therapeutic intervention. The biochemical markers proposed for the study of sarcopenia may be classified in two groups. The first group evaluates the musculoskeletal status, made up by myostatin/follistatin, N-terminal Type III Procollagen and the sarcopenia index. The second evaluates causal factors, where the measurement of the following is suggested: hormones insulin-like growth factor-1 (IGF-I), dehydroepiandrosterone sulphate (DHEAS), cortisol, inflammatory factors [C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-a (TNF-a)]. The recommendations made are based on scientific evidence currently available and the appropriate methodology availability for each biomarker. (AU)

Acute and Chronic Effects of Strength Training on Plasma Levels of Adipokines in Man.

Adipose tissue is specialized cells that produce and release adipokines. Exercise may modulate adipokine production in adipocytes. The aim of this longitudinal study was to evaluate the acute and chronic effects of strength training (ST) on plasma levels of adiponectin, leptin, and resistin. Twelve untrained young male participants (23.42±2.67 years) were selected. The training protocol consisted of 3 exercises, with 3 sets of 65% of 1RM (one-repetition maximum) with pause of 90 s between sets with duration of 5 s/repetition (2 s conc/3 s ecc), 3 times a week for 10 weeks. Blood was collected at four time points: before and after the first ST session and before and after the last ST session. The comparisons between adipokine levels before and after the same training session showed acute changes, while the comparisons between levels before or after the first session versus before or after the last session revealed chronic alterations. ST increased adiponectin levels after the first exercise session in comparison to levels before this session [50 952 (46 568-51 894) pg/mL vs. 52 981 (49 901-54 467) pg/mL, p=0.019]. Similar differences were observed for resistin levels, which were higher after the last session compared to before [4 214.4 (±829) pg/mL vs. pre-S30 2 251.3 (±462.2) pg/mL, p=0.0008] and in the comparison between after the last and after the first ST sessions [4 214.4 (±829.0) pg/mL vs. 1 563.7 (±284.8) pg/mL, p=0.004]. Leptin levels acutely changed in the last training session. ST produced acute and chronic changes in plasma adipokines.

Higher serum uric acid is associated with body fat, retinol-binding protein 4, and antioxidative status in Brazilian children.

OBJECTIVE: The aim of this study was to evaluate the association of serum uric acid (SUA) with adiposity, adipokines, and anti- and oxidative markers in Brazilian children. METHODS: This was a cross-sectional investigation with 378 children ages 8 to 9 y in Viçosa, Minas Gerais, Brazil. Information on sociodemographic and lifestyle characteristics was obtained via questionnaires, and body fat was determined by dual energy x-ray absorptiometry. We compared the distributions of adiposity (total and central), adipokines (adiponectin, chemerin, leptin, and retinol-binding protein 4 [RBP4]), anti- and oxidative markers (plasma ferric reducing antioxidant power [FRAP], superoxide dismutase [SOD], and malondialdehyde [MDA]) by SUA categories using linear regression. RESULTS: SUA was positively associated with total and central fat. Every standard deviation (SD) of SUA was related, respectively, to a 3.4 (95% confidence interval [CI], 2.4-4.4), 4 (95% CI, 2.8-5.1), 4.2 (95% CI, 2.9-5.5), and 3.5 (95% CI, 2.4-4.6) units higher of total, truncal, android, and gynoid fat. We found a positive association of SUA with RBP4 and FRAP, and a negative association with MDA. Every SD of SUA was related, respectively, to 0.1 (95% CI, 0.01-0.1) and 7.8 (95% CI, 5.5-10.1) units higher of RBP4 and FRAP; and to -0.3 (95% CI, -0.5 to -0.1) units lower of MDA. CONCLUSIONS: SUA was positively associated with adiposity, RBP4, and antioxidative status in Brazilian children.

Adiponectin: A "Friendly adipokine" in Diabetic Retinopathy?

PURPOSE: Adiponectin has also been associated with diabetic retinopathy, a diabetic microvascular complication. However, the mechanism of action of adiponectin in retinopathy is still under investigation. This review summarizes emerging evidence on the association with diabetic retinopathy in type 2 diabetes. METHODS: We reviwed papers from 2004 to 2022 and included studies related to retinopathy and its association with blood and intraocular adiponectin in type 2 diabetes. RESULTS: Most of the studies analyzed in this review suggested an association between the diabetic retinopathy progression and intraocular, serum, or plasma adiponectin levels. Increased levels of adiponectin contributed to the development of the disease in diabetic patients. In a minority of studies, it was indicated an inversely proportional relationship between adiponectin concentration and diabetic retinopathy severity. CONCLUSION: The high levels of adiponectin in diabetic patients may be related to the decrease in renal clearance. Under this situation, if the predominant isoform is globular adiponectin, this may explain the retinopathy progression, considering a pro-inflammatory response induced by this isoform. However, the actions of adiponectin in diabetic retinopathy pathophysiology are still controversial.