Adiponectin modulates endometrial prostaglandin production during early pregnancy in pigs: An in vitro study.

Adiponectin and central nervous system disorders: Regulatory mechanisms and therapeutic potential.

To investigate the associations of adiponectin (APN), body mass index (BMI), and waist-to-hip ratio (WHR) with insulin resistance (IR) in patients with type 2 diabetes mellitus (T2DM), and to evaluate a combined model for discriminatory performance and potential clinical value for the identification of IR. A total of 394 hospitalized patients with T2DM were retrospectively analyzed. Participants were divided into low-IR and high-IR groups based on the median HOMA-IR. Clinical data were then analyzed by Spearman's correlation, trend analysis, multiple linear regression, logistic regression, and receiver operating characteristic (ROC) curve analysis. Compared with the low-IR group, patients in the high-IR group exhibited a higher BMI and WHR but lower APN levels (P < 0.05 for all). Furthermore, APN was negatively correlated with HOMA-IR, whereas BMI and WHR were positively correlated (all P < 0.01). Multivariable analysis further revealed that APN (β = -0.335), BMI (β = 0.243), and WHR (β = 0.138) were independently associated with IR (P < 0.01 for all). The combined model showed better discrimination (AUC = 0.82) than APN (0.78), WHR (0.72), and BMI (0.69) alone. APN, BMI, and WHR were independently associated with IR in patients with T2DM. Our combined model demonstrates superior discriminative performance to individual indicators and may be useful for identifying individuals at high risk of IR. Not applicable.

Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality worldwide, with aging as a major risk factor. This study aimed to investigate age-related proteins potentially involved in COPD pathogenesis. A total of 70 plasma samples (35 healthy controls, 35 COPD patients) were analyzed by data-independent acquisition mass spectrometry (DIA-MS), with each group stratified into young (≤ 50years) and aged (≥ 70years) subgroups. Differentially expressed proteins were identified using the limma package in R, followed by functional enrichment and protein-protein interaction analyses. Spearman's correlation and multivariable linear regression were used to assess associations between protein levels and lung function. Receiver operating characteristic curves (ROC) were generated to evaluate the diagnostic value of aging-related proteins in COPD. A total of 534 proteins were detected by DIA-MS. Following missing value imputation and quality filtering, 413 proteins were retained for analysis. Comparative analysis revealed 20 proteins differentially expressed between young and aged COPD patients (11 upregulated, 9 downregulated), which were significantly enriched in pathways including glutathione metabolism, nitrogen metabolism, endoplasmic reticulum protein processing, and PI3K-Akt signaling. Notably, expression levels of polymeric immunoglobulin receptor (PIGR), thrombospondin-1 (TSP1), secreted protein acidic and rich in cysteine (SPRC), and adiponectin (ADIPO) were correlated with FEV₁/FVC ratio in COPD patients; PIGR and ADIPO remained independently associated after adjusting for covariates. An exploratory model integrating these four proteins with age demonstrated reasonable discriminatory ability for COPD (AUC 0.818; 95% CI: 0.718-0.917). Our findings identify four plasma proteins-PIGR, SPRC, TSP1, and ADIPO-as age-related biomarkers in COPD that may offer value for patient stratification and endotyping. These results provide new insights into the role of aging in COPD pathogenesis and warrant further validation.

Acute lung injury (ALI) is the initial complication in the pathogenesis of sepsis and a leading cause of mortality in patients with sepsis. Adiponectin (APN), an important downstream effector of fibroblast growth factor 21 (FGF21), exerts metabolic regulatory effects; however, the specific role of FGF21 in alleviating sepsis-induced ALI through APN remains to be fully elucidated. The present study established a sepsis-induced ALI model in C57BL/6J mice via intraperitoneal injection of lipopolysaccharide (LPS, 15.0 mg/kg). Three FGF21 treatment groups were set up (intraperitoneal injection of 0.5 mg/kg, 1.0 mg/kg, and 2.0 mg/kg FGF21 6 hours after LPS administration) to explore the optimal usage concentration of FGF21 in this study. Additionally, adeno-associated virus (AAV)-mediated APN overexpression and knockdown were performed to verify the mediating role of APN. LPS-induced sepsis significantly increased FGF21 levels in mouse serum (p < 0.05) and lung tissues (p < 0.01), while reducing APN expression (p < 0.01), increasing percent weight loss (%WL ≈ 15%), elevating lung wet-to-dry (W/D) ratio by ~125%, upregulating mRNA levels of inflammatory factors (IL-1β, IL-6, TNF-α; p < 0.001), and promoting pulmonary fibrosis (increased α-SMA and TGF-β1 expression; p < 0.05 or p < 0.01). Among the FGF21 treatment groups, the medium dose (1.0 mg/kg) exhibited the most potent therapeutic effects: it reduced %WL by approximately 40%, decreased lung W/D ratio by approximately 30%, significantly downregulated the expression of inflammatory factors, and attenuated pulmonary fibrosis. APN overexpression mimicked the protective effects of FGF21, whereas APN knockdown partially abolished FGF21's therapeutic benefits. Mechanistically, FGF21 administration significantly reversed the sepsis-induced decrease in APN expression, inhibited pulmonary collagen deposition, and reversed the dysregulated Nrf2-Keap1-HO-1 pathway (upregulating Nrf2 and HO-1, downregulating Keap1; p < 0.05 or p < 0.01), which in turn restored redox homeostasis by increasing serum levels of catalase (CAT), glutathione (GSH), and superoxide dismutase (SOD) (p < 0.05 or p < 0.001). The present study revealed that APN mediates FGF21 to alleviate sepsis-induced ALI in mice, and its mechanism of action may be related to the alleviation of pulmonary fibrosis, the improvement of redox imbalance, and the down-regulation of inflammatory factor expression. This discovery provides a new strategy for the treatment of ALI. APN mediates FGF21's protective effects against sepsis-induced ALI in mice. The underlying mechanism involves reversing the sepsis-induced decrease in APN expression, inhibiting pulmonary fibrosis, downregulating inflammatory factor expression, and restoring redox homeostasis via the Nrf2-Keap1-HO-1 pathway. This discovery provides a novel therapeutic strategy for the treatment of sepsis-induced ALI.

Introduction: Type 2 diabetes mellitus (T2DM) is a rising health concern all over the world, often associated with obesity, poor glycemic control, and increased cardiometabolic risk. Nutritional interventions like pumpkin seeds may have beneficial metabolic health effects. The objective of this study was to assess how supplementing with powdered pumpkin (Cucurbita) seed affected the glycemic profile, serum magnesium (Mg), and adiponectin (ADPN) in T2DM patients. Methods and Material: In an open-label randomized trial, 195 T2DM patients completed follow-up (intervention group: n=101; control group: n=94). The intervention group received 10 gm/day of pumpkin seed powder (PSP) in addition to conventional T2DM medication for six months, while the control group continued their conventional T2DM medication alone. At baseline and six months after the intervention, anthropometric, clinical, and biochemical markers such as fasting blood sugar (FBS), postprandial glucose (PPG), HbA1c, Mg, and ADPN levels were measured. Results: The intervention group patients’ body weight and BMI decreased significantly (both p&lt;0.001), while in the control group, changes were not significant. Subsequently, significant reductions were also observed for FBS (p&lt;0.05), PPG (p&lt;0.001), and HbA1c (p&lt;0.001) in the intervention group. Mg and ADPN both showed a modest increase of 4.7% and 11%, respectively, in the intervention group, while a decline of 3.3% and 5.7%, respectively, was seen in controls. BP changes were minimal and statistically non-significant in both groups. Conclusions: PSP supplementation improved body weight, BMI, glycemic regulation and upheld Mg and ADPN levels in patients with T2DM. PSP may serve as a safe, accessible, nutrition-based addition to conventional diabetes management.

BACKGROUND:Obesity and cardiovascular diseases (CVD) are major public health concerns in Indonesia, especially among women who face a higher risk of obesity-related complications due to biological and lifestyle factors. Chronic low-grade inflammation, involving markers such as interleukin-6 (IL-6), high-sensitivity C-reactive protein (hs-CRP), and adiponectin (ADP), plays a crucial role in linking obesity to CVD.AIM:This study aimed to examine the association of sociodemographic, body composition, dietary intake, and physical activity factors with plasma IL-6, hs-CRP, and ADP levels in obese young adult women.MATERIALS AND METHODS:A cross-sectional study was conducted among obese women in Bandung City, Indonesia. Thirty-eight women aged 18–25 years with body fat >35% were selected through purposive sampling. Anthropometric measurements (weight, height, waist/hip circumference, body composition) were taken using calibrated tools. Dietary intake was assessed through two 24-h recalls (weekday and weekend), and physical activity was recorded using a structured questionnaire. Inflammatory and adipokine biomarkers (IL-6, hs-CRP, ADP) were analyzed from fasting blood samples using enzyme-linked immunosorbent assay kits. All tools were standardized and validated. Bivariate analysis (Chi-square test) identified candidate variables (P < 0.25) for multivariate logistic regression. Multiple linear regression was used to determine independent predictors of biomarker levels.RESULTS:Most participants had low energy intake and high fat consumption. No significant associations were found between the studied variables and IL-6 or hsCRP levels. However, lower education and decreased skeletal muscle and leg muscle mass were significantly associated with reduced ADP levels (P < 0.001). In multivariate analysis, leg skeletal muscle was the only significant predictor of ADP levels (P < 0.001) supporting the hypothesis that muscle mass, particularly in the lower limbs, influences anti-inflammatory adipokine levels. Besides, there is high pulse as a predictor of hsCRP level (P = 0.027).CONCLUSIONS:Leg skeletal muscle mass is a key determinant of ADP levels in obese young women, while pulse for hsCRP. This emphasizes the importance of strength-focused interventions to reduce cardiometabolic risk. These findings support health policy benchmarks that promote equitable access to physical activity and nutrition education, particularly for populations with lower educational attainment.

It has been reported that DNA methylation in the epigenetic profile of the genes LEP and ADIPOQ is associated with obesity. To the best of our knowledge, there are no previous reports assessing the methylation of the LEP, LEPR, and ADIPOQ genes in subjects with metabolically healthy obesity (MHO). Therefore, the aim of this study was to determine the association between methylation of the LEP, LEPR, and ADIPOQ genes with the MHO phenotype. Healthy men and women aged 20-55 years of age with a body mass index ≥30 kg/m2 were enrolled in a case-control study. Exclusion criteria were pregnancy, alcohol intake, smoking, diabetes, hypertension, hepatic disease, cardiovascular disease, renal disease, thyroid disease, cancer, and/or any type of drug therapy. Individuals with MHO were allocated to the case group, while those with metabolically unhealthy obesity (MUO) were assigned to the control group. A total of 78 individuals were enrolled and allocated into the groups with MHO (n = 39) or MUO (n = 39). In the MHO group, the methylation percentage of the LEP gene was significantly higher than in the MUO group, while the LEPR and ADIPOQ genes did not show differences between the study groups. Finally, the methylation of the LEP gene (OR = 1.67; 95% confidence interval (CI): 1.29-2.16; p < 0.001), but not of LEPR (OR = 0.77; 95% CI: 0.45-1.32; p = 0.350) and ADIPOQ (OR = 1.01; 95% CI: 0.97-1.05; p = 0.411), presented a positive association with the MHO phenotype. In conclusion, the LEP gene hypermethylation is positively associated with the MHO phenotype. In addition, the LEPR gene overexpression was significantly associated with the MHO.

Cell-type-specific killing by black phosphorus nanosheets in colorectal cancer: Unraveling the ADIPOQ-redox homeostasis axis.

Background: Adiponectin (ADPN) is a key adipokine with osteogenic potential, but its clinical translation for bone regeneration is hindered by poor in vivo stability. This study aimed to develop poly lactic-co-glycolic acid (PLGA) microparticles as a stable and biocompatible carrier for sustained ADPN delivery to enhance bone repair. Methods: ADPN-loaded PLGA microparticles (ADPN-MPs) were fabricated via emulsion solvent evaporation. Their physicochemical properties were characterized using scanning electron microscopy (SEM) and circular dichroism (CD) spectroscopy. Loading efficiency and drug loading were quantified. In vitro release kinetics and stability under physiological conditions were assessed. Biocompatibility was evaluated using MC3T3-E1 osteoblasts and BMSCs, and in vivo efficacy was tested in a fracture model via gait analysis. Results: Employing CD to evaluate the secondary structure of ADPN, emulsion solvent evaporation for microparticles preparation, and SEM for morphological analysis, we quantitatively assessed the loading efficiency (69.83 ± 4.24%) and drug loading (0.97 ± 0.06%) of ADPN-MPs. Results indicated that ADPN-MPs maintained significant stability under varied pH and temperature conditions and exhibited a controlled release profile, with an average initial rapid release of 14.25% within 24 h and an average cumulative release of 55.00% by day 28. Furthermore, ADPN-MPs promoted the proliferation of MC3T3-E1 and BMSCs without toxicity, demonstrating excellent biocompatibility. Notably, gait analysis in a fracture model showed improved healing in both ADPN and ADPN-MPs groups compared to controls, with ADPN-MPs demonstrating comparable efficacy to free ADPN, supporting its potential as a stable delivery system for bone regeneration. Conclusions: PLGA microparticles serve as an effective, stable, and biocompatible delivery platform for ADPN, significantly promoting bone regeneration in vitro and in vivo. This delivery system enhances the therapeutic potential of ADPN for clinical bone repair applications.

Purpose: Obesity, characterized by abnormal fat accumulation with comorbidities, continues to increase dramatically, particularly in the pediatric population. Identifying the environmental and genetic causes underlying the development of obesity during early childhood is crucial for establishing preventive and protective treatments for this complex disease. We aimed to investigate genetic variants related to non-syndromic early-onset childhood obesity. Methods: Whole-exome sequencing was performed in three independent consanguineous families with obesity, including three index cases and two additional affected siblings. Non-synonymous variants with minor allele frequency < 0.01 in all normal populations were filtered using the Genomize-SEQ Platform. Variant confirmations and familial segregations were analyzed by Sanger sequencing. Results: WES revealed a shared ATXN3 gene variant and two known variants of the SH2B1 and ADIPOQ genes, which were reported to be associated with obesity. Additionally, five heterozygous novel gene variants of the ANKK1, NEGR1, OGDH, ABCB1, and GSK3B genes were identified, which are predicted to cause excessive fat accumulation and disruption of energy balance in individuals. Conclusions: We suggest that the cumulative effects of all obesity-associated detected variants lead to the early-onset obesity phenotype observed in individuals. Hence, periodic follow-up and treatment opportunities are recommended for index cases, alongside the adoption of a more active lifestyle and healthy nutrition practices.

Selenium nanoparticles (Se NPs) play a substantial role in human body. Therefore, they were newly and greenly synthesized by using phlorizin (PHZ). The antidiabetic effects of PHZ and its greenly synthesized PHZ-SeNPs were tested in STZ-induced diabetes. The PHZ-SeNPs were red in color, UV-visible spectrophotometry (λmax 322 nm). Infrared spectroscopy verifies the production of Se NPs' coated with PHZ. TEM image represents spherically shaped particles (smaller average size, 5-11 nm). Zeta potential was -28.77 ± 9.5 mV with size distribution of 395 nm for PHZ-SeNPs. The loading capacity (LC) and encapsulation efficiency (EE) were 42.8% and 38.96%, respectively. FBG, HbA1c, calculating HOMA-IR, oral glucose tolerance test as well as insulin, adiponectin (ADP) and leptin using anti-rat were done. In addition, Leptin/Adiponectin ratio (LAR) were calculated. The LD50 of PHZ-SeNPs was 173.68 mg/kg. FBG level of diabetic rats was 477.67 ± 30.4 mg/dL, that after PHZ-SeNPs treatment was 206.83 ± 34.69 mg/dL and that of insulin-treated rats (237.17 ± 54.04 mg/dL). HOMA-IR levels were positively and significantly correlated with FBG, insulin level, lipid profile; expect HDL and that of leptin levels but were negatively and significantly correlated with ADP levels, and LAR. In addition, diabetes reduces liver content of glycogen which was elevated after treatments. As an in vitro study, IC50 of free PHZ was found to be 4.87 mM which was reduced up to 3.28 mM if PHZ-SeNPs were used (DPPH assay). The treatments improve liver, kidney and pancreatic histopathological finding. In conclusion: PHZ-SeNPs can be usefully used to reduce blood sugar and prevent diabetic complications. The mechanisms may involve both the intrinsic radical scavenging activity of PHZ and PHZ-SeNPs (as evidenced by DPPH assay) and the enhancement of endogenous antioxidant defenses (increased reduced glutathione, superoxide dismutase, and catalase levels), in addition to improved insulin secretion, ADP stimulation, leptin inhibition and increment in erythrocytes-glucose uptake.Supplementary InformationThe online version contains supplementary material available at 10.1186/s40643-026-01034-3.

Background This study investigated the association between gestational serum adiponectin (APN) levels and postpartum glycaemic outcomes in women with gestational diabetes mellitus (GDM). Methods A total of 96 GDM patients were enrolled. Baseline demographic and biochemical data were collected. Serum APN levels were measured longitudinally across three gestational stages and postpartum using an enzyme-linked immunosorbent assay. Based on 1-year follow-up data, patients were classified into favourable (normal glucose metabolism) and unfavourable (prediabetes or type 2 diabetes mellitus [T2DM]) outcome groups. Statistical analyses included t-tests, non-parametric tests, Cox proportional hazards models, and Kaplan-Meier survival curves to assess the associations between APN levels and outcomes. Results At 1-year follow-up, 54.17% had favourable outcomes with higher APN levels, while 45.83% had unfavourable outcomes characterised by older age, higher BMI, and a higher prevalence of family history. T2DM patients had lower APN than those with prediabetes. Cox regression identified postpartum APN as an independent protective factor (Hazard Ratio [HR] = 0.720, 95% confidence interval [CI]: 0.60–0.85, P < 0.001), with each 1-μg/mL increase reducing risk by 27%. Significant risk factors included age (HR = 1.10, 95% CI: 1.01–1.20), pre-pregnancy BMI (HR = 2.06, 95% CI: 1.03–4.14), family history (HR = 2.58, 95% CI: 1.22–5.46), fasting glucose (HR = 1.41, 95% CI: 1.17–1.70), and 1-hour OGTT glucose (HR = 1.20, 95% CI: 1.02–1.40). The low-APN group showed significantly higher cumulative incidence of metabolic dysfunction. Conclusions Gestational APN levels are strongly associated with postpartum metabolic outcomes in GDM. Low APN is an independent risk factor for adverse outcomes, and its dynamic changes reflect metabolic recovery capacity.

Objective: to study the association of muscle, adipose, and bone tissue markers with abnormal body composition phenotypes in women with rheumatoid arthritis (RA). Material and methods. A total of 163 women (median age 61.0 [52.0; 66.0] years) with a confirmed diagnosis of RA were examined. Dualenergy X-ray absorptiometry was performed; based on the results, the following body composition phenotypes were identified: normal (NP), osteoporotic (OP), sarcopenic (SP), and osteosarcopenic (OSP). Serum levels of myostatin, insulin-like growth factor 1 (IGF-1), leptin (LEP), adiponectin (ADPN), resistin (RES), interleukin 6 (IL-6), irisin, and sclerostin (SOST) were measured. Results and discussion. In patients with OP and OSP, LEP, RES, and SOST levels were significantly lower than in women with NP. In those with OSP, ADPN levels were higher than in patients with NP (p=0.031). IGF-1 levels in NP were significantly higher than in OP, SP, and OSP. Logistic regression showed an association of IGF-1 with OP, SP, and OSP (odds ratio, OR 0.96, 95% confidence interval, CI 0.93–0.99; OR 0.94, 95% CI 0.89–0.99; and OR 0.97, 95% CI 0.95–0.99, respectively; p&lt;0.05). ADPN levels were associated with OP and OSP (OR 1.30, 95% CI 1.02–1.66 and OR 1.23, 95% CI 1.02–1.48, respectively; p&lt;0.05); SOST levels associated with OP and OSP (OR 0.90, 95% CI 0.86–0.95 and OR 0.92, 95% CI 0.87–0.96, respectively; p&lt;0.001); and LEP and RES levels with OP (OR 0.72, 95% CI 0.53–0.99 and OR 0.72, 95% CI 0.58–0.89, respectively; p&lt;0.05). Conclusion. Associations were identified between OP and levels of LEP, ADPN, RES, SOST, and IGF-1; between OSP and levels of ADPN, SOST, and IGF-1; and between SP and IGF-1 only. For IGF-1, the positive predictive value was 100% at the identified cut-off points, which allows it to be considered a predictive marker of abnormal body composition phenotypes in patients with RA.

Prenatal exposure to metal(loid)s and hormone profile in umbilical cord serum: Evidence of sex-specific association.

ADIPOQ Genotypes, Adiponectin Isoforms, and Hypertension Risk in Pediatric Obesity.

Individuals with abnormal glucose metabolism are at high risk of developing metabolic dysfunction-associated steatotic liver disease (MASLD). Severe hepatic steatosis represents a critical transition stage from simple fat accumulation to liver fibrosis and significantly increases the risk of adverse liver outcomes. This study aimed to construct a nomogram model integrating serological markers and clinical parameters for predicting the risk of severe hepatic steatosis in this population. This prospective study enrolled 186 patients with abnormal glucose metabolism (including prediabetes and diabetes mellitus) who underwent FibroScan examination and serological testing between February 2023 and May 2024. According to the controlled attenuation parameter (CAP) cutoff values recommended by the manufacturer, patients were classified into severe (n = 56) and non-severe (n = 130) hepatic steatosis groups and randomly divided into training and validation cohorts at a 7:3 ratio. Least absolute shrinkage and selection operator (LASSO) regression was applied to select potential predictive variables, followed by multivariate logistic regression to identify independent predictors. Restricted cubic spline (RCS) analysis was used to assess potential nonlinear associations between independent predictors and severe hepatic steatosis, and Spearman correlation analysis was performed to evaluate their correlations with CAP values.A nomogram prediction model was constructed based on the identified independent predictors. Predictive performance was evaluated, and internal validation using 1,000 bootstrap resamples was performed to assess model stability. Multivariate logistic regression identified body mass index (BMI), triglycerides (TG), adiponectin (ADPN), and chemerin as independent predictors of severe hepatic steatosis. RCS analysis revealed approximately linear associations of BMI, ADPN, and chemerin with the risk of severe hepatic steatosis, whereas TG demonstrated a nonlinear relationship. Spearman correlation analysis showed that the CAP was positively correlated with BMI, TG, and chemerin and negatively correlated with ADPN. A nomogram incorporating these four variables was established. The area under the receiver operating characteristic curve (AUC) was 0.862 in the training cohort and 0.889 in the validation cohort, indicating good discriminative ability. Calibration and decision curve analysis (DCA) curves confirmed favorable calibration and clinical utility. Internal validation with 1,000 bootstrap resamples further demonstrated the stability of the nomogram. The nomogram based on BMI, TG, ADPN, and chemerin can predict severe hepatic steatosis in patients with abnormal glucose metabolism to a certain extent, providing a novel and practical tool for individualized clinical decision-making.

This study investigated whether ovarian adipokines exhibit uniform or stage-specific expression patterns across different follicular stages under hyperandrogenic conditions using a letrozole-induced polycystic ovary syndrome (PCOS) mouse model. Adult female mice received oral letrozole treatment for 21days to induce hyperandrogenism, and ovarian tissues were analyzed by immunohistochemistry and western blot to examine the localization and expression of adiponectin (ADPN), adipoR1, adipoR2, leptin (Ob), leptin receptor (ObR), apelin (APLN), apelin receptor (APJ), chemerin, CMKLR1, and visfatin. Intense immunostaining for Ob, ObR, APJ, APLN, adipoR2, and visfatin was observed in primary, secondary, and Graafian follicles, whereas ADPN, adipoR1, and CMKLR1 showed reduced reactivity. In follicular cysts, adipoR2, APLN, APJ, and Ob were markedly upregulated compared with the corpus luteum of control ovaries, whereas ADPN, adipoR1, chemerin, CMKLR1, and ObR were downregulated. These findings indicate that hyperandrogenism disrupts adipokine signaling in a follicle-dependent manner, with differential expression patterns contributing to altered follicular maturation and cyst formation. The enhanced activation of adiponectin, apelin, and leptin signaling observed in cystic follicles may indicate disrupted adipokine-mediated regulation of ovarian physiology in letrozole-induced PCOS. Given the established roles of these adipokines in folliculogenesis and steroidogenesis, their dysregulation may contribute to follicular arrest and impaired ovarian function. These alterations are likely reflective responses to an altered endocrine and metabolic environment rather than direct causal mechanisms. Nonetheless, they may participate in the pathophysiological processes underlying cyst formation in PCOS.

Currently, there are many studies on the relationship between the ADIPOQ gene polymorphisms and the onset of type 2 diabetes (T2D), and the research results vary among different regions and ethnic groups. However, there are relatively few studies on the relationship between ADIPOQ gene polymorphisms and the occurrence and severity of diabetic kidney disease (DKD). This study aims to investigate the association of DKD with the ADIPOQ gene polymorphisms rs2241766 and rs1063537 in patients with T2D in the Han population in southern China. A total of 347 patients with type 2 diabetic kidney disease (T2DKD) from the Jinhua area in central Zhejiang between 2021 and 2023 were enrolled as the case group, which was divided into the microalbuminuria phase (group I: urinary albumin-to-creatinine ratio [UACR] 30–299 mg/g, 185 cases) and the macroalbuminuria phase (group II: UACR ≥ 300 mg/g, 162 cases) based on UACR. Meanwhile, 191 patients with T2D and without kidney disease were recruited as the control group during the same period. The KASP-PCR (competitive allele-specific polymerase chain reaction) technique was used for genotyping of the rs2241766 and rs1063537 loci in the ADIPOQ gene, aiming to explore their associations with the occurrence and severity of T2DKD. The frequency of the TT genotype at the rs1063537 locus was 8.6% in group I and 15.4% in group II, with a statistically significant difference in distribution between the 2 groups (P < .05). After adjusting for age, gender, body mass index (BMI), diabetes duration, hypertension status, creatinine, and fasting plasma glucose, this genotype was significantly associated with the macroalbuminuria phase of T2DKD (P = .016), meaning that carriers of the TT genotype had a 2.47-fold higher risk of developing macroalbuminuria compared with those with the CC genotype. No statistically significant differences were observed in the genotype distributions of the rs2241766 and rs1063537 loci in the ADIPOQ gene between the case group and the control group (P > .05). In the Han population in southern China, the TT genotype at the rs1063537 locus of the ADIPOQ gene in patients with T2DKD is significantly associated with the presence of the macroalbuminuria stage.

To analyze the clinical value of Adiponectin (APN) combined with lipoprotein phospholipase A2 (Lp-PLA2) in predicting the prognosis of patients with cerebral infarction undergoing intravenous thrombolysis with recombinant tissue- plasmin activator (rt-PA). Total 100 patients admitted to our hospital with cerebral infarction underwent intravenous thrombolysis with rt-PA during June 2022 to June 2023 were chosen as the cerebral infarction group. The healthy control group were composed of 100 healthy people during the same period. The levels of APN and Lp-PLA2 was examined use enzyme-linked immunosorbent assay (ELISA). Patients with cerebral infarction were divided into two groups based on different functional outcomes after 3 months of treatment using the modified Rankin Scale (mRS) score: 55 patients in the good outcome group (mRS score 0–2, patients independently complete daily activities without assistance from others) and 45 patients in the poor outcome group (mRS score 3–6). Multivariate logistic regression analysis was adopted to investigate the influencing factors. Pearson correlation analysis was performed to analyze the correlation. The predictive value of APN and Lp-PLA2 was assessed using receiver operating characteristic (ROC) curves. Patients in the cerebral infarction group had much lower serum APN levels and higher Lp-PLA2 levels than those in the control group (P < 0.001). Patients were categorized into large artery atherosclerosis (LAA), cardioembolic embolism (CE), and small vessel disease (SVD) according to the TOAST classification. Lp-PLA2 levels were significantly higher in the LAA and SVD groups compared to the CE group (P < 0.05), while APN levels were significantly lower in these groups (P < 0.05). At three months post-intravenous thrombolysis with rt-PA, patients in the poor outcome group exhibited significantly higher values for age, pre-treatment NIHSS score, pre-stroke mRS score, maximum infarct diameter, serum Lp-PLA2 level, and total complication rate compared to those in the favorable outcome group. Serum APN levels were significantly lower in the poor outcome group. All differences were statistically significant (P < 0.01). Age, NIHSS score before thrombolysis, serum Lp-PLA2 and total complication rate were independent risk factors affecting adverse outcomes after rt-PA intravenous thrombolysis in patients with cerebral infarction (P < 0.05), and APN level was an independent protective factor (P < 0.05). Pearson correlation analysis showed a significant negative correlation between APN and mRS scores (r=-0.677, P < 0.001); Lp-PLA2 was significantly positively correlated with mRS score (r = 0.2334, P = 0.001). The ROC curve showed that the area under the curve (AUC) of serum APN and Lp-PLA2 for predicting functional outcomes after thrombolysis in cerebral infarction was 0.886 and 0.785, respectively. The AUC of serum APN + Lp-PLA2 was 0.913, with a sensitivity of 88.89% and a specificity of 81.82% (P < 0.05). Abnormally expressed serum APN and Lp-PLA2 in patients with cerebral infarction were correlated with mRS scores. APN and Lp-PLA2 had a certain clinical value in predicting functional outcome after rt-PA intravenous thrombolytic therapy in patients with cerebral infarction.