Transforming growth factor-beta 1 (TGF-β1)-stimulated clone 22 domain (TSC22D) family genes (including TSC22D1-TSC22D4) were identified as transcription factors. It has been demonstrated that they display multiple functions due to proteins’ isoforms, redundancy, and other factors. Formerly, researchers mainly focused on its functions, like controlling cell growth and development, cell apoptosis, and balance of osmotic pressure in vivo. Nowadays, growing evidence indicates that they also play an important role in metabolic regulation and the immune system and are expected to be a new potential target for the treatment of diabetes or obesity. Despite this, it has been shown that TSC22D family genes have an inhibitory effect in multiple tumors. In this review, we significantly synthesized advances in metabolism, showing that TSC22D3 could control lipid accumulation via modulating adipogenesis and adipose differentiation, while TSC22D4 could regulate insulin sensitivity and gluconeogenesis by affecting Akt (serine/threonine kinase, also known as protein kinase B, or PKB) phosphorylation. Moreover, we provide novel insights, including the fact that TSC22D family genes function as a double-edged sword in cancer due to the type of tumor and tumor microenvironment (TME).

This article reports the synthesis and functionalization of 1-(4-chlorobenzyl)-2-(4-chlorophenyl)-4-fluoro-1H-benzo[d]imidazole (CCFB) with SiO2 nanoparticles, demonstrating significant improvements in its photophysical and biological properties. Detailed spectroscopic investigations (UV-Vis, fluorescence, and FT-IR) confirm strong adsorption of CCFB on SiO2 surfaces, accompanied by fluorescence quenching through photoinduced electron transfer and interfacial energy transfer mechanisms. ZnO nanocatalyst-assisted synthesis afforded high yields under mild conditions, underscoring the catalytic relevance of nanomaterials. Computational analyses further elucidated the molecular interactions, validating the experimental findings. Biological evaluation revealed that SiO2 functionalization markedly enhanced the anti-inflammatory and alpha-amylase inhibitory activities of CCFB, surpassing both the unmodified compound and standard drug references. The dual advantage of improved stability and bioactivity highlights the potential of SiO2-functionalized benzimidazoles in drug design and nanomedicine. Overall, this study provides molecular-level insights into nanomaterial-drug conjugation, with implications for photophysics-driven biomedical and therapeutic applications.

Metabolic and cardiometabolic diseases are closely associated with mitochondrial dysfunction and redox imbalance. Ubiquinol-cytochrome c reductase core protein 2 (UQCRC2), a non-catalytic structural core subunit of mitochondrial respiratory chain Complex III, is increasingly recognized as a regulator of Complex III integrity, electron transfer, oxidative phosphorylation, and mitochondrial redox homeostasis. Under metabolic stress, reduced expression or functional impairment of UQCRC2 may promote electron leakage, mitochondrial reactive oxygen species (mtROS) generation, lipid peroxidation, impaired antioxidant defense, and disrupted glucose-lipid metabolism. These alterations may contribute to insulin resistance (IR), metabolic dysfunction-associated steatotic liver disease (MASLD), obesity, and cardiovascular disease (CVD). This review summarizes current evidence linking UQCRC2 dysfunction to mitochondrial bioenergetic failure, oxidative stress, inflammatory signaling, and cardiometabolic injury. We further discuss redox-regulatory pathways, including Nrf2, AMPK-SIRT1-PGC-1α, glutathione metabolism, and mitophagy, as well as pharmacological agents and natural compounds that may modulate UQCRC2-related mitochondrial responses. Collectively, these findings highlight UQCRC2 as a redox-sensitive mitochondrial node linking Complex III dysfunction to cardiometabolic injury and targeted redox-based interventions.

Pregnancy zone protein (PZP) is an antiprotease-resistant immunosuppressant belonging to the α-macroglobulin (αM) protein family. PZP is secreted by the liver and was found to be upregulated in plasma during pregnancy. α-2-macroglobulin (Α2M) shares 71 % serial homology with PZP, but low PZP levels do not lead to increased A2M levels in pregnancy. PZP can interact with several factors such as low-density lipoprotein receptor-associated protein (LRP), transforming growth factor-β (TGF-β), 78 kDa glucose-regulated protein (GRP78), and glycoside A (GdA). PZP is involved in the development of glycolipid metabolism disorders, bronchiectasis, Alzheimer's disease (AD), rheumatoid arthritis (RA), myocardial infarction (MI) and inflammatory bowel disease (IBD). PZP is also associated with the progression of tumorigenesis such as breast cancer (BC), homologyepatocellular carcinoma (HCC), lung adenocarcinoma (LAC), and colorectal cancer (CRC). Therefore, this review analyzes the role of PZP in pathophysiology of various diseases.

Citrate is a potential biomarker for early stage detection of prostate cancer (PC), its concentration significantly dropped to 2-20 mM in PC patients. Herein, a cheap, simple, and reliable citrate sensor was proposed based on the biogenic synthesis of nitrogen-doped carbon dots (N-CDs) derived from the biowaste of Syzygiumcumini (S. cumini) seeds. The prepared N-CDs were characterized by TEM, FT-IR and spectral studies. The average size of the N-CDs was found to be 2.4 nm, the presence of -OH and -NH2 functional groups on the surface of N-CDs was confirmed by FT-IR analysis. The N-CDs possess the highest emission at 414 nm and cause quenching after reacting with citrate, which is due to the possible hydrogen bonding interactions between the probe and citrate. The probe expressed the lowest limit of detection of 3.5 nM, high selectivity, high interfering ability (1000-fold), provided a stable response at 5 min of reaction time, good biocompatibility, and delivered a contrast bioimage with different concentrations of citrate. The N-CDs were utilized to detect citrate in human urine samples, obtained good recovery results, and validated with the high-performance liquid chromatography method.

Fyn is widely involved in diverse cellular physiological processes, including cell growth and survival, and has been implicated in the regulation of energy metabolism and the pathogenesis of diabetes mellitus through multiple pathways. Fyn plays a role in increasing fat accumulation and promoting insulin resistance, and it also contributes to the development of diabetic complications such as diabetic kidney disease and diabetic retinopathy. The primary mechanism by which Fyn modulates lipid metabolism is that it inhibits AMP-activated protein kinase (AMPK). Additionally, it affects energy homeostasis through regulating specific signal pathways affecting lipid metabolism including pathways related to CD36, through enhancement of adipocyte differentiation, and through modulating insulin signal transduction. Inflammatory stress is one of the fundamental mechanisms in diabetes mellitus and its complications. Fyn also plays a role in inflammatory stress-related signaling cascades such as the Akt/GSK-3β/Fyn/Nrf2 pathway, exacerbating inflammation in diabetes mellitus. Therefore, Fyn emerges as a promising therapeutic target for regulating glucolipid metabolism and alleviating type 2 diabetes mellitus. This review synthesizes research on the role of Fyn in the regulation of energy metabolism and the development of diabetes mellitus, while exploring its specific regulatory mechanisms.

Luteolin and quercetin, which are flavonoids, are present in various traditional Chinese medicines. Although they have been shown to improve obesity, the specific mechanisms of action remain unclear. This study aimed to determine pivotal targets and major regulatory pathways involved in their mechanisms of action using network pharmacology and transcriptome sequencing. Data on luteolin/quercetin-related targets were acquired from the PharmMapper platform, and data on known obesity-related targets were collected from the OMIM and GeneCards databases. Differentially expressed genes (DEGs) involved in luteolin and quercetin action that regulate adipogenic differentiation were identified using RNA sequencing (RNA-seq). Bioinformatic analyses were performed to identify potential target genes and pathways regulated by luteolin/quercetin during adipogenesis. Finally, key genes and pathways were validated through quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting. Network pharmacology showed that luteolin/quercetin was closely associated with anti-obesity targets. The related pathways were metabolic, PI3K/AKT, and MAPK pathways. RNA-seq revealed 91 common DEGs involved in luteolin/quercetin regulation of adipogenic differentiation. Finally, nine potential target genes (including CIDEC, Mgll, Slc2a4, Pck1, and PNPLA3) were identified, and the AMPK and AKT signaling pathways were verified. The present study provides novel information regarding the molecular mechanism of luteolin and quercetin action in treating obesity and demonstrates their therapeutic effects through multiple targets and pathways.

Background:The inflammatory microenvironment disrupts the ovarian niche, impairing granulosa cell function and leading to aberrant follicular development, a key pathological feature of polycystic ovary syndrome (PCOS). However, the precise mechanisms by which inflammation influences granulosa cell function remain poorly understood. Methods:Differentially expressed genes (DEGs) were identified from the GSE34526 dataset, with the inflammatory marker CD163 selected for further investigation due to its upregulation in ovarian granulosa cells in PCOS. Serum levels of soluble CD163 (sCD163) were measured in patients with PCOS, and a dehydroepiandrosterone (DHEA)-induced PCOS mouse model was utilized to examine the relationship between CD163 expression, inflammatory mediators, and macrophage activity in the ovaries and uterus. Granulosa cell apoptosis, inflammatory cytokine secretion, and sCD163 release from conditioned media (CM) of differently polarized macrophages co-cultured with COV434 cells were assessed. Results:Elevated serum sCD163 levels were observed in patients with PCOS. The DHEA-induced PCOS mice exhibited characteristic oestrous cycle abnormalities, as well as morphological and pathological alterations in the ovaries and uterus. Increased CD163 expression was detected in ovarian and uterine macrophages of PCOS mice, alongside elevated inflammatory cytokines. Conditioned media from M1-polarized macrophages induced apoptosis in COV434 granulosa cells, with concomitant increases in pro-inflammatory cytokines (IL-1β and IL-6) and sCD163 secretion. Furthermore, CD163+ cell apoptosis was heightened in the ovaries of PCOS mice. Conclusion:These findings suggest that ovarian macrophages, through elevated CD163 expression, contribute to granulosa cell apoptosis and the secretion of sCD163, which may play a critical role in the pathogenesis of PCOS.

Polycystic ovary syndrome (PCOS) and obesity share a bidirectional relationship. While previous studies have indicated the anti-obesity effects of luteolin, its role in PCOS exacerbated by obesity remains unclear. This study aimed to investigate the ameliorative effects of luteolin on obese rats with PCOS and explore its underlying mechanisms. We established a rat model of PCOS with obesity and administered luteolin to evaluate its mitigating effects on the metabolic phenotype. Liver transcriptomics and fecal metagenomics were employed to analyze potential targets and alterations in the gut microbiota composition associated with luteolin's effects. Results showed that luteolin reduced body weight, improved estrous cycles, polycystic ovarian morphology, and glucose tolerance, and lowered serum levels of triglycerides (TG), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-c) in the model rats. Importantly, luteolin significantly alleviated hepatic steatosis and reversed the expression of 138 key differentially expressed genes (DEGs) in the liver, including UQCRC2, IRS2, NFIX, and ALDH6A1. In addition, luteolin significantly increased the alpha diversity of the gut microbiota and modulated its composition, specifically increasing the relative abundance of Bacteroidota and decreasing that of Firmicutes. Our findings suggest that luteolin exerts beneficial effects on PCOS with obesity, potentially mediated through the improvement of hepatic lipid metabolism and the restoration of gut microbiota homeostasis. Luteolin emerges as a promising therapeutic candidate for managing PCOS with obesity.

Objective:Tsukushi (TSK) is a recently identified hepatic factor that has gained prominence for its distinctive function in glycolipid metabolism and energy homeostasis. However, the role of TSK in gestational diabetes mellitus (GDM) remains largely unexplored. In this study, we conducted a pioneering investigation by determining serum TSK levels in patients with GDM and examining the correlation between these levels and various metabolic parameters in gestational diabetes patients. Methods:A total of 176 pregnant women (mean age 29.5 ± 3.2 years) were recruited from September 2023 to December 2024. Serum TSK levels and clinical markers related to glycolipid metabolism were measured at 24-28 weeks of gestation. All subjects underwent an oral glucose tolerance test (OGTT). Results:Serum TSK was significantly higher in patients with GDM than in the normal glucose tolerance group [0.60(0.47,0.73 vs 0.52(0.42,0.67) ng/mL; P <0.05]. Correlation analysis showed that TSK was significantly and positively correlated with diastolic blood pressure (DBP), alanine aminotransferase (ALT), direct bilirubin (Dbil), free triiodothyronine (FT3), 1-h post-OGTT glucose (1hPG), low-density lipoprotein cholesterol (LDL-C), and total cholesterol (TC). Logistic regression analysis showed that Logistic regression analysis showed that higher TSK levels were independently associated with increased odds of GDM. Conclusion:TSK levels were higher in GDM than in NGT (P=0.013), and higher TSK tertiles were independently associated with increased odds of GDM (Model 3 OR=2.883, 95% CI 1.173-7.084; P=0.021). After FDR correction, only the association with total cholesterol remained significant (FDR-adjusted P=0.023).

PurposeThe Chinese Visceral Adiposity Index (CVAI), a measure of visceral adiposity dysfunction, is used to assess visceral fat (VFA) malfunction. This research was performed to evaluate the relationship between CVAI and serum uric acid levels in type 2 diabetes mellitus (T2DM) patients.MethodsA total of 2268 patients with T2DM were enrolled in this study. We collected the general clinical information of patients, measured the basic anthropometric indicators, tested glycolipid metabolism and biochemical indicators, and measured the visceral and subcutaneous fat area with bioelectrical impedance technology. According to the quartiles of the CVAI, the T2DM patients were classified into four groups: group A (CVAI ≤ 94.43), group B (94.43<CVAI ≤ 118.75), group C (118.75<CVAI ≤ 143.95), and group D (CVAI≥143.95), each group has 567 participants. Participants were divided into hyperuricemia (HUA) and non-HUA groups, and the clinical data between the two groups was compared.ResultsAmong quartiles of CVAI, as CVAI increased, the proportion of patients with HUA gradually increased. The correlation analysis showed that the majority of basal measures, glycolipid metabolism and biochemical indicators were positively correlated with CVAI. By comparison, the level of CVAI in the HUA group was significantly higher than non-HUA group. Meanwhile, through using the ROC curve, our study observed the more predictive value of CVAI than other obesity indicators for T2DM with HUA.ConclusionCVAI is a simple but effective indicator, which is significantly correlated with HUA in T2DM and can reflect the incidence of HUA in T2DM patients. As CVAI increased, the risk of HUA in T2DM patients increased. Therefore, we should pay more attention to the application of CVAI in T2DM.

Sleep plays a crucial biological role, and mounting evidence suggests that sleep disorders negatively impact health. In contemporary society, sleep disorders, such as sleep deprivation, insomnia, disrupted sleep-wake disorders, and circadian rhythm disorders, are widespread. Sleep disorders affect hormone production and secretion, which lead to endocrine changes, including impaired glucose tolerance, decreased insulin sensitivity, hepatic steatosis, and increased inflammatory responses, all of which accelerate the onset of various diseases. To support optimal metabolic and cardiovascular health, maintaining a consistent sleep schedule and practicing good sleep hygiene are essential.

Obesity is a chronic metabolic disease that is closely related to type 2 diabetes mellitus, cardiovascular diseases, nonalcoholic fatty liver disease, obstructive sleep apnea, and osteoarthritis. The prevalence of obesity is increasing rapidly every year and is recognized as a global public health problem. In recent years, the role of epigenetics in the development of obesity and related diseases has been recognized and is currently a research hotspot. N6-methyladenosine (m6A) methylation is the most abundant epigenetic modification in the eukaryotic RNA, including mRNA and noncoding RNA. Several studies have shown that the m6A modifications in the target mRNA and the corresponding m6A regulators play a significant role in lipid metabolism and are strongly associated with the pathogenesis of obesity-related diseases. In this review, the latest research findings regarding the role of m6A methylation in obesity and related metabolic diseases are summarized. The authors' aim is to highlight evidence that suggests the clinical utility of m6A modifications and the m6A regulators as novel early prediction biomarkers and precision therapeutics for obesity and obesity-related diseases.

Background: The association between serum uric acid (SUA) levels and serum proprotein convertase subtilisin/kexin type 9 (PCSK9) levels has not yet been uncovered. This study aimed to explore the potential link between SUA levels and serum PCSK9 levels and quantify the mediating effect of metabolic factors and inflammation in Chinese adults. Furthermore, it assessed whether gender differences modified this association. Methods: In total, 2624 participants were enrolled and categorized based on their SUA levels as the hypouricemic (n = 432) and normouricemic group (n = 2192). Stepwise multivariable regression analysis, binary logistic regression analysis and mediation analyses were performed. Results: Participants with hyperuricemia had higher serum PCSK9 levels than those with normouricemia (73.74 +/- 30.25 vs 68.55 +/- 29.01 ng/mL, P < 0.05), especially in women (69.11 +/- 28.84 vs 87.86 +/- 27.90 ng/mL, P < 0.001). SUA levels were positively associated with serum PCSK9 levels in all participants (r = 0.06, P < 0.01) and in women (r = 0.22, P < 0.01), but not in men (r = 0.03, P = 0.18). Multiple linear regression and binary logistic regression analyses indicated that serum PCSK9 levels were significantly correlated with SUA levels and hyperuricemia in women. However, when the model was adjusted for triglyceride (TG), the associations of serum PCSK9 levels with SUA levels and hyperuricemia disappeared. In mediation analyses, TG, low-density lipoprotein cholesterol (LDL-C), body mass index (BMI), total cholesterol (TC), white blood cell count and neutrophil count explained 35.08%, 20.58%,19.99%, 14.37%, 7.10% and 3.24% of SUA levels association with serum PCSK9 levels, respectively. Conclusion: Serum PCSK9 levels are positively associated with SUA levels in women. Furthermore, this association is partially mediated through metabolic factors and inflammation.

Type 2 diabetes mellitus (T2DM) has become one of the most serious public healthcare challenges, contributing to increased mortality and disability. In the past decades, significant progress has been made in understanding the pathogenesis of T2DM. Mounting evidence suggested that gut microbiota (GM) plays a significant role in the development of T2DM. Communication between the GM and the brain is a complex bidirectional connection, known as the “gut-brain axis,” via the nervous, neuroendocrine, and immune systems. Gut-brain axis has an essential impact on various physiological processes, including glucose metabolism, food intake, gut motility, etc. In this review, we provide an outline of the gut-brain axis. We also highlight how the dysbiosis of the gut-brain axis affects glucose homeostasis and even results in T2DM.

Olfactory receptors (ORs) are G protein coupled receptors (GPCRs) with seven transmembrane domains that bind to specific exogenous chemical ligands and transduce intracellular signals. They constitute the largest gene family in the human genome. They are expressed in the epithelial cells of the olfactory organs and in the non-olfactory tissues such as the liver, kidney, heart, lung, pancreas, intestines, muscle, testis, placenta, cerebral cortex, and skin. They play important roles in the normal physiological and pathophysiological mechanisms. Recent evidence has highlighted a close association between ORs and several metabolic diseases. Cardiovascular diseases (CVDs) are the leading cause of morbidity and mortality globally. Furthermore, ORs play an essential role in the development and functional regulation of the cardiovascular system and are implicated in the pathophysiological mechanisms of CVDs, including atherosclerosis (AS), heart failure (HF), aneurysms, and hypertension (HTN). This review describes the specific mechanistic roles of ORs in the CVDs, and highlights the future clinical application prospects of ORs in the diagnosis, treatment, and prevention of the CVDs.

Background: The aim of this study was to explore the associations of serum remnant cholesterol (RC) levels with the progression and regression of metabolic dysfunction-associated steatotic liver disease (MASLD) in Chinese adults.Methods: We conducted a cross-sectional study in 13903 individuals who underwent transient elastography tests (cohort 1) and a longitudinal study in 17752 individuals who underwent at least two health check-up exams with abdominal ultrasound (cohort 2). Anthropometric and biochemical parameters were collected. Serum RC levels were calculated. Noninvasive fibrosis indices such as FIB-4 were evaluated in cohort 2.Results: In cohort 1, serum RC levels were positively and independently associated with the severity of hepatic steatosis and liver fibrosis according to logistic regression analysis. In cohort 2, baseline serum RC levels were increased in participants with the incidence of MASLD and decreased in participants with the regression of MASLD during the follow-up period. Baseline serum RC levels were independently associated with an increased risk of development and a decreased likelihood of regression of MASLD: the fully adjusted hazard ratios (HR) were 2.785 (95% CI 2.332-3.236, P <0.001) and 2.925 (95% CI 2.361-3.623, P <0.001), respectively. In addition, when we used FIB-4 to evaluate liver fibrosis, baseline serum RC levels were positively correlated with the incidence of high-intermediate probability of advanced fibrosis. However, we did not find an association between serum RC levels and the regression of liver fibrosis.Conclusion: Serum RC levels are independently correlated with the progression and regression of MASLD in Chinese adults, suggesting that RC may participate in the pathophysiological process of MASLD.

Basement membranes (BMs) are widely distributed and highly specialized extracellular matrix (ECM). The goal of this study was to explore novel genes associated with nonalcoholic fatty liver disease (NAFLD) from the perspective of BMs. Sequencing results of 304 liver biopsy samples about NAFLD were systematically obtained from the Gene Expression Omnibus (GEO) database. Biological changes during NAFLD progression and hub BM-associated genes were investigated by differential gene analysis and weighted gene co-expression network analysis (WGCNA), respectively. The nonalcoholic steatohepatitis (NASH) subgroups were identified based on hub BM-associated genes expression, as well as the differences in Kyoto Encyclopedia of Genes and Genomes (KEGG) signaling pathways and immune microenvironment between different subgroups were compared. Extracellular matrix (ECM) seems to play an important role in the development of NAFLD. Three representative BM-associated genes (ADAMTS2, COL5A1, and LAMC3) were finally identified. Subgroup analysis results suggested that there were significant changes in KEGG signaling pathways related to metabolism, extracellular matrix, cell proliferation, differentiation, and death. There were also changes in macrophage polarization, neutrophils, and dendritic cells abundance, and so on. In conclusion, the present study identified novel potential BM-associated biomarkers and further explored the heterogeneity of NASH that might provide new insights into the diagnosis, assessment, management, and personalized treatment of NAFLD.

Objective To explore the correlation between monocyte to high-density lipoprotein cholesterol ratio（MHR）and insulin resistance（IR） in male patients with type 2 diabetes mellitus（T2DM） combined with metabolic-related fatty liver disease（MAFLD）.Methods A total of 454 male patients with T2DM combined with MAFLD in National Metabolic Management Center（MMC） of the Affiliated Hospital of Jiangsu University from May 2018 to July 2020 were enrolled. The general clinical data of subjects were collected, blood routine and biochemical indexes were tested, homeostasis model insulin resistance index（HOMA-IR） was calculated, visceral fat area（VFA） and subcutaneous fat area（SFA） were measured.Accordingtothe MHR quartile, patients were divided into group Q1（MHR≤0.38）, group Q2（0.38＜MHR≤0.48）, group Q3（0.48＜MHR≤0.64） and group Q4（MHR＞0.64） to compare the differences in measured indicators above. In addition, patients were divided into two groups according to HOMA-IR, HOMA-IR＜2.5 and HOMA-IR≥2.5, and the differences in MHR were compared.Results The patients were divided into four groups according to MHR:group Q1（n=115）, group Q2（n=110）, group Q3（n=120） and group Q4（n=109）. Fasting insulin（FINS） were respectively 6.17（4.20,9.76）, 7.73（4.94,10.66）, 8.92（5.32,11.33）and 9.13（5.25,12.27） mU/L, 2-hour postprandial insulin were 22.75（12.87,39.59）, 27.55（16.44,39.77）, 30.98（17.46,43.11） and 31.28（18.54,45.92） U/L. HOMA-IR were 3.12（1.63,4.25）, 3.72（2.26,4.66）, 3.87（2.48,5.44） and 3.95（2.42,5.31）. Neutrophil（Neu） were 3.10（2.60,3.70）, 3.20（2.50,3.93）, 3.60（2.80,4.28）, 4.20（3.30,5.00）×10~9/L. Subcutaneous fat area（SFA） were（181.27±53.60）,（192.64±62.41）,（199.53±61.40） and（203.69±71.51） cm~2. They all increased gradually. However, the levels of highdensity lipoprotein cholesterol（HDL-c） [1.18（1.06,1.35）, 1.02（0.86,1.17）, 0.96（0.80,1.03） and 0.80（0.69,0.92） mmol/L] and low-density lipoprotein cholesterol（LDL-c） [（3.00 ± 0.79）,（2.76 ± 0.83）,（2.67 ± 0.85） and（2.59 ± 0.92） mmol/L] decreased gradually. Pearson’s or Spearman’s correlation analysis showed that MHR was positively correlated with FINS, 2-hour postprandial insulin（2hINS）, HOMA-IR, VFA and SFA（r=0.190, 0.153, 0.184, 0.114, 0.127, P＜0.05）. The coronary heart disease history, systolic blood pressure,diastolic blood pressure,fasting plasmaglucose（FPG）, FINS, alanine aminotransferase（ALT）, aspartate aminotransferase（AST）, blood uric acid（Ur）, body mass index（BMI）, VFA, SFA and MHR of patients in group HOMA-IR≥2.5 were higher than group HOMA-IR＜2.5（P＜0.05）.Conclusion MHR is positively correlated with IR in male patients with T2DM combined with MAFLD, and as MHR increases, the degree of IR is higher.

Polycystic ovary syndrome (PCOS) is a common endocrine gynecological disorder, and the specific pathogenesis of PCOS has not been elucidated. Obesity is a current major public health problem, which is also vital to PCOS. It can exacerbate PCOS symptoms via insulin resistance and hyperandrogenemia. The treatment of PCOS patients depends on the prevailing symptoms. Lifestyle interventions and weight loss remain first-line treatments for women with PCOS. The gut microbiota, which is a current research hot spot, has a substantial influence on PCOS and is closely related to obesity. The present study aimed to elucidate the function of the gut microbiota in obesity and PCOS to provide new ideas for the treatment of PCOS.