Metabolic dysfunction-associated steatotic liver disease (MASLD) is driven by complex immune and inflammatory mechanisms. Visceral adiposity, a key contributor, worsens inflammation, immune dysregulation, and insulin resistance. This study examines correlations between inflammatory genes, insulin resistance markers, and inflammatory markers across visceral adiposity levels in patients with MASLD. This cross-sectional study included 102 patients with MASLD. Assessments included body mass index, visceral adiposity index (VAI), a body shape index (ABSI), inflammatory markers, gene expression from peripheral white blood cells, and serologic inflammatory proteins. We calculated insulin resistance markers, such as homeostasis model assessment-insulin resistance index (HOMA-IR), triglyceride/high-density lipoprotein cholesterol (TG/HDL-C) ratio, triglyceride-glucose (TyG) index, and neutrophil-to-HDL ratio (NHR). Pearson correlation coefficients evaluated parameter associations between low and high VAI and ABSI groups. The higher VAI group presented with some elevated markers, such as HOMA-IR (5.21 ± 3.42 vs. 4.34 ± 4.62), TG/HDL-C (4.08 ± 1.97 vs. 2.20 ± 1.07), TyG (9.03 ± 0.48 vs. 8.70 ± 0.51), and NHR (1.86 ± 0.75 vs. 1.45 ± 0.64) compared with the low VAI group, indicating potentially greater insulin resistance and systemic inflammation. Monocyte chemoattractant protein-1and interleukin-6 genes were strongly correlated in the low VAI group (R = 0.94, P < 0.001) but more weakly correlated in the high VAI group (R = 0.63, P < 0.001). These findings highlight differential immune changes across visceral adiposity levels in MASLD, supporting the need for tailored interventions based on adiposity profiles.

BackgroundIncreasing evidence suggests obstructive sleep apnea (OSA) is an independent risk factor for type 2 diabetes. Insulin resistance is the primary mechanism in the early stage of type 2 diabetes. The aim of this study was to assess the prevalence of OSA among patients with type 2 diabetes mellitus and to examine the association between OSA severity and insulin resistance.MethodsThis study adopted a cross-sectional observational design. We enrolled patients hospitalized for poorly controlled type 2 diabetes mellitus from the Endocrine Department of Beijing Chao-Yang Hospital and recorded their demographic and clinical data in an electronic case report form. Polysomnography (PSG) monitoring was performed for all the subjects. According to the apnea hypopnea index (AHI), the subjects were classified into the following three groups: the control group, AHI <5 events per hour; the mild-OSA group, 5 events per hour ≤ AHI <15 events per hour; and the moderate-to-severe-OSA group, AHI ≥15 events per hour.ResultsA total of 96 patients with type 2 diabetes were enrolled in this study, among whom 78 (81.28%) were diagnosed with OSA. The participants were categorized into three groups: a control group of 18 patients without OSA, a mild-OSA group of 54 patients, and a moderate-to-severe OSA group of 24 patients. Analysis revealed that the C-peptide area under the curve (AUCcp) was significantly greater in the moderate-to-severe OSA group compared to the control group. Additionally, the homeostasis model assessment of insulin resistance (HOMA-IR) was significantly higher in both the moderate-to-severe OSA and mild OSA groups relative to the control group. Multiple stepwise regression analysis revealed that the AHI and AUCcp were positively correlated (r=0.323, P=0.001). Both the AHI and body mass index (BMI) were positively correlated with the HOMA-IR index (P=0.007 and 0.02, respectively).ConclusionsA high prevalence of OSA was observed among patients hospitalized for poorly controlled type 2 diabetes; further, its severity was positively correlated with insulin resistance.

We investigated whether vitamin D (VD) alleviates type 2 diabetes mellitus (T2DM) by modulating autophagy and inflammation. In wild-type diabetic mice, VD supplementation significantly improved glucose tolerance, reduced fasting blood glucose, and the HOMA-IR (homeostasis model assessment of insulin resistance) index (P<0.05). Serum levels of IL-1β, TNF-α, and tissue reactive oxygen species were markedly elevated in T2DM mice but significantly decreased after VD treatment (P<0.05). Histopathological and ultrastructural analyses revealed that VD preserved pancreatic and kidney tissue integrity and increased autophagic structures. Consistently, VD upregulated Beclin-1 and LC3-II while downregulating IL-1β and NF-κB p65 expression in these tissues (P<0.05). In contrast, these beneficial effects of VD were largely absent in NLRP3-knockout T2DM mice. Collectively, vitamin D exerts therapeutic effects in T2DM by promoting autophagy and inhibiting inflammation, primarily through the ROS-NLRP3-IL-1β-NF-κB signaling pathway.

To observe the effect of electroacupuncture (EA) at "Sanyinjiao" (SP6) and "Zusanli" (ST36) on the expressions of peroxisome proliferator-activated γ receptor (PPAR-γ), nuclear factor-κB (NF-κB) and glucose transporter 4 (GLUT4) in skeletal muscle of Zucker Diabetic Fatty (ZDF) rats with type 2 diabetes mellitus (T2DM), so as to explore its possible mechanism in improving insulin resistance (IR). Eighteen male 2-month-old ZDF (Leprfa/fa) rats were fed with a high-fat diet for 4 weeks to establish a diabetic model. After the model was confirmed, the rats were randomly divided into model, EA and medication groups, with 6 rats in each group. Additionally, 6 Zucker lean rats (Lepr+/fa) of the same age were used as the control group. EA (15 Hz, 1 mA) was applied to bilateral SP6 and ST36 for 20 min;the medication group was administered pioglitazone solution (10 mg/kg) via gastric gavage;both groups were treated once daily, 5 d a week for 4 weeks. Fasting body weight (FBW) was measured weekly, fasting blood glucose (FBG) was measured the day before sampling. The levels of serum fasting insulin (FINS), free fatty acid (FFA), low density lipoprotein (LDL), total cholesterol (TC), triglyceride (TG), tumor necrosis factor-α (TNF-α), C peptide and C reactive protein (CRP) were detected by ELISA, and the homeostasis model assessment of insulin resistance (HOMA-IR) index was calculated. HE staining and oil red O staining were used to observe the pathological changes and lipid droplet accumulation of skeletal muscle in rats respectively. The protein expression levels of PPAR-γ, NF-κB and phosphorylated (p) -NF-κB in skeletal muscle tissue of rats were detected by Western blot. The positive expressions of TNF-α and GLUT4 in skeletal muscle of rats were detected by immunofluorescence. Compared with the control group, the FBW, FBG, HOMA-IR index, the serum levels of FINS, FFA, LDL, TG, TC, TNF-α, C-peptide and CRP, NF-κB phosphorylation level, as well as the positive expression of TNF-α and p-NF-κB/NF-κB in skeletal muscle were increased (P<0.01), while the PPAR-γ expression and the positive expression of GLUT4 in skeletal muscle were decreased (P<0.01) in the model group. Oil red O staining showed a large number of bright red lipid droplets and serious lipid accumulation in skeletal muscle cells, HE staining showed that the skeletal muscle fibers were broken in the model group. Compared with the model group, the FBW of the medication group, the expression levels of PPAR-γ and GLUT4 of both EA and medication groups were increased (P<0.01). Conversely, the levels of FBG, HOMA-IR index, FINS, FFA, LDL, TG, TC, TNF-α, C-peptide and CRP, the phosphorylation level of NF-κB protein and TNF-α expression were decreased (P<0.05, P<0.01) in the EA and medication groups. The oil red O staining showed that the lipid droplets in the skeletal muscle cells were significantly reduced, and the degree of lipid accumulation was alleviated, whereas HE staining showed reduced skeletal-muscle fiber disruption in the EA and medication groups compared to those in the model group. EA can ameliorate energy metabolism disorders in T2DM rats, reduce ectopic lipid accumulation in skeletal muscle, and alleviate inflammatory responses, which may be related to the regulation of the PPAR-γ/NF-κB signaling pathway.

We aimed to assess the sex-specific associations of different measures of body size, composition, and fat distribution with data from an oral glucose tolerance test (OGTT) and to compare their effect sizes in a population-based study. sCross-sectional data of 3628 (1898 women, 52%) subjects aged between 20 and 84 years were taken from the Study of Health in Pomerania (SHIP-Trend-0). We investigated associations of markers from body anthropometry, bioelectrical impedance analysis, and magnetic resonance imaging with markers from an OGTT including fasting glucose, fasting insulin, the homeostasis model assessment-insulin resistance index, 2-h post-load (glucose and insulin) and glucose tolerance categories. For this, we used linear and multinomial logistic regression models stratified by sex and adjusted for confounding. All body composition markers were significantly associated with all OGTT parameters in both sexes. In women, visceral adipose tissue and liver fat content were most strongly associated with the OGTT parameters, while in men, the waist-to-height ratio showed the strongest association. Relative fat-free mass was the only marker, which was inversely associated with the OGTT parameters in both men and women. Overall, the associations of all body composition markers wee more pronounced in men than in women. Our study highlights that associations between body composition markers and OGTT parameters differ between men and women with a tendency of stronger associations in men than in women. Sex-specific body composition markers may have to be considered in clinical practice to predict future prediabetes and type 2 diabetes.

This research explored whether vitamin D status is related to Insulin Resistance (IR) and pancreatic β-cell performance among non-diabetic obese employees at Dr. M. Djamil Padang Hospital, West Sumatra, Indonesia. Insulin resistance and β-cell activity were assessed using the Homeostatic Model Assessment—specifically Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) as an indicator of insulin resistance and Homeostasis Model Assessment of Beta-Cell Function (HOMA-B) to evaluate β-cell function. The study applied a cross-sectional design conducted from January to July 2020 and involved 81 obese hospital staff without diabetes. Measurements included Fasting Blood Glucose (FBG), Fasting Insulin (FI), and Serum 25-Hydroxyvitamin D [25(OH)D], all analyzed with automated instruments. HOMA-IR and HOMA-B indices were derived from FBG and FI using standard formulas. Statistical analysis used the Spearman correlation test with a significance threshold of p&lt;0.05, followed by multivariate linear regression. The participants were predominantly female (58%), aged 18–58 years, with a mean Body Mass Index (BMI) of 31.46±3.99 kg/m². Average vitamin D levels were 14.84±5.48 ng/mL, while median values for HOMA-IR and HOMA-B were 2.30 and 193.09%, respectively. The results indicated that vitamin D concentrations did not show a meaningful correlation with either HOMA-IR (r=0.071; p=0.530) or HOMA-B (r=−0.106; p=0.347). BMI demonstrated the strongest association with HOMA-IR (β=0.165), and HOMA-IR was the variable most strongly related to HOMA-B (β=21.83). Overall, this study concludes that baseline vitamin D levels are not significantly linked to insulin resistance or pancreatic β-cell function, as reflected by HOMA-IR and HOMA-B measurements, among non-diabetic obese staff at Dr. M. Djamil Padang Hospital.

Background:According to the genome-wide association studies (GWASs), zinc transporter 8 (ZnT8; SLC30A8) is among the loci containing variants linked to type 2 diabetes (T2D) risk. The variants rs11558471 and rs13266634 are two GWAS-suggestive single nucleotide variations (SNVs), however, their synergistic effects have received less attention, particularly in populations with the high prevalence of diabetes. This study, was thus conducted to determine their synergistic effects on insulin resistance.Methods:A total of 261 subjects were included in this study. Insulin and fasting glucose concentrations were used to calculate the homeostasis model assessment for insulin resistance (HOMA-IR) index. The study variants were genotyped by polymerase chain reaction (PCR)-based restriction analysis.Results:For both variants, the HOMA-IR index is enhanced in the order of risk allele-carrying genotypes (GG<GA<AA for rs11558471 and TT<CT<CC for rs13266634). For rs13266634, in the CT + CC group, this insulin resistance index was significantly higher in T2D patients than in control subjects (P < 0.001). For rs11558471, in both the GA + AA group and GG genotypes, HOMA-IR was higher in patients than in control subjects; however, only the difference in the GA+AA group was statistically significant (P < 0.001). Individuals with 3–4 risk alleles had a significantly higher HOMA-IR than that of individuals with 0–2 risk alleles (P = 0.02).Conclusions:In addition to individual effects on T2D risk, the risk alleles of rs13266634 and rs11558471 seem to collectively work in an additive manner to influence insulin resistance. The combination of their risk alleles may be helpful to diagnose people at high risk for the development of T2D.

To investigate the association between insulin resistance (IR) and obesity and uterine fibroids (UFs) in non-diabetic populations using data from the National Health and Nutrition Examination Survey (NHANES). This cross-sectional study analyzed data from NHANES (1999-2006) and included 867 non-diabetic women aged 20-54 years. IR was assessed using the triglyceride-glucose (TyG) index, TyG-waist-to-height ratio (TyG-WHtR), TyG-body mass index (TyG-BMI), and the homeostasis model assessment of insulin resistance (HOMA-IR). Obesity was assessed by WHtR, weight-adjusted waist index (WWI), waist circumference (WC) and BMI. Logistic regression, restricted cubic spline curves (RCS), subgroup analyses, and interaction tests were performed to evaluate the associations. HOMA-IR index (OR = 1.17, p = 0.004) and BMI (OR = 1.04, p = 0.036) were significantly positively correlated with UFs. Subgroup analyses in those not using female hormones show that among women aged 20-38 years, the association between BMI and UFs was stronger (P < 0.05), while in women aged 39-54 years, HOMA-IR was stronger (P < 0.05). The RCS models indicated significant positive linear associations between HOMA-IR, as well as BMI, and UFs. Our study demonstrates that IR and BMI are independently and positively associated with the presence of UFs in non-diabetic women, indicating that they may be potentially modifiable factors associated with UFs development.

Endometrial hyperplasia (EH) accounts for 10–18% of gynecological pathology and is associated with a risk of malignancy, particularly in patients with metabolic syndrome and impaired liver function. Nonalcoholic fatty liver disease, with a prevalence of 25–30% among the adult population, promotes proliferative processes in the endometrium.The objective: to evaluate the effectiveness of comprehensive treatment of EH in patients with concomitant hepatic steatosis by individualizing therapy based on metabolic status.Materials and methods. A total of 114 women with histologically confirmed non-atypical EH and hepatic steatosis were exa-mined and divided into two groups. The patients in the I group received monotherapy with dydrogesterone 20 mg/day from the 16th to 25th days of the menstrual cycle. The II group received dydrogesterone in combination with the phytotherapeutic agent Artigel, which contains artichoke and dandelion extracts, choline and inositol. The treatment duration was 6 months. Effectiveness was evaluated based on transvaginal ultrasound of the endometrium, biochemical liver function parameters, lipid metabolism indicators, HOMA (Homeostasis Model Assessment of Insulin Resistance) index, estradiol and sex hormone-binding globulin (SHBG) levels.Results. After the 6-month treatment course, the combined therapy group showed a significant reduction in transaminase levels, in particular, the level of aspartate aminotransferase decreased by 1.5 times (from 42.7 ± 3.1 to 28.4 ± 2.6 U/L), alanine aminotransferase – by 1.4 times (from 46.2 ± 3.5 to 32.8 ± 2.9 U/L); a 1.5-fold reduction in HOMA index (from 4.8 ± 0.6 to 3.1 ± 0.4); improvement in lipid profile, in particular, level of triglycerides decreased from 2.4 ± 0.3 to 1.6 ± 0.2 mmol/L, low-density lipoproteins – from 3.9 ± 0.4 to 2.6 ± 0.3 mmol/L, while the level of high-density lipoproteins increased in 1.4 times (from 1.0 ± 0.1 to 1.4 ± 0.2 mmol/L). These changes were not observed in the monotherapy group. Unlike the dydrogesterone monotherapy group, in the II group of patients an increased level of SHBG (from 95.1 ± 2.1 to 128.5 ± 11.6 nmol/L) was recorded, which was accompanied by a decrease in bioavailable estradiol by 35% (from 118.9 ± 12.5 to 88.4 ± 8.9 pmol/L). The recurrence rate of EH was lower in the combined therapy group – 17.2% versus 37.5% (p &lt; 0.05).Conclusions. Combined therapy with dydrogesterone and the phytotherapeutic agent Artigel demonstrated higher effectiveness in the treatment of EH compared with dydrogesterone monotherapy, as it not only reduced the recurrence rate of EH but also corrected key pathogenetic mechanisms such as insulin resistance, dyslipidemia and hormonal imbalance. These findings confirm the rationale for a comprehensive treatment approach to EH in patients with metabolic disorders.

BackgroundThe incidence of insulin resistance (IR) among cancer survivors is significantly higher than that in the general population. Current diagnostic methods for IR are complex, often requiring fasting blood samples, specialized laboratory tests, and sometimes invasive procedures, which limit their routine clinical application. This study investigated the association between platelet-to-lymphocyte ratio (PLR), a readily available marker from routine blood tests, and IR in cancer survivors, aiming to find a more straightforward predictor of IR that could potentially simplify screening and monitoring processes in this high-risk population.MethodsThis cross-sectional study analyzed data from 1,418 cancer survivors from the NHANES 2005-2018 database. IR was assessed by three indicators: homeostasis model assessment of insulin resistance (HOMA-IR), quantitative insulin sensitivity check index (QUICKI), and the triglyceride-glucose (TyG) index. Multivariable logistic regression models were used to examine the relationship between PLR quartiles and IR, with restricted cubic spline (RCS) analyses to evaluate non-linear relationships. Covariates included demographic (age, gender, race/ethnicity), socioeconomic (marital status, education, family poverty income ratio), lifestyle (smoking status, alcohol consumption, sleep duration, physical activity) and health status variables (body mass index (BMI), history of cardiovascular disease, hypertension status). Subgroup analyses were conducted to identify sensitive populations.ResultsThe 1,418 cancer survivors (weighted population: 20,233,847; median age 69.0 years; 58.4% female) with low HOMA-IR (< 2.5), high QUICKI (≥ 0.33) and low TyG index (< 4.68) demonstrated more favorable metabolic profiles, including lower PLR values, better socioeconomic status, better lifestyle, and lower chronic disease burden. Compared to the lowest PLR quartile (Q1), individuals in the highest quartile (Q4) showed significantly increased IR risk when assessed by QUICKI (hazard ratio (HR) = 1.61, 95% confidence interval (CI): 1.02 - 2.53, P = 0.040) and the TyG index (HR = 1.56, 95% CI: 1.02 - 2.45, P = 0.035). Each increment in PLR quartile was associated with a 19% (QUICKI) and 15% (TyG) increased risk of IR. Receiver operating characteristic (ROC) analysis results indicated that PLR cutoff values in the range of 124 - 137 can serve as screening thresholds for IR in cancer survivors. In the subgroup analysis, the PLR and IR showed no significant interaction across all examined subgroup characteristics in both the HOMA-IR and QUICKI models (P > 0.05). However, in the TyG index model, individuals in the Q4 compared to the Q1 demonstrated greater susceptibility to IR in those with physical activity < 600 metabolic equivalent of task (MET)-mins/week (odds ratio (OR) = 2.28, 95% CI: 1.12 - 4.61); and those with a history of hypertension (OR = 1.95, 95% CI: 1.05 - 3.63), with P values for interaction of 0.007 and 0.036, respectively.ConclusionsHigher PLR levels indicated a significantly increased risk of IR in cancer survivors, especially when assessed by QUICKI and the TyG index. This relationship showed no significant interaction between subgroups in the HOMA-IR and QUICKI models, but in the TyG index model, and the association was more pronounced among individuals with low physical activity and those with a history of hypertension. As a simple, cost-effective biomarker derived from routine blood tests, PLR offers potential clinical value for the assessment of IR risk in cancer survivors, especially in high-risk subgroups.

BackgroundChronic hepatitis C (CHC) is associated with an increased risk of type 2 diabetes mellitus (T2DM). However, regional variations in HCV genotypes and clinical characteristics may influence this association. This study aimed to investigate the association between chronic hepatitis C virus (CHC) infection and the development of T2DM in CHC patients in Southern China.MethodsA retrospective case-control cohort study analyzed 442 CHC patients (242 without T2DM, 200 with T2DM) from 2010 to 2018. Biochemical parameters, HCV genotypes, and clinical characteristics were compared. Multivariate logistic regression and ROC analysis were performed to evaluate predictors of T2DM.ResultsThe CHC + T2DM group exhibited significantly higher age (P < 0.001), BMI (P = 0.001), fasting blood glucose (P < 0.001), fasting insulin (P = 0.015), HOMA-IR (Homeostasis Model Assessment-Insulin Resistance) index (P < 0.001), transaminases alanine transaminase (ALT) (P < 0.001) and aspartate transaminase (AST) (P < 0.001), total bilirubin (P < 0.001), γ-Glutamyl Transferase (GGT) (P < 0.001), and cirrhosis prevalence (P < 0.001). Logistic regression analysis showed that age (OR: 1.09), fasting blood glucose (OR: 16.20), fasting insulin (OR: 1.23), HOMA-IR (OR: 0.48), and GGT (OR: 1.01), cirrhosis (OR: 15.32) and hypertension (OR: 31.00) were the risk factors of T2DM in CHC patients. HCV genotype distribution differed significantly between CHC and CHC + DM groups (P = 0.008), with genotype 3a more prevalent in CHC + DM (2.07% vs. 11.36%, P = 0.032). Receiver Operating Characteristic curve analysis highlighted fasting glucose (AUC = 0.904) as the strongest predictor.ConclusionAge, metabolic dysregulation, liver cirrhosis, hypertension, and HCV genotype 3a are key risk factors for T2DM in CHC patients. Early screening for glucose intolerance and genotype-specific interventions are critical in high-risk populations.

This study investigated the potential therapeutic effects of Lactobacillus rhamnosus PB01 supplementation on metabolic and reproductive dysfunctions in Type 1 diabetes mellitus (T1DM) rat model. Diabetic rats treated with L. rhamnosus PB01 (1 × 10⁹ CFU/day) showed significant improvements in metabolic and reproductive outcomes. Specifically, diabetes-induced weight loss was mitigated by approximately 13%, and the percentage of hyperactivated sperm in the treatment group was significantly 2.5 times higher than that of the diabetic controls. Additionally, testosterone levels were significantly elevated by 27%, further supporting the positive effects on reproductive health. The probiotic supplementation also led to improvements in insulin sensitivity, as evidenced by a 34.12% reduction in homeostasis model assessment index of insulin resistance (HOMA-IR). L. rhamnosus PB01 (DSM 14870) demonstrated potential as an adjunct therapy for managing T1DM-associated complications in the rat model, by improving insulin sensitivity, supporting weight management, and partially restoring diabetes-related fertility impairments, likely through modulation of hormonal pathways. However, further studies are needed to translate the results to humans and refine optimal dosing and supplementation duration for sustained benefits.

Abstract Psoriasis is associated with metabolic syndrome and insulin resistance (IR). Recent studies have shown IR to be a predictor of response to various biologic treatments in patients with psoriasis (Huang D, Zhong X, Jiang Y et al. Insulin resistance impairs biologic agent response in moderate-to-severe plaque psoriasis: insights from a prospective cohort study in China. Br J Dermatol 2024; 191: 616–23). We hereby tried to analyse treatment response to the systemic nonbiologic modalities with respect to IR in patients with moderate-to-severe psoriasis. This single-centre retrospective study was carried out at a tertiary care institute. Data were retrieved and analysed for patients with moderate-to-severe psoriasis registered in the psoriasis clinic from January 2023 to June 2024 who received systemic nonbiologic treatment with a minimum follow-up of 12 weeks. Psoriasis severity was assessed using the Psoriasis Area and Severity Index (PASI). IR was calculated using triglyceride glucose–body mass index (TyG-BMI) and homeostasis model assessment of insulin resistance (HOMA-IR). Treatment response was assessed as ≥ 75% improvement in PASI (PASI 75) at 12 weeks. In total 34 patients with moderate-to-severe psoriasis were analysed. The mean (SD) age of the study population was 42.7 (13.6) years; 22 patients were male and 12 female ratio. Of the 34 patients, 11 had metabolic syndrome and five had psoriatic arthritis. The mean duration of the disease was 9.5 (SD 6.9) years. The mean (SD) baseline body surface area (BSA) and PASI were 19.1% (17.4) and 9.1 (5.7), respectively. Twenty-four patients received methotrexate and 10 patients received apremilast. The mean (SD) TyG-BMI index was 222 (33.4). Mean (SD) insulin and HOMA-IR were 13.5 mIU L−1 (8.8) and 3.2 (1.9), respectively. Among the patients with a high TyG-BMI index (i.e. above the median of 223), nine of 17 (53%) achieved PASI 75, while seven of 17 patients (41%) with a low TyG-BMI index achieved PASI 75 at week 12 (P = 0.73). However, among patients with high HOMA-IR (&amp;gt; 2.9), only 4 of 15 (27%) achieved PASI 75 at week 12, compared with 12 of 19 (63%) with low HOMA-IR (P = 0.04). Significant differences were observed in the decrease in BSA and PASI at week 12 between patients with high and low HOMA-IR (P = 0.02 and P = 0.03, respectively). In contrast, no such significance was observed with respect to TyG-BMI (P = 0.6 and P = 0.8, respectively). In conclusion, our study shows that a high HOMA-IR index, not a TyG-BMI index, impairs treatment response to systemic drugs in patients with moderate-to-severe psoriasis. However, our study has limitations such as the small sample size and retrospective design. Thus, prospective studies with larger patient populations are needed to evaluate the long-term impact of IR in psoriasis.

Background: Frozen shoulder (FS) is a common musculoskeletal condition with significant socioeconomic impact. Despite its prevalence, the condition lacks a definitive understanding and universally effective treatment approach. Objective: To evaluate the effects of an intervention combining manual therapy, conventional exercises, and strategies to improve sleep quality and circadian rhythm on recovery and biomarkers in patients with FS. Methods: A single-blind, randomized, controlled trial was conducted with 34 participants divided into control and experimental groups (n = 17 each). Both groups received manual therapy and conventional exercises, while the experimental group (EG) also received sleep and circadian rhythm optimization instructions. Biomarkers (fasting glucose, insulin, Homeostasis Model Assessment of Insulin Resistance (HOMA) index, leptin, triglycerides, total cholesterol, HDL cholesterol, uric acid, CRP, IL-1β, IL-6, IL-17, IL-10, IL-33, HMGB1, and TNF-α) and functional outcomes (SPADI, ROM, and PSQI) were assessed pre- and post-intervention. Results: After six weeks, the EG showed significant improvements in IL-10 levels (mean change: 2.5 pg/mL vs. 0.5 pg/mL in the control group (CG), p = 0.03), IL-6 reduction (-1.8 pg/mL vs. -0.4 pg/mL, p = 0.02), and HOMA index (-0.8 vs. -0.2, p = 0.04). ROM improved by 20 degrees in the EG versus 10 degrees in the CG (p = 0.01), SPADI scores decreased by 25 points versus 15 points (p = 0.03), and PSQI improved by 4 points compared to 2 points (p = 0.05). Conclusion: The integration of sleep quality and circadian rhythm optimization into conventional rehabilitation significantly enhances recovery, particularly IL-10 modulation, but these did not translate into superior clinical improvements within the study period. Further long-term studies are needed to confirm whether early biological effects lead to sustained functional recovery in FS patients.

Objectives: This study aims to examine the mechanism by which white turmeric extract inhibits insulin resistance in experimental animals. Methods: Twenty-five male Wistar rats were divided into five groups: Normal control, high-fat diet (HFD), drug control (metformin), and two dose groups of white turmeric extract (200 mg/kg and 400 mg/kg). A HFD was administered for 10 days to induce insulin resistance, except in the normal control group. The drug control and two extract groups received metformin (45 mg/kg), and white turmeric extract (200 mg/kg and 400 mg/kg) for an additional 10 days. Insulin resistance was assessed using fasting blood glucose, insulin levels, homeostasis model assessment of insulin resistance (HOMA-IR) index, fat profiles, and tissue morphology of liver and brain organs. Results: Rats given 400 mg/kg of white turmeric extract showed significantly lower fasting blood glucose (45.04±9.08 mg/dL), insulin levels (1.58±0.37 mU/L), and HOMA-IR index (0.17±0.02) compared to the HFD group (81.55±13.94 mg/dL, 2.28±0.20 mU/L, and 0.46±0.08, respectively). The extract improved fat profiles and caused morphological changes in liver and brain tissue, with liver cells appearing smaller and nerve cells showing longer axons. Conclusion: White turmeric extract effectively inhibits insulin resistance by improving fat profiles.

Abstract Introduction The relationship between muscular strength and metabolic markers is poorly understood. Previous studies demonstrated that higher muscular strength was associated with lower prevalence of diabetes mellitus possibly due to better glycemic metabolism. We investigated the relations of handgrip strength (HGS) with oral glucose tolerance test (OGTT) markers: fasting glucose (FG) and insulin (FI), the homeostasis model assessment-insulin resistance index (HOMA-IR), 2-hour postload glucose (2HG) and insulin (2HI), and glucose tolerance categories in the general population. Methods We analyzed data from 3,125 women and men, aged 20-82 years, from the population-based Study of Health in Pomerania (SHIP-TREND-0). HGS, in kilograms, was assessed by a hand-grip dynamometer. Plasma FG was measured using a hexokinase method, and serum FI through electrochemiluminescence immunoassay. For OGTT examination, 75 grams of anhydrous glucose was given to study participants without known type 2 diabetes or taking glucose-lowering agents. Following the criteria of the American Diabetes Association, we classified individuals as having normal glucose tolerance (NGT), isolated impaired fasting glucose (i-IFG), isolated impaired glucose tolerance (i-IGT), combined IFG and IGT (IFG + IGT), and unknown type 2 diabetes (UT2D). The associations of HGS with glucose and insulin parameters were analyzed using multivariable linear regression models adjusted for appropriate confounders. Results HGS was inversely associated with glycemic and insulin levels. A 10 kg lower HGS was associated with a 0.07 mmol/L (95% confidence interval [CI]: 0.02 to 0.12; p=0.003) higher FG, a 0.57 µlU/mL (95% CI: 0.23 to 0.92; p=0.001) higher FI, a 0.23 mmol/L (95% CI: 0.11 to 0.35; p&amp;lt;0.001) higher 2HG, and a 0.12 (95% CI: 0.03 to 0.21; p=0.007) higher HOMA-IR. There was no association with 2HI. HGS was lower in individuals with metabolic impairments compared to NGT. Specifically, a 1kg (95% CI: 0.38 to 1.61; p=0.045), a 0.99kg (95% CI: 0.53 to 1.45; p=0.021) and 1.92kg (95% CI: 1.35 to 2.49; p&amp;lt;0.001) lower HGS was found in study participants with i-IGT, IFG+IGT and UDM, respectively. Conclusions/Outlook In a general population, HGS was inversely associated with glucose and insulin levels and resistance. The postprandial hyperglycemia seems to be associated the strongest with HGS when compared with the nocturnal hepatic gluconeogenesis dependent on hepatic insulin sensitivity.Figure 1

Metabolic syndrome (MetS) poses considerable toxicological risks due to its association with an increased likelihood of metabolic dysfunction-associated steatotic liver disease (MASLD), and is characterized by hypertension, hyperglycemia, dyslipidemia, and obesity. This study aimed to investigate the therapeutic potential of flavonoid-rich lotus seedpod extract (LSE) in alleviating MetS and MASLD-related hepatic disturbances. In vivo, mice subjected to a high-fat diet (HFD) and streptozotocin (STZ) injection were supplemented with LSE or simvastatin for 6 weeks. Obesity indicators included body weight and epididymal fat, while insulin resistance was measured by fasting serum glucose, serum insulin, homeostasis model assessment-insulin resistance index (HOMA-IR), and oral glucose tolerance (OGTT). Also, the levels of serum lipid profiles and blood pressure were evaluated. Adipokines, proinflammatory cytokines, liver fat droplets, and peri-portal fibrosis were analyzed to clarify the mechanism of MetS. LSE significantly reduced the HFD/STZ-induced MetS markers better than simvastatin, as demonstrated by hypoglycemic, hypolipidemic, antioxidant, and anti-inflammatory effects. In vitro, LSE improved oleic acid (OA)-triggered phenotypes of MASLD in hepatocyte HepG2 cells by reducing lipid accumulation and enhancing cell viability. This effect might be mediated through proteins involved in lipogenesis that are downregulated by adenosine monophosphate-activated protein kinase (AMPK). In addition, LSE reduced reactive oxygen species (ROS) generation and glycogen levels, as demonstrated by enhancing insulin signaling involving reducing insulin receptor substrate-1 (IRS-1) Ser307 phosphorylation and increasing glycogen synthase kinase 3 beta (GSK3β) and protein kinase B (PKB) expression. These benefits were dependent on AMPK activation, as confirmed by the AMPK inhibitor compound C. These results indicate that LSE exhibits protective effects against MetS-caused toxicological disturbances in hepatic carbohydrate and lipid metabolism, potentially contributing to its efficacy in preventing MASLD or MetS.

Goat's milk casein hydrolysates combined or not with zinc have interesting nutraceutical properties that limit the multiple complications of type 2 diabetes (T2D). This study aimed to evaluate the effect of goat’s milk casein hydrolysates and zinc (Zn) on insulin resistance, renal function and pancreatic and kidney histopathology, in type 2 diabetic rats (T2D). T2D was induced in rats by high fat diet (HFD) followed by intraperitoneal injection of streptozotocin (35 mg/kg body weight). Diabetic rats (n = 21) were divided into three groups: HFD or HFD combined with casein hydrolysates (HFD-CH) or HFD-CH combined with Zinc (HFD-CH-Zn). The control group (C) fed a standard diet. In high fat diet fed group vs control group HFD vs C, increased glucose levels, Glycated Hemoglobin (HbA1c), Oral Glucose Tolerance Test (OGGT) and Homeostasis model assessment Index-Insulin resistance (HOMA-IR) as well as renal dysfunction were observed while decreased serum insulin levels and Homeostasis model assessment Index-Pancreatic beta cells (HOMA- β ) (p&lt;0.01) was noted. Treatment of diabetic rats with CH and CH-Zn increased insulin levels and HOMA-β index vs HFD group (p&lt;0.01). Both treatments also prevented kidney injury by reducing serum creatinine, urea and uric acid. Histopathological analysis of the pancreas and kidney revealed tissue damages in the HFD vs C. These histological disturbances were reduced by the CH diet associated or not with Zn. Casein hydrolysates when used alone or in combination with zinc showed a beneficial effect on hyperglycaemia and improved renal function and repaired pancreatic and kidney histological damages induced by diabetes.

Background: The triglyceride-glucose (TyG) index has emerged as a novel surrogate marker of insulin resistance, but its changes after hepatitis C virus (HCV) eradication remain unclear. This study aimed to evaluate changes in the TyG index following direct-acting antiviral (DAA) treatment. Methods: HCV-infected patients achieving sustained virological response 12 weeks post-treatment (SVR12) were prospectively enrolled from May 2015 to June 2023. Exclusion criteria included the following: (1) failure to achieve SVR12; (2) use of anti-diabetes or anti-hyperlipidemia medications; and (3) hepatitis B virus or human immunodeficiency virus co-infection. Changes in lipid profiles, TyG index, and homeostasis model assessment of insulin resistance (HOMA-IR) were evaluated from baseline to SVR12. Insulin resistance was defined as HOMA-IR ≥ 2.5. The optimal TyG index cut-off for predicting insulin resistance was determined using the Youden Index. Results: A total of 111 patients (median age: 61.0 years; 45.9% male) were included. The TyG index correlated positively with HOMA-IR (Pearson's r = 0.32, p < 0.001). Among patients with pre-existing insulin resistance, significant improvements were observed at SVR12 in both HOMA-IR (4.0 [IQR: 3.1-5.4] vs. 2.5 [IQR: 2.0-3.9]; p < 0.001) and TyG index (8.47 [IQR: 8.08-8.68] vs. 8.36 [IQR: 8.00-8.71]; p = 0.028). Using 8.27 as the optimal TyG index cut-off, similar improvements were noted in HOMA-IR (2.8 [IQR: 2.0-4.3] vs. 2.3 [IQR: 1.5-3.8]; p = 0.031) and TyG index (8.62 [IQR: 8.46-8.83] vs. 8.52 [IQR: 8.27-8.89]; p = 0.003). Conclusions: The TyG index is a valuable tool for monitoring changes in insulin resistance after HCV eradication, particularly in patients with baseline insulin resistance.

Background and Purpose: Older adults are more susceptible to the development of type 2 diabetes mellitus (T2DM) due to age-related changes in insulin secretion and signaling pathways. Given the multifactorial nature of metabolic disorders, the use of robust multivariate models is justified to explore associated risk factors. This study aimed to identify latent classes of metabolic profiles among older adults based on a cluster of variables associated with cardiovascular risk. Methods: The study included community-dwelling individuals aged 60 years or older residing in urban areas who participated in all three phases of data collection: questionnaires, clinical examinations, and blood sampling. Latent class analysis (LCA) was applied using dichotomized variables, with model selection based on criteria such as Akaike Information Criterion, Bayesian Information Criterion, G², log-likelihood value, and entropy estimation. Results: A total of 210 older adults were evaluated. Three latent classes were identified: low, moderate, and high metabolic risk. The high-risk class was characterized by a higher probability of altered HbA1c and triglyceride-glucose (TyG) index values (0.96), elevated fasting blood glucose, and a prior diagnosis of hypertension (0.87), as well as impaired homeostasis model assessment of insulin resistance (HOMA-IR) index and a prior diagnosis of T2DM (0.79). The moderate-risk class showed a greater likelihood of hypertension (0.87), altered TyG (0.87), and impaired HOMA-IR index (0.56). Conclusions: LCA proved to be a valuable tool in Public Health by enabling the identification of homogeneous subgroups within a heterogeneous population. These findings support the development of more targeted and effective preventive strategies based on specific metabolic risk profiles.