Comparison of in vitro degradation of immunoreactive adrenocorticotropic hormone and insulin in equine blood measured by two immunoassay methods.

Bombesin receptor-activated protein homolog deficiency reduces food intake and alleviates metabolic dysfunction in high-fat diet treated mice.

Effectiveness and safety of preoperative carbohydrate loading in pediatric patients: A systematic review and meta-analysis of randomized controlled trials.

Down syndrome (DS) is the most common chromosomal abnormality associated with intellectual disabilities. Many metabolic issues begin in childhood, and children without DS are reported to have a high prevalence of metabolic syndrome (MS) according to various studies. However, our understanding of the risk of MS in children with DS is limited. A cross-sectional study assessed the prevalence of MS in DS children aged 10-18 during 2022-2024. Demographic details and anthropometric measurements were recorded for all participants. Fasting blood samples were collected for blood glucose, insulin, and lipid profile analysis. The modified NCEP-ATP III criteria were used to classify the MS. We also evaluated insulin resistance (IR) using HOMA-IR and body adiposity patterns with a DEXA scan in DS children aged 6-18. Seventy-six children aged 10-18 and 38 aged 6-9 were enrolled. The prevalence of MS was 18% in our cohort. Dyslipidemia (high triglycerides and low HDL) was observed in 21% and 15.8% of children aged 6-9 and 10-18, respectively. IR was observed in 27.6% and 7.8% of children aged 10-18 and 6-9, respectively. IR was positively correlated with BMI, whereas no correlation was observed with MS or dyslipidemia. Total body fat mass was positively correlated with MS. Our study observed a higher prevalence (18.0%) of MS than age-matched general population studies (pooled prevalence: 5.0%). Additionally, we observed a high prevalence of dyslipidemia and IR from 6 years of age. The results indicate the need to review the management guidelines and consider incorporating metabolic workups.

Lithium is the gold-standard pharmacotherapy for both acute episodes and long-term management of bipolar disorder (BD). Lithium treatment is associated with metabolic changes including weight gain; however, the exact mechanisms mediating weight increase are poorly understood. This systematic review assesses the effects of lithium on glucose, glucose-tolerance and insulin in persons with BD. A systematic search was conducted on PubMed, MEDLINE, Embase, CENTRAL, APA PsychINFO, Scopus and Web of Science. Primary studies assessing validated metrics of serum glucose or insulin in bipolar patients receiving lithium treatment were included. 16 studies were included in this review. Fasting plasma glucose (FPG) was the most studied metabolic biomarker. Most studies did not report an association between lithium and changes in FPG. Lithium treatment did increase glucose tolerance in the short-term, however most short-term effects appear to be transient and do not persist. There is a lack of a consistent criteria for BD across the reviewed studies. Many included studies lack controls and do not stratify for relevent metabolic factors such as body mass index (BMI) and age. Lithium does not appear to consistently affect FPG in persons with BD. Current evidence does not suggest that lithium directly and consistently affects FPG; instead changes to FPG in persons receiving lithium may be indirectly affected by BMI, age or mood status.

Association between hemodynamic parameters, insulin resistance, and body composition in primary care

Polycystic ovarian syndrome (PCOS) is a prevalent endocrine and metabolic disorder affecting women of reproductive age, frequently associated with infertility, metabolic complications, and chronic inflammation mediated by NF-κB activation. This is the first study to examine the effects of linalool (Lin), an acyclic monoterpene, on PCOS-related complications in rats. Adult female rats were randomly assigned to six experimental groups (n = 6): control, Lin 100, PCOS, PCOS + Lin 50, PCOS + Lin 100, and PCOS + Metformin (Met). To induce PCOS, letrozole (1mg/kg) was administered orally to the rats for 21 days. After PCOS induction, the rats were orally treated with Lin (50 and 100mg/kg) and Met (300mg/kg) for 14 days. Linalool remarkably mitigated ovarian histopathological alterations and fibrosis and significantly improved fasting blood glucose levels and insulin sensitivity in PCOS rats. Hormonal disturbances in PCOS rats, including elevated LH and testosterone levels, decreased FSH levels, and increased LH/FSH ratio, were considerably ameliorated after Lin treatment. Additionally, Lin treatment markedly decreased oxidative stress and inflammatory responses in PCOS rats, as demonstrated by enhanced glutathione peroxidase activity and decreased malondialdehyde, NF-κB p65, and TNF-α levels. Linalool partially restored impaired autophagy in PCOS rats by upregulating LC3-I and LC3-II. Conversely, Lin administration significantly inhibited excessive ovarian apoptosis in PCOS rats through downregulating cleaved caspase-3 and reducing the cleaved caspase-3/procaspase-3 ratio. In summary, Lin improved PCOS-induced ovarian and metabolic abnormalities in rats by regulating oxidative stress, inflammation, autophagy, and apoptosis, highlighting its potential for PCOS management.

Pemafibrate, a selective peroxisome proliferator-activated receptor alpha (PPARα) modulator, has shown potential in improving metabolic parameters. However, its effects on key metabolic biomarkers and fibroblast growth factor 21 (FGF21), have not been fully elucidated. To evaluate the effects of Pemafibrate on fasting blood glucose (FBG), insulin, HbA1c, HOMA-IR, and FGF21 through a systematic review and meta-analysis of randomized controlled trials (RCTs). A comprehensive literature search was conducted in PubMed, Web of Science, SCOPUS, and Embase databases from their inception until November 2025. RCTs assessing the effects of Pemafibrate on the selected metabolic biomarkers were included and the weighted mean differences (WMD) for each outcome were calculated using a random-effects model. A total of 14 RCTs with 4084 participants were included in the present meta-analysis. Pemafibrate significantly reduced FBG (11 studies, 3273 patients, WMD = -0.47 mmol/L, 95% CI: -0.70 to -0.24), insulin levels (7 studies, 2102 patients, WMD = -30.72 pmol/L, 95% CI: -42.08 to -19.36), and HOMA-IR (8 studies, 2381 patients, WMD = -1.60, 95% CI: -2.27 to -0.93). Additionally, FGF21 levels were significantly increased (7 studies, 2178 patients, WMD = 3.30 pg/mL, 95% CI: 2.57 to 4.04). The effect on HbA1c was marginally non-significant (10 studies, 3065 patients, WMD = 0.02%, 95% CI: 0.00 to 0.05). Subgroup analysis revealed that lower duration of Pemafibrate intake were associated with significant improvements in FBG, while higher doses (> 0.2mg/day) had more pronounced effects on FGF21 and glucoe metabolism. Meta-regression indicated that treatment duration was positively correlated with reductions in insulin levels. The overall GRADE quality assessment was rated as very good, supporting a moderate-to-high level of confidence. Pemafibrate significantly improves glucose metabolism, insulin sensitivity, and increases FGF21 levels, making it a promising therapeutic option for patients with metabolic disorders.

To assess the prevalence and risk factors of diabetic retinopathy (DR) in northern Xinjiang. A hospital-based cross-sectional study was performed on patients above 20 years old who were enrolled in chronic diabetes management in six areas of northern Xinjiang. All subjects received a standardized questionnaire interview of baseline characteristics. Fundus photographs were captured and reviewed by optometrists and ophthalmologists using DR grading software to determine the diagnosis and severity of DR according to the UK guidelines. A total of 3253 patients with diabetes were surveyed, among whom 2972 subjects with graded fundus photographs. The age-standardized prevalence of DR was 17.9% and vision-threatening diabetic retinopathy (VTDR) was 8.7%. In the binary logistic regression model, younger age, male gender, longer duration of diabetes, higher fasting blood glucose, hypertension, and treatment methods (insulin use compared to diet only) were independent risk factors for DR. These risk factors were associated with VTDR except the male gender. The prevalence of DR and VTDR in diabetic patients in northern Xinjiang was 17.9% and 8.7%, respectively. The younger age, male gender, higher fasting blood glucose, hypertension, and insulin use were the main risk factors for DR.

Polycystic ovary syndrome (PCOS) is characterized by insulin resistance, hyperandrogenism, oxidative stress, and disrupted folliculogenesis. The present study aimed to investigate whether combined alpha-lipoic acid (ALA) and vitamin D therapy exerts synergistic effects on metabolic, oxidative, endocrine, and histomorphological parameters in a letrozole-induced rat model of PCOS. Sixty female Wistar Albino rats were randomly divided into six groups: Control, PCOS, PCOS+Metformin (500mg/kg/day), PCOS+Vitamin D (1000 IU/kg/day), PCOS + ALA (100mg/kg/day), and PCOS + ALA+Vitamin D. PCOS was induced with letrozole (1mg/kg/day) for 21 days, followed by 30 days of treatment. Fasting blood glucose (FBG), insulin, and HOMA-IR were assessed to evaluate metabolic status. Ovarian oxidative stress markers (MDA, SOD, CAT, GSH), serum hormonal parameters (testosterone, LH, FSH, LH/FSH ratio), and detailed histomorphometric analyses were performed. Statistical analyses included one-way and two-way ANOVA. Letrozole administration induced persistent diestrus, hyperandrogenemia, increased ovarian weight, elevated HOMA-IR (6.61 ± 1.18 vs. 2.24 ± 0.42, p < 0.001), and marked oxidative stress (MDA: 5.84 ± 0.72 vs. 2.31 ± 0.34 nmol/mg, p < 0.001). ALA and vitamin D monotherapies significantly improved metabolic, oxidative, and endocrine parameters compared with untreated PCOS rats (p < 0.05). The combination therapy group demonstrated the most pronounced improvements, with HOMA-IR (2.43 ± 0.47), MDA (2.52 ± 0.39 nmol/mg), testosterone (1.29 ± 0.27 ng/mL), and LH/FSH ratio (1.03 ± 0.19) values approaching control levels (all p < 0.01 vs. PCOS). Histologically, combined treatment markedly reduced cystic follicles and restored granulosa and theca thickness. Two-way ANOVA revealed significant interaction effects for HOMA-IR, MDA, testosterone, and LH/FSH ratio (p < 0.05). Combined ALA and vitamin D therapy produced enhanced improvements in insulin resistance, oxidative stress, endocrine imbalance, and ovarian morphology in experimental PCOS. Simultaneous targeting of mitochondrial redox dysfunction and endocrine-metabolic signaling pathways may represent a promising multidimensional therapeutic approach in PCOS.

Type 2 diabetes mellitus (T2DM) is characterized by insulin resistance and chronic low-grade inflammation. Pro-inflammatory cytokines, particularly tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), contribute to impaired insulin signaling and metabolic dysfunction. Vitamin D possesses immunomodulatory properties and may influence inflammatory pathways associated with insulin resistance. This study aimed to evaluate the association between serum vitamin D levels, TNF-α and IL-6 expression, and glycemic control among insulin-resistant patients with T2DM. A hospital-based case-control study was conducted between September 2025 and February 2026 among 556 participants, including 426 insulin-resistant patients with T2DM and 130 age- and sex-matched healthy controls. Fasting blood samples were analyzed for serum vitamin D, TNF-α, IL-6, fasting blood glucose, insulin, and HbA1c. Insulin resistance was assessed using the Homeostatic Model Assessment of Insulin Resistance (HOMA-IR). Serum cytokine concentrations were measured using enzyme-linked immunosorbent assay (ELISA), while adipose tissue TNF-α and IL-6 gene expression was evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). Correlation and multivariable regression analyses were performed to examine associations between vitamin D status, inflammatory markers, insulin resistance, and glycemic indices. Serum vitamin D levels were significantly lower among T2DM patients than controls (17.9 ± 6.8 ng/mL vs. 31.4 ± 7.6 ng/mL, p < 0.001). Conversely, serum TNF-α (18.4 ± 5.2 pg/mL vs. 9.8 ± 3.1 pg/mL, p < 0.001) and IL-6 (12.6 ± 4.7 pg/mL vs. 5.3 ± 2.0 pg/mL, p < 0.001) were significantly elevated in T2DM patients. Adipose tissue analysis demonstrated a 2.8-fold increase in TNF-α expression and a 3.2-fold increase in IL-6 expression among cases compared with controls (p < 0.001). Vitamin D levels were inversely correlated with TNF-α (r = - 0.42), IL-6 (r = - 0.38), HbA1c (r = - 0.35), and HOMA-IR (r = - 0.39) (all p < 0.001). Multivariable regression analysis demonstrated that vitamin D remained an independent negative predictor of TNF-α and IL-6 expression after adjustment for potential confounding variables. Vitamin D deficiency was significantly associated with increased TNF-α and IL-6 expression, greater insulin resistance, and poorer glycemic control among patients with T2DM. These findings support a potential role of vitamin D in metabolic inflammation; however, prospective studies and randomized controlled trials are needed to determine whether improving vitamin D status can favorably influence inflammatory and metabolic outcomes in T2DM.

Lactobacillus casei Zhang modulates hippocampal metabolism and cognition in T2DM rats: A microbiota-gut-brain axis study.

3013-LB: Metabolomic and Proteomic Signatures of Difficult-to-Control Type 2 Diabetes in East Asians with Type 2 Diabetes

BackgroundOptimizing insulin dosing and predicting future glucose levels for people with type 1 diabetes is challenging due to the dynamic nature of glucose metabolism. Traditional static insulin regimens fail to adapt to individual variability in diet, physical activity, stress, and metabolic fluctuations, leading to suboptimal glycemic control. Reinforcement learning (RL) offers a promising alternative by enabling personalized, real-time insulin adjustments that improve the balance between hyperglycemia and hypoglycemia.ObjectiveThis study aims to develop a deep Q-network (DQN)–based RL system that dynamically personalizes insulin dosing recommendations using continuous glucose monitoring data, meal intake, and physical activity levels. By leveraging real-time data, the model adapts to patients’ evolving physiological states, enhancing glucose control and patient safety.MethodsWe used the OhioT1DM dataset (2018 and 2020), which includes 8 weeks of continuous glucose measurements, insulin dosing records, and physical activity data for twelve people with type 1 diabetes. The RL agent was designed with a state representation consisting of recent blood glucose levels, insulin doses, and lifestyle factors over a 2-hour window. The 2-hour window was selected based on the known pharmacodynamic profile of rapid-acting insulin (peak action within 90‐120 min), as well as the typical lag in glycemic response following meals or exercise. This window size captures both recent and delayed physiological effects while balancing data density and model stability. The action space included discrete insulin dose recommendations (eg, 0.5 U, 1 U, and 1.5 U). A reward function incentivized glucose levels within the target range (70‐180 mg/dL) while penalizing extreme deviations. The DQN model was trained to maximize reward by learning optimal dosing strategies through iterative trial and error.ResultsPerformance evaluation was conducted using both qualitative and quantitative metrics. Time-series analysis compared actual and predicted glucose levels, demonstrating effective glucose regulation. The RL model achieved a mean glucose level of 80.06 mg/dL, with a reward score of 10 during evaluation, indicating that most glucose predictions were maintained within the desired clinical range. This suggests the model has learned to regulate blood glucose effectively through adaptive insulin dosing. The root mean square error (12.39 mg/dL) was slightly higher than the mean absolute error (9.85 mg/dL), indicating stable predictions. Additionally, the percentage time in target range was 64.06%, suggesting that the model-maintained glucose within the clinically safe range for a majority of the time.ConclusionsThe DQN-based RL model demonstrated its effectiveness in personalized insulin dosing while minimizing the risk of hypo- and hyperglycemia. This suggests the model has learned to regulate blood glucose effectively through adaptive insulin dosing. This approach represents a significant advancement over conventional methods, offering a scalable and adaptive strategy for real-world diabetes management, along with enhancing clinical trust and transparency through explainability techniques.

Effects of vatinoxan in horses sedated with detomidine and butorphanol for gastroscopy: A randomized clinical study.

This study examined the effects of coffee berry pulp (CBP) extract on hepatic lipid accumulation and blood lipid levels in mice fed on a high-fat, high-fructose (HFHF) diet. Male C57BL/6J mice were divided into the following four groups and fed their respective diets for 15 weeks: normal diet, HFHF diet, and HFHF diet supplemented with 100 or 200 mg/kg body weight CBP extract. CBP inhibited weight gain and normalized blood glucose and insulin levels. CBP supplementation also inhibited lipid and lipoprotein accumulation in the liver, thereby effectively regulating triglyceride (TG) levels in both the blood and liver. Analysis of liver lipid metabolism revealed that CBP suppressed the increased messenger RNA (mRNA) expression of sterol regulatory element-binding protein-1C induced by HFHF and downregulated both mRNA and protein levels of peroxisome proliferator-activated receptor-γ. Liver X receptor regulation occurred at the mRNA level, and the adenosine monophosphate-activated protein kinase (AMPK)/phosphorylated AMPK ratio was modulated at the protein level. Among the lipid catabolic enzymes, adipose TG lipase expression was specifically modulated by CBP treatment. These findings suggest that CBP supplementation modulates key hepatic lipid regulators and reduces blood and liver TG accumulation. Although CBP shows promise in regulating TG synthesis and storage in a mouse model, further studies, including clinical validation, are required to confirm its potential as a treatment for human non-alcoholic fatty liver disease.

Chronic hyperglycaemia accompanied by impaired pancreatic β-cell function defines Type 2 diabetes mellitus(T2DM), a disorder linked to progressive complications. This study identified flavonoids, phenols and prenol lipids as the major bioactive constituents of Cynanchum auriculatum Royle ex Wight ethanol extract (CRE) and investigated its therapeutic potential on the gut microbiota(GM) in T2DM mice. After a four-week intervention, CRE markedly ameliorated glycemic control, liver function and insulin resistance. It effectively improved key indicators, encompassing body weight, fasting blood glucose, insulin resistance and hepatic function, with CRE-H showing superior efficacy. Critically, CRE restored gut microbial balance. CRE-H increased beneficial Faecalibaculum while suppressing pathogenic Angelakisella, thereby mitigating hepatic inflammation. Predictive analysis further identified genera like Eubacterium, Faecalibaculum and Mailhella as being strongly linked to hypoglycaemic effects, indicating their potential function as intestinal biomarkers. In conclusion, the amelioration of hyperglycaemia in T2DM by CRE is crucially mediated through its positive modulation of the GM.

Cold-induced thermogenesis (CIT) mediated by brown adipose tissue (BAT) and skeletal muscle holds therapeutic utility for obesity, but relative tissue contribution to CIT-driven metabolic flexibility (MetF) and its correlation to insulin resistance remain undefined across diverse ethnicities. This study aimed to investigate ethnic differences in cold-induced MetF and its link to insulin sensitivity in Chinese and Asian Indian individuals with overweight. Forty-one participants with pre-metabolic or metabolic syndrome of two ethnic groups (31 Chinese, 10 Indian), with an average body mass index (BMI) of 27.5 kg/m2 underwent whole-body calorimetry following 1-h cold exposure (~14.5 °C) and oral glucose tolerance test (OGTT) in a crossover design. Resting metabolic rate (RMR), respiratory exchange ratio (RER), carbohydrate oxidation (COX), and fat oxidation (FOX) were assessed. Blood glucose and insulin were measured to assess insulin sensitivity. Asian Indians had significantly higher fasting insulin levels and lower insulin sensitivity than Chinese participants. Chinese participants had greater increase in energy expenditure and a more pronounced fuel switch (RER, COX and FOX) with cold. For Chinese individuals, better cold-induced MetF was independently associated with lower fasting insulin and insulin resistance, even after adjusting for age, sex, and body fat. This association was not observed in Asian Indians. Significant ethnic differences exist in the association of CIT-driven MetF to insulin resistance. Chinese individuals exhibited robust MetF-insulin sensitivity correlation, whereas Asian Indians showed a blunted response without such independent association. This suggests that ethnicity-specific strategies targeting MetF are crucial for addressing metabolic health disparities.

Temporal variation in incretin and insulin secretion in ponies in association with dietary macronutrients.

USP47 alleviates metabolic-associated fatty liver disease by activating the PPARα signaling pathway through the stabilization of SIRT1.