Search Results (2,172)

Type 2 diabetes (T2D) is often accompanied by chronic low-grade inflammation, with altered cytokine balance. Although cytokine profiles have often been compared between patients with T2D and healthy individuals, less is known about how they differ among patients with varying disease duration. The aim of this exploratory study was to compare selected pro-inflammatory and anti-inflammatory cytokines in patients with shorter and longer duration of clinically diagnosed T2D. Anonymized surplus serum samples from 18 patients with T2D were analyzed. Patients were divided into two groups according to disease duration: 1–7 years and 8–16 years post-T2D diagnosis. Serum concentrations of six pro-inflammatory cytokines (IL-1β, IL-5, IL-6, IL-8, TNF-α and IFN-γ), three cytokines with anti-inflammatory or immunoregulatory functions (IL-2, IL-4, IL-10), and pro- and anti-inflammatory ratios were measured. All tests were performed using MAGLUMI X8 (Snibe Diagnostics, Shenzhen, China) high-sensitivity chemiluminescent immunoassay according to the manufacturer’s guidelines. Statistical analysis of the data obtained was performed using GraphPad Prism (Boston, MA, USA). The longer-duration T2D group showed higher median concentrations of several pro-inflammatory cytokines, particularly IL-6, IL-8, TNF-α, and IFN-γ, compared with the shorter-duration group. Several values in the longer-duration group exceeded the assay-specific reference intervals provided by the diagnostic platform. Anti-inflammatory and immunoregulatory cytokines showed less consistent differences between groups. Correlation analysis indicated stronger correlations among pro-inflammatory cytokines than among anti-inflammatory or immunoregulatory cytokines. This cross-sectional study suggests that cytokine profiles may differ between patients with shorter and longer durations of T2D, with a pattern consistent with a more pro-inflammatory profile in the longer-duration group. Because of the small sample size, absence of healthy controls, and limited availability of clinical covariates, these findings should be interpreted as descriptive rather than confirmatory and require validation in larger, longitudinal studies with detailed metabolic characterization. Full article

Background/Objectives: Type 2 diabetes (T2D) remission can be defined as a return to a HbA1c < 6.5% (<48 mmol/mol) sustained without ongoing treatment for at least 3 months. Prevalence estimates and factors associated remain unknown for LMIC and resource-limited settings. Methods: We conducted a retrospective observational analysis of electronic medical records from 8463 adults who received multidisciplinary care at Mexico’s primary care specialized units (UNEMES-EC) between 2015 and 2019 and who were referred for inadequate metabolic control. Remission was defined per 2021 ADA criteria as HbA1c <6.5% sustained for ≥3 months without glucose-lowering medications. After estimating the prevalence of T2D remission, logistic regression models were used to evaluate its sociodemographic and clinical predictors, with particular attention to weight change and baseline adiposity interactions. Results: RT2D prevalence was 0.87% (95% CI: 0.68–1.10) over a median 393-day follow-up. Weight loss ≥10% (adjusted OR 2.75; 95% CI: 1.21-6.27) and systolic blood pressure (tertile 3 vs tertile 1: OR 2.49; 95% CI: 1.17–5.26) were positively associated with RT2D, while elevated baseline HbA1c (tertile 3 vs. tertile 1: OR 0.09; 95% CI: 0.02–0.33), triglyceride levels (tertile 3 vs. tertile 1: OR 0.49; 95% CI: 0.24–0.98) and intensive pharmacotherapy were inversely associated with RT2D. No associations with HDL and total cholesterol were found. Age, sex, educational attainment, and income demonstrated no independent associations with remission. Among lifestyle-treated patients achieving ≥5% weight loss, remission prevalence reached approximately 11%. No significant interaction between baseline BMI and weight change was detected (p = 0.60). Conclusions: This first large-scale Mexican study establishes RT2D as an achievable endpoint in patients with poor baseline metabolic control. The findings suggest that remission could be achieved with equity-focused, weight-centered interventions even in resource-constrained health systems and populations. Full article

The global prevalence of type 2 diabetes mellitus (T2DM) has increased more than twofold over the last thirty years. T2DM is associated with multiple complications, among which diabetic encephalopathy and accompanying cognitive impairment have drawn considerable interest. This systematic review synthesizes findings from advanced diffusion magnetic resonance imaging (dMRI) studies (published from 2009 to 2025) on T2DM-related brain microstructural abnormalities. The most common technique, diffusion tensor imaging (DTI), consistently reveals reduced white-matter integrity (lower fractional anisotropy, higher diffusivity) associated with cognitive impairment. DTI-based network analysis further identifies disrupted structural network topology, characterized by reduced global and nodal efficiency. To overcome DTI’s limitations, newer techniques provide more specific insights: diffusion kurtosis imaging shows reduced tissue complexity in white matter, gray matter, and crossing-fiber regions via non-Gaussian modeling; neurite orientation dispersion and density imaging quantifies decreased neurite density; intravoxel incoherent motion assesses combined microstructural and microvascular alterations; diffusion spectrum imaging maps complex fiber architecture. These dMRI metrics may provide promising imaging markers for characterizing T2DM-related brain microstructural alterations. However, most available evidence remains cross-sectional, and further longitudinal, multicenter validation is required before these measures can be considered clinically validated biomarkers for prediction, diagnosis, or monitoring. Full article

People living with HIV (PLWHIV) have an increased risk of developing metabolic disorders, including type 2 diabetes (T2D), partly driven by chronic low-grade inflammation and immune dysregulation. This study evaluated the potential role of circulating miR-23a-3p as a possible early biomarker of prediabetes (preT2D) in PLWHIV. In this cross-sectional study, 80 adults were divided into five groups (n = 16 each): normoglycemic PLWHIV, PLWHIV with preT2D, PLWHIV with T2D, HIV-negative individuals with T2D, and controls. Clinical, anthropometric, biochemical, inflammatory, and insulin resistance (IR) markers were assessed, while plasma miR-23a-3p was quantified by digital PCR (dPCR). Bioinformatic network analysis was performed to identify potential molecular targets. PLWHIV with T2D showed the most unfavorable metabolic and inflammatory profile, including higher HbA1c, triglycerides, IL-6, TNF-α, hs-CRP, and GDF-15. In contrast, PLWHIV with preT2D exhibited significant overexpression of miR-23a-3p, whereas lower levels were observed in normoglycemic PLWHIV. miR-23a-3p correlated positively with IL-6 and GDF-15. ROC analyses showed good discriminative performance of miR-23a-3p for preT2D in PLWHIV (AUC = 0.80), and logistic regression confirmed its association with preT2D. In silico network analysis suggested potential inflammatory and metabolic targets of miR-23a-3p; however, these findings require experimental validation. These findings suggest that miR-23a-3p may represent a potential early biomarker of preT2D and immunometabolic dysfunction in PLWHIV. Full article

Background/Objectives: This study aims to systematically deconstruct the shared genetic architecture underlying the comorbidity of hypertension (HTN) and type 2 diabetes (T2D) and evaluate how these divergent genetic architectures are associated with differential cardiovascular risk in East Asian population. Methods: This two-stage study first leveraged the largest genetic dataset from >300,000 East Asian individuals to identify pleiotropic loci between hypertension and type 2 diabetes using conjunctional false discovery rates, classifying them into coupling and uncoupling types based on effect directions. Corresponding polygenic risk scores (PRSs) were then constructed and validated in an independent family-based cohort. A logistic regression model was used to examine the associations between different genetic architectures and cardiovascular risk, including comorbidity onset and cardiovascular outcomes. Results: A total of 463 pleiotropic loci were identified, including 439 coupling loci and 24 uncoupling loci. The coupling PRS showed a significant association with single T2D (OR = 1.53; 95% CI: 1.08–2.18; p = 0.017), whereas the other associations were not significant, although the effect estimates were directionally consistent with our hypothesis. Crucially, coupling and uncoupling PRSs showed divergent cardiovascular risk profiles and exhibited distinct gene–environment interactions. Conclusions: Our findings suggest that coupling and uncoupling pleiotropy between hypertension and type 2 diabetes may contribute to the heterogeneity of cardiovascular risk in East Asians. Deconstructing genetic pleiotropy offers a potential framework for precision prevention strategies, although these findings are exploratory and warrant further validation in larger cohorts. Full article

Metformin, widely prescribed for type 2 diabetes mellitus (T2D), has emerged as a systemic immunomodulator with effects that extend far beyond glycemic control. Recent advances in immunometabolism reveal that metformin modulates innate immune responses through coordinated cellular metabolic reprogramming and epigenetic modification, which collectively modulate the functional phenotype of innate immune cells. This narrative review summarizes current evidence regarding the immunomodulatory effects of metformin on the innate immune system, with a focus on immunometabolism and epigenetic regulation. It explores how metformin modulates innate immunity by altering cellular energy sensing, mitochondrial function, and nutrient utilization. Such metabolic changes and alterations further reshape chromatin structure and architecture, as well as transcriptional profiles and programs. Through the regulation of glycolysis, fatty acid oxidation, and histone modification landscapes, metformin regulates the phenotypes of innate immune cells, which can be pro-inflammatory, tolerogenic, or homeostatic. This conceptual framework presents a new understanding of metformin. As well as acting as an anti-inflammatory agent, it may regulate immune memory. Full article

Type 2 diabetes (T2D) is a prevalent disease worldwide that increases the risk of cardiovascular (CV) complications, disability and mortality. While excessive alcohol consumption is harmful, the effects of moderate wine consumption remain debated. This review evaluates whether moderate wine intake affects the risk of developing T2D and its impact on subjects with T2D. Twenty-eight studies were analysed. Evidence suggests an association between moderate wine consumption and the risk of developing T2D, with a J-shaped relationship, and reduced risk observed at low levels. This effect appears more pronounced with red wine, likely related to its higher polyphenol content, and when consumed with meals. On the other side, in patients with T2D, moderate wine consumption has been associated with a reduced risk of CV complications, nephropathy and mortality. It has also been linked to improved lipid profiles and reduced inflammatory markers, without adversely affecting body weight or glycaemic control in well-managed patients. These effects may be enhanced within a Mediterranean dietary pattern, suggesting synergistic actions. However, alcohol intake may increase the risk of hypoglycemia, particularly in patients receiving glucose-lowering therapies. It should be avoided by vulnerable individuals, and those with comorbidities such as MASLD and other significant liver diseases, peripheral neuropathy or other severe conditions. In conclusion, moderate wine consumption may be associated with a reduction in the risk of developing T2D and with several CV benefits in patients with T2D. Vulnerable patients should abstain and individuals who currently do not drink alcohol should not start drinking. If wine is consumed, intake should always remain moderate (as low as possible), within healthy meals and only after individual clinical assessment. Full article

Background: Type 2 diabetes mellitus (T2DM) is a global health challenge characterized by chronic hyperglycemia and oxidative stress. Pithecellobium dulce root has long been recognized for its antidiabetic potential; however, its specific bioactive constituents and mechanisms of action remain poorly defined. This study aimed to evaluate the antidiabetic and antioxidant properties of extracts and isolated molecules from P. dulce root bark. Methods: The DCM/MeOH crude extract of P. dulce root bark was fractionated with n-hexane (PDEH) and ethyl acetate (PDAE), followed by chromatographic purification and spectroscopic characterization, yielding seventeen compounds (1–17). The antioxidant activity (DPPH, ABTS, FRAP) and antidiabetic potential of PDEH, PDAE, and 1–17 were assessed in vitro using yeast-derived enzymes and in silico (targeting human α-glucosidase [PDB: 2QLY] and human α-amylase [PDB: 4GQR]). The in vitro α-glucosidase experiments used saccharomyces cerevisiae enzyme, which varies from the human target. Therefore, these results should be taken as preliminary screening data that needs confirmation with human enzymes. Results: Compound 1 was identified as new, while 2 was isolated for the first time from a natural source. The cell-free chemical tests DPPH, ABTS, and FRAP measured antioxidant capability. These tests quantify radical-scavenging and electron-transfer capabilities in vitro and are preliminary chemical screening methods. They do not directly represent biological antioxidant activity in cells or organisms. PDEH demonstrated strong radical scavenging against DPPH (IC₅₀ = 15.30 μg/mL) and ABTS (IC₅₀ = 12.80 μg/mL), while pristriol (16) showed ferric reducing power (EC₅₀ = 4200 μM FeSO₄/g). Enzyme inhibition assays demonstrated activity against α-amylase (IC₅₀ 53.88–112.24 µg/mL; acarbose IC₅₀ = 91.20 µg/mL) and α-glucosidase (IC₅₀ 18.38–136.88 µg/mL; acarbose IC₅₀ = 11.31 µg/mL). Compounds 15, 1, and 2 showed superior activity compared to acarbose for α-amylase, with effect sizes (Cohen’s d) of 2.15, 0.94, and 0.82, respectively, and IC₅₀ values of 53.88, 88.15, and 92.62 µg/mL; for α-glucosidase, IC₅₀ values were 18.38, 39.25, and 36.40 µg/mL, respectively. Docking studies supported these findings, revealing binding energies of −9.08, −8.34, and −7.22 kcal/mol for compounds 1, 2, and 15 with α-amylase, and −10.35 and −9.79 kcal/mol for compounds 1 and 2 with α-glucosidase. ADME profiling further identified 1 and 2 as promising lead candidates for dual-enzyme inhibition. Conclusions: P. dulce root bark represents a potent source of bioactive molecules with both antioxidant and dual-enzyme-inhibitory properties. These findings validate its traditional use and highlight its potential in the development of multitarget therapies for T2DM management. Full article

Dipeptidyl peptidase-4 (DPP-4) is a key therapeutic target for type 2 diabetes (T2D). Several synthetic anti-DPP-4 drugs are currently available for the treatment of T2D; however, the need for safe and effective therapies remains unmet due to the side effects associated with existing DPP-4 inhibitors. This study aimed to integrate structure-based and machine learning (ML)-based virtual high-throughput screening to identify natural DPP-4 inhibitors. Random forest, logistic regression, support vector machine (SVM), and multilayer perceptron (MLP) models were trained on DPP-4 IC₅₀ datasets. Among these, the SVM and MLP models achieved high predictive performance, with areas under the curve of 0.928 and 0.923, respectively. Screening of a natural compound database identified 107 compounds for further analysis. Subsequent structure-based screening, using sitagliptin as a positive control, identified sennidin B and doxorubicin hydrochloride as promising candidates with strong binding affinity for DPP-4. Molecular dynamics simulations (200 ns) and MM-PBSA calculations confirmed stable interactions with DPP-4. Further, sennidin B and doxorubicin hydrochloride inhibited DPP-4 activity in a concentration-dependent manner, with estimated IC₅₀ values of 39.39 and 19.78 μM, respectively. Sennidin B also reduced DPP-4 mRNA and protein expression levels in Caco-2 cells. Overall, sennidin B shows promise as a natural DPP-4 inhibitor and warrants further investigation as a potential antidiabetic agent. Full article

Background/Objectives: Diabetic retinopathy (DR) is a major microvascular complication of type 2 diabetes (T2D) and a leading cause of visual impairment. The relationships among Mediterranean diet adherence, dietary components, DR, and vision-related quality of life remain incompletely defined. This cross-sectional study evaluated Mediterranean Diet Score (MDS) as the primary dietary endpoint, individual MDS components as secondary endpoints, and micronutrient intakes as exploratory endpoints. Methods: In this single-centre study, 129 subjects with long-standing T2D were classified as no DR (NDR; n = 85), non-proliferative DR (NPDR; n = 36), or proliferative DR (PDR; n = 8). Dietary intake was assessed using a food frequency questionnaire and vision-related quality of life using the NEI-VFQ-25. Results: Subjects with DR had longer diabetes duration than those without DR (18 vs. 16 years, p < 0.01). Overall MDS did not differ by DR status, indicating a null finding for the primary dietary endpoint. In secondary analyses, lower legume consumption was observed among participants with DR and was associated with higher odds of DR in multivariable models. Participants with PDR showed poorer vision-related quality of life, although this finding was limited by the small PDR subgroup and high NEI-VFQ-25 scores in other groups. Exploratory analyses suggested associations between selected micronutrient intakes and NEI-VFQ-25 domains. Conclusions: Overall Mediterranean diet adherence was not associated with DR status. Secondary and exploratory findings should be considered hypothesis-generating and require confirmation in prospective studies. Full article

Background: Vitamin D (25(OH)D) deficiency affects over one billion people globally and is associated with type 2 diabetes (T2D) and cardiometabolic diseases. However, causal relationships remain unclear, as vitamin D supplementation has shown limited benefit in reducing the risk of T2D. Genetic studies have identified variants that influence circulating 25(OH)D levels, but whether genetically determined vitamin D status predicts cardiometabolic outcomes remains uncertain. Methods and Results: Using multi-ethnic populations from the UK Biobank (471,861) and the Asian Indian Diabetic Heart Study (3486), we performed genome-wide univariate and polygenic risk score (PRS)-based bidirectional MR analyses to determine the causal association between vitamin D and T2D. A polygenic score of vitamin D–raising alleles did not affect the risk of T2D or cardiovascular disease. In contrast, a higher T2D PRS was strongly associated with an increased risk for 25(OH)D deficiency. Genetically instrumented per SD increase in T2D PRS was predicted to significantly (p = 9.5 × 10⁻³¹) reduce circulating 25(OH)D (β = −9.1 nmol/L; 95% CI: −8.9 to −9.3). The ancestry-specific univariate MR and sensitivity analyses confirmed that vitamin D levels reduced significantly with increasing T2D risk across all ancestries. Conclusions: Our findings suggest low circulating vitamin D levels are unlikely to causally predict T2D risk but may serve as a marker for secondary prevention in endocrine and cardiovascular health. Instead, genetic susceptibility to T2D appears to contribute to vitamin D insufficiency, which may lead to cardiovascular complications. Further studies are needed to clarify the mechanisms underlying vitamin D deficiency in diabetes. Full article

Type 2 diabetes mellitus (T2D) is associated with dyslipidemia, characterized by elevated plasmatic triglycerides and free fatty acids, particularly palmitate (PA), which may cause lipotoxicity in skeletal muscle cells. This leads to inflammation, activation of the unfolded protein response (UPR), insulin resistance, and cell death. Herbal medicines such as Uncaria tomentosa (UT) have shown potential as complementary treatments for T2D due to their protective effects. Purpose and study design: This study investigates the effect of UT aqueous extract on UPR and insulin resistance induced by PA in C2C12 myotubes. C2C12 myoblasts were grown in DMEM medium supplemented with 10% fetal bovine serum and differentiated into myotubes with 3.5% horse serum. The myotubes were incubated with 100 or 500 μM PA, 2–100 µM thapsigargin (Tg) or tunicamycin (Tn), in the presence or absence of 250 μg/mL UT extract or 100 µM TUDCA, for 2 or 6 h. The myotubes treated with UT extract for 6 h, after the incubation with 20 µM Tg, Tn or 500 µM PA, presented reduction in the expression of UPR-related genes ATF4 and CHOP by approximately 1.5-fold, and increased by 3-fold the expression of IRS-1, an insulin-signaling protein, when compared to myotubes incubated with only 20 µM Tg, Tn or 500 µM PA. These findings suggest that UT extract may serve as a modulator against skeletal muscle dyslipidemia by downregulating ATF4 and CHOP, reducing cell stress and death, while enhancing IRS-1 expression, which supports the use of the UT extract in managing insulin resistance and T2D. Full article

This paper analyzes the role of cereal products in the diet of individuals with disorders of carbohydrate metabolism, with particular emphasis on their impact on postprandial glycemia and the risk of developing type 2 diabetes (T2D). Cereal products, as the main source of dietary carbohydrates, also provide dietary fiber, minerals, B vitamins, and key bioactive compounds such as β-glucans, arabinoxylans, resistant starch (RS), and polyphenols. These components may reduce the rate of starch digestion and glucose absorption in the small intestine by increasing the viscosity of intestinal contents or by directly inhibiting digestive enzymes such as α-glucosidase. It has been shown that fermentation of these compounds by the gut microbiota leads to the production of short-chain fatty acids (SCFAs), which improve insulin sensitivity and stimulate the secretion of incretin hormones such as GLP-1. A literature review confirms that regular consumption of whole-grain products is associated with a reduced risk of T2D, whereas refining processes and excessive grain fragmentation lead to an increased glycemic index of products. Based on clinical guidelines and a narrative synthesis of the available literature, minimally processed whole-grain products were identified as a fundamental component of dietary therapy for diabetes, which is illustrated by the cereal product pyramid presented in the paper. This review involved a comprehensive literature search in PubMed, Scopus, and Web of Science using relevant keywords. Peer-reviewed articles, reviews, and meta-analyses (mainly 2000–2025) were included based on their relevance. Full article

Background/Objectives: Nocturnal glycemic variability in pediatric type 1 diabetes (T1D) disrupts caregiver sleep and quality of life; advanced hybrid closed-loop (AHCL) systems may be associated with reduced caregiver burden by providing more stable overnight glucose control. We aimed to evaluate changes in caregiver-reported sleep quality and continuous glucose monitoring (CGM) targets three months after transition to an AHCL system. Methods: We conducted a prospective single-center real-world study in a tertiary pediatric diabetes unit that included children aged 6–17 years with T1D who switched from continuous subcutaneous insulin infusion (MiniMed) and intermittently scanned CGM (FreeStyle Libre 2) to an AHCL system (MiniMed 780G) with Guardian 4 sensor. Caregivers completed the Pittsburgh Sleep Quality Index (PSQI) at baseline and after 3 months; CGM metrics (TIR 70–180 mg/dL, TAR1 180–250 mg/dL, TAR2 > 250 mg/dL, TBR1 54–70 mg/dL, TBR2 < 54 mg/dL) were extracted at the same time points. Analyses used Shapiro–Wilk, Wilcoxon signed-rank, Spearman correlations, and McNemar tests (α = 0.05). Results: Twenty-two caregivers completed baseline PSQI; 16 provided PSQI data at three months. The proportion with PSQI > 5 decreased from 56.3% to 18.8% (p = 0.034), and 81.3% showed lower global PSQI at 3 months (p = 0.018). The largest mean improvements were observed in daytime dysfunction (−0.94), subjective sleep quality (−0.81), and sleep duration (−0.63), with slight increases in sleep disturbance (+0.13) and sleep-medication use (+0.13). The proportion of participants meeting international CGM consensus targets improved: the percentage achieving TIR > 70% increased from 26.7% to 80.0% (p = 0.008); those meeting TAR > 180 mg/dL < 30% increased from 26.7% to 80.0% (p = 0.008); and those meeting TAR2 > 250 mg/dL < 5% increased from 20.0% to 53.3% (p = 0.008). Hypoglycemia-related targets showed no significant change, and no episodes of symptomatic or level 3 hypoglycemia were reported. Exploratory analyses suggested that poorer PSQI at 3 months was associated with greater Δ TBR1, and increases in TAR2 with higher sleep disturbance and sleep-medication use. Conclusions: Transition to an AHCL system was associated with improvements in caregiver-reported sleep and attainment of CGM consensus targets within three months. Residual nocturnal hyperglycemia was associated with features of ongoing sleep disturbance, highlighting the potential relevance of individualized alert settings, sleep-focused education, and inclusion of objective sleep measures in future studies. Full article

Background/Objectives: Type 2 diabetes (T2D)-associated sarcopenia is characterized by impaired insulin signaling, lipotoxicity, oxidative stress, and progressive muscle loss. Although liraglutide improves glucose control and reduces lipid burden, its ability to preserve muscle integrity under diabetic lipotoxic conditions remains limited. This study investigated whether β-hydroxy-β-methylbutyrate (HMB) could enhance liraglutide-mediated protection against high-glucose plus free fatty acid (HG+FFA)-induced injury in skeletal muscle cells. Methods: Differentiated C2C12 myotubes were exposed to HG+FFA to establish a sublethal lipotoxic model and treated with liraglutide, HMB, or their combination. Cell viability, lipid accumulation, myotube morphology, insulin signaling, glucose uptake, mitochondrial function, reactive oxygen species (ROS), antioxidant gene expression, and atrophy-related signaling were assessed. Results: HG+FFA induced marked lipid droplet accumulation, impaired insulin signaling, reduced glucose uptake, disrupted mitochondrial membrane potential, increased ROS production, suppressed antioxidant gene expression, and promoted an atrophic phenotype characterized by increased atrogin-1 and MuRF1 and reduced myogenic markers. Liraglutide alone reduced large lipid droplets and partially improved insulin signaling but showed limited efficacy in preserving the myotube phenotype. HMB alone exerted modest effects on lipid accumulation but preserved myotube area. Notably, combined HMB and liraglutide treatment more effectively reduced lipid burden, restored insulin signaling and glucose uptake, attenuated mitochondrial dysfunction and oxidative stress, restored antioxidant gene expression, and preserved MyHC-positive area and myotube diameter while suppressing atrogin-1/MuRF1 activation. These protective effects were largely attenuated by rapamycin, indicating at least partial dependence on mTOR-associated signaling. Conclusions: Overall, HMB and liraglutide exert complementary protective effects against diabetic lipotoxic and atrophic stress, supporting the potential utility of this combination strategy for T2D-associated sarcopenia. Full article