Search Results (1,053)

The growing demand for aquaculture has driven the search for sustainable practices and utilization of agro-industrial residues. Brown rice bran, an abundant and low-cost by-product, has emerged as a promising raw material. This dissertation aimed to evaluate solid-state fermentation (SSF) of rice bran using the fungus Rhizopus oryzae and the yeast Saccharomyces cerevisiae with the goal of improving its nutritional value for use in diets formulated for zebrafish (Danio rerio). Proximate composition analyses revealed the strong biotransformation potential of Rhizopus oryzae. Fermentation with this fungus resulted in a significant 36.45% increase in protein content, a 51.62% increase in total polyphenols, and a 13.7% reduction in lipid content. In an in vivo experiment, zebrafish fed a diet containing rice bran fermented by R. oryzae showed the best zootechnical performance, with higher weight gain, specific growth rate, and improved feed conversion. Gene expression analysis showed a significant difference only for glut6, which is related to glucose transport. In summary, the fermentation of brown rice bran with Rhizopus oryzae represents an effective strategy to enhance its nutritional profile, establishing it as a viable alternative for the formulation of more sustainable and efficient diets in aquaculture. Full article

Reprogramming is a hallmark of cancer, enabling tumour cells to sustain rapid proliferation, resist cell death, and adapt to hostile microenvironments. This review explores the expression profiles of key metabolic enzymes and transporters involved in glucose, amino acid, and lipid metabolism across the five most deadly cancers worldwide: lung, breast, colorectal, liver, and gastric cancers. Through a comparative analysis, we identify consistent upregulation of glycolytic enzymes such as LDHA, PKM2, and HK2, as well as nutrient transporters like GLUT1, ASCT2, and LAT1, which contribute to cancer progression, metastasis, and therapy resistance. The role of enzymes involved in glutaminolysis (e.g., GLS1, GDH), one-carbon metabolism (e.g., SHMT2, PHGDH), and fatty acid synthesis (e.g., FASN, ACLY) is also examined, with emphasis on their emerging relevance as diagnostic, prognostic, and predictive biomarkers. While several metabolic proteins show strong potential for clinical translation, only a few, such as tumour M2-pyruvate kinase (TuM2-PK) and serum LDH measurement, have progressed into clinical use or trials. This review addresses some of the challenges in biomarker development. Ultimately, our findings underscore the importance of metabolic proteins not only as functional drivers of malignancy but also as promising candidates for biomarker discovery. Advancing their clinical implementation could significantly enhance early detection, treatment stratification, and personalized oncology. Full article

Background: Small-molecule tyrosine kinase inhibitors (SMTKIs), widely used in cancer chemotherapy, have been reported to variably affect glycaemic control and metabolism, with some agents demonstrating hypoglycaemic effects while others show hyperglycaemic properties. This study aims to elucidate how small-molecule tyrosine kinase inhibitors affect glucose metabolism in C2C12 cells in vitro. Specifically, this study investigated their impact on glucose uptake, AKT expression, GLUT4 expression and translocation, and IL-6 expression. Methods: In this study, skeletal muscle (C2C12) preparations were separately treated with small-molecule tyrosine kinase inhibitors; imatinib, dasatinib, axitinib, and erlotinib for 24 h. Thereafter, the effect of the test drugs was assessed on cell viability using the MTT assay, while glucose uptake was determined by measuring residual glucose concentrations in the culture medium with a glucometer. The expression of AKT, GLUT4, and IL-6 and translocation of GLUT4 were evaluated using ELISA. Furthermore, the effect of the drugs was assessed on insulin-stimulated AKT phosphorylation and GLUT4 translocation. Imatinib, dasatinib, axitinib, and erlotinib were selected due to their effect of glucose metabolism, highlighted in the literature. Results and Discussion: C2C12 cells treated with SMTKIs were viable after 24 h. A concentration-dependent increase in glucose uptake in C2C12 cells treated with imatinib was observed as the concentration of imatinib increased. Axitinib, dasatinib, and erlotinib demonstrated glucose uptake levels comparable to the control across all concentrations. SMTKIs demonstrated an increase in GLUT4 translocation in the absence of insulin. GLUT4 expression was unchanged in cells treated with small-molecule tyrosine kinase inhibitors compared to the control. Small-molecule tyrosine kinase inhibitors showed an increase in AKT expression. C2C12 cells treated with SMTKI were observed to have elevated IL-6 expression compared to the control. Conclusions: The results show that SMTKIs, in particular dasatinib, impact glucose metabolism in C2C12 cells via their effect on GLUT4 translocation and expression and AKT expression. Dasatinib shows promising potential with regard to antidiabetic capabilities. Further research is needed to better understand SMKI effects on metabolic homeostasis, which can perhaps inform future therapeutic strategies. Full article

Background/Objectives: Bioactive peptides derived from animal venoms, toxins, and secretions demonstrate considerable pharmacological potential for use in the management of diabetes mellitus—a highly prevalent metabolic disorder of substantial global health significance. This integrative review systematically evaluated the current evidence regarding the pharmacological mechanisms underlying the antidiabetic properties of these bioactive peptides. Methods: This study was guided by the research question “What are the mechanisms of action of peptides derived from animal venoms in modulating parameters associated with diabetes?” developed using the PECo framework. A comprehensive literature search was executed across Scopus, PubMed, and Web of Science, focusing on studies from the last five years. Out of 190 identified articles, 17 satisfied the inclusion criteria. Results: Twenty-eight distinct peptides were characterized, exhibiting structural diversity with 7–115 amino acid residues and molecular weights of 900–13,000 Da. These compounds were sourced from venomous taxa including sea anemones, marine snails, spiders, centipedes, scorpions, and snakes. Their antidiabetic mechanisms encompassed glucagon-like peptide-1 (GLP-1) receptor agonism, insulin receptor activation, potassium channel inhibition, glucose transporter type 4 (GLUT4) upregulation, and α-amylase inhibition. Sequence analyses revealed substantial homology among peptides with analogous mechanisms—notably Con-Ins and ILP-Ap04, plus SpTx1 and SsTx-4—suggesting that structural determinants underlie their functional characteristics. Toxicological evaluations of nine peptides demonstrated low-toxicity profiles despite originating from toxic venom, crucial for therapeutic development. Conclusions: These peptides exhibited exceptional pharmacological potency with effective doses in nanogram-to-nanomole per kilogram ranges. Collectively, our findings underscore the therapeutic potential of venom-derived peptides as innovative candidates for use in diabetes management. Full article

Heat stress induced by high temperature and humidity in southern China during summer reduce goat production efficiency and meat quality. Taurine (TAU), one of the most abundant amino acids in animal tissues, plays a vital role in alleviating heat stress and regulating energy metabolism through its involvement in glucose uptake and glycogen turnover. This study aimed to investigate the effects of rumen-protected (RP)-TAU on the meat quality, hepatic gluconeogenesis, and muscle energy metabolism of heat-stressed goats. During summer, twenty-four male crossbred Gan-xi goats (20.45 ± 2.95 kg) aged 5 months were randomly allocated to two groups treated with or without 0.4% RP-TAU (on a diet weight basis). After feeding for 60 days, six goats per treatment were slaughtered. Compared with the control group, RP-TAU supplementation significantly improved the growth performance of goats, as evidenced by increased final body weight, average daily gain, and average daily feed intake (p < 0.05). The goats in the RP-TAU group showed a reduced splenic index (p < 0.05), lower serum cortisol levels (0.05 < p < 0.1), and decreased muscle crude fat content (p < 0.01). Crucially, meat quality was improved with reduced hardness, gumminess, and chewiness (p < 0.05), indicating better textural properties. Nutritionally, RP-TAU supplementation modulated the muscle fatty acid profile, significantly reducing the concentrations of palmitic (a saturated fatty acid), palmitoleic (a monounsaturated fatty acid), and nervonic acids (p < 0.05), while cystine content was reduced (p < 0.05). RP-TAU supplementation significantly enhanced the muscle contents of glucose and glycogen, glycolytic potential, phosphofructokinase activity, and ATP level, while decreasing the pyruvate level and AMP/ATP ratio (p < 0.05). Gene expression analysis revealed the upregulation of GLUT4 and PYGM and the downregulation of GSK3β in muscle (p < 0.05). These results indicated that dietary supplementation of RP-TAU might be beneficial to improve stress resistance and meat quality by increasing muscle energy supply and glucose uptake in Gan-xi goats. Full article

Hyperuricemia (HUA) is a metabolic disorder characterized by abnormal purine metabolism within the body. Ampelopsis japonica (Thunb.) Makino has traditionally been utilized in the treatment of various kidney diseases; however, its specific anti-hyperuricemic effects and the underlying mechanisms warrant further investigation. This study investigates the mechanism of action by which A. japonica extract (AJE) addresses HUA using a combination of pharmacology techniques, including network pharmacology and metabolomics. A HUA mouse model was established using potassium oxonate and hypoxanthine. AJE intervention significantly reduced serum uric acid and creatinine levels in HUA mice and markedly decreased glomerular atrophy and renal tubular degeneration. Metabolic profiling revealed distinct metabolic profiles between AJE-intervention and control groups, further demonstrating that AJE corrected disruptions in arginine biosynthesis, purine metabolism, pyrimidine metabolism, and arachidonic acid metabolism. The results of the network pharmacology-based study indicate that AJE can alleviate HUA by modulating the TNF pathway and the Toll-like receptor pathway. The mechanisms of action of AJE in HUA involve the inhibition of xanthine oxidase (XOD) to reduce uric acid synthesis, downregulation of URAT1 and GLUT9 to decrease uric acid reabsorption, and suppression of the TLR4/NF-κB pathway to mitigate inflammation in the HUA mouse model. Therefore, AJE demonstrates significant potential as a therapeutic intervention for HUA and its associated renal complications. Full article

Background: Hypoxia-induced glycolysis represents a hallmark of colorectal cancer (CRC) progression and contributes significantly to therapeutic resistance. Curcumol, a natural sesquiterpenoid derived from Curcumae Rhizoma, has demonstrated promising anti-tumor properties. However, its impact on metabolic reprogramming under hypoxic conditions remains largely undefined. Objective: The objective of this study was to elucidate the potential of Curcumol in inhibiting glycolytic reprogramming and impede CRC progression via regulation of the VHL/HIF-1α signaling pathway. Methods: CRC cells and orthotopic mouse models were treated with Curcumol under chemically induced hypoxic conditions. Metabolic alterations were evaluated using Seahorse extracellular flux analysis, Western blot analysis, quantitative real-time PCR (qRT-PCR), immunohistochemistry (IHC) and co-immunoprecipitation (Co-IP). Functional validation of glycolysis and epithelial–mesenchymal transition (EMT) phenotypes was conducted through in vitro and in vivo assays. Results: Curcumol inhibited HIF-1α-mediated metabolic reprogramming by upregulating VHL expression, thereby promoting HIF-1α degradation. This effect led to the downregulation of key glycolytic genes (HK2, LDHA, and GLUT1), decreased glycolytic flux, and lactate production, ultimately suppressing CRC cell proliferation and invasion. The anti-tumor efficacy of Curcumol was validated in both in vitro and in vivo models. Moreover, Curcumol effectively reversed the hypoxia-induced epithelial–mesenchymal transition (EMT) phenotype, suggesting that its metabolic regulatory effects may contribute to reduced metastatic potential. Conclusions: Curcumol suppresses glycolysis and CRC progression by activating the VHL/HIF-1α signaling axis. These findings underscore the potential of Curcumol as a natural metabolic regulator capable of reversing tumor metabolic reprogramming, offering a promising therapeutic strategy for CRC treatment. Full article

The liver and gut play a central role in modulating bile acid metabolism. Our recent study found that supplementation with sodium butyrate (NaB) from microbiota might slow diabetes progression and ameliorate liver function in diabetic mice. The role of NaB in the homeostasis of mitochondrial energy metabolism and bile acid metabolism needs to be investigated further, so this study was conducted by us. We used an ELISA kit to detect biochemical indicators related to mice; HE and PAS were used to stain and analyze tissues; CCK8 was used to detect cell viability; and WB was used to detect related indicators. We found here that NaB administration enormously reduced liver hypertrophy and steatosis in diabetic mice, improved liver and gut function and the release of inflammatory factors in diabetic mice, and ameliorated mitochondrial function both in vitro and in vivo. NaB incubation significantly increased bile acid metabolism-related receptors under diabetic conditions; the intracellular content of enzymes related to liver function was elevated within liver cells. Glucose transport proteins GLUT2 and NaB receptor GPR43 were upregulated by NaB on the cell membrane. The actuation of the intracellular signaling proteins PI3K, AKT, and GSK3 was inhibited by NaB under diabetic conditions. The present study proved that the microbiota metabolite NaB has positive effects on bile acid metabolic homeostasis by promoting mitochondrial energy metabolism in enterocytes and the liver, and the GPR43-PI3K-AKT-GSK3 signaling pathway should contribute to this effect. Full article

The impact of maternal dietary restriction and hydroxytyrosol (HT) supplementation during the last third of gestation on plasma malondialdehyde (MDA) concentration, total antioxidant capacity (ABTS assay), and peripheral blood gene expression related to antioxidant defence, immune response, and energy metabolism was evaluated in beef cows and calves. Two feeding treatments in late gestation (T100% vs. T60% of nutrient requirements) and two HT levels (Control vs. HT at 180 mg/kg of diet) were evaluated during gestation (n = 46 cows) and lactation (n = 37 cows and calves). In pregnant cows, undernutrition led to inhibition of glucose oxidation (PDK4), decreased lipid synthesis (HMGCS1 and SCD) and TLR signalling; T60% cows showed higher plasma MDA (p < 0.05) with no positive effect of HT on antioxidant capacity. Contrarily, during lactation, earlier HT supplementation upregulated antioxidant capacity and modulated antioxidant gene expression (p < 0.05). In calves, there was an increase in SOD1, CAT, and GPX1, especially in the T60%-HT group (p < 0.05). Interestingly, HT supplementation increased glucose transport (SLC2A1/GLUT1) during pregnancy and lactation (p < 0.05). However, it caused different effects on immunometabolic regulation in both dams and calves, depending on maternal diet. Overall, maternal HT supplementation under restricted nutritional conditions promoted postpartum antioxidant capacity and modulated immune and metabolic gene expression in cows and calves. Full article

Background: The dysregulation of both glucose and lipid metabolism is the main clinical features of type 2 diabetes. Qihua Tongtiao Formula (QHTTF) is our team’s current clinical empirical formula, and the related patent has been granted. It is composed of Astragalus membranaceus, Atractylodes macrocephala koidz, Aurantii Fructus Immaturus, Radix Bupleuri, Ligusticum chuanxiong hort, Angelicae sinensis radix, Raphanus sativus, and Polyporus umbellatus. It can alleviate tissue pathological damage in type 2 diabetic rats by improving glycolipid metabolism disorders. Nevertheless, the specific mechanisms of QHTTF in the treatment of type 2 diabetes remain unclear. Purpose: This research aims to explore the fundamental effect and underlying mechanism of the QHTTF formula in ZDF rats via network pharmacology, biological validation, and metabolomics technology. Methods: The chemical compounds of QHTTF were initially identified via UHPLC-MS/MS analysis. Meanwhile, drug targets, genes, related diseases, and differential metabolites of QHTTF in the treatment of T2DM were obtained through network pharmacology, molecular docking, and metabolomics. Then, we conducted animal experiments to further explore the therapeutic molecular mechanism of QHTTF in ZDF rats. Results: A total of 39 main chemical components were recognized through LC-MS/MS technology, and 22 remained after the second screening. Network pharmacology and molecular docking results revealed that 59 intersection targets were involved in the treatment of glycolipid metabolic disorders, and the PPARα, PPARγ, and TNF proteins were identified as crucial targets through PPI network analysis. Additionally, serum metabolomics analysis of ZDF rats showed that QHTTF could regulate linoleic acid metabolism, fructose and mannose metabolism, galactose metabolism, fatty acid biosynthesis, and other related signaling pathways. The results of biological experiments proved that QHTTF effectively lowered blood glucose and lipid levels, alleviated hepatic and pancreatic pathological damage, increased the expression of IRS-1 and GLUT4 in the pancreas, and improved insulin resistance, while inhibiting the inflammatory response and oxidative stress, as well as enhancing the expression of liver PPARα, PPARγ, and AMPK proteins in ZDF rats. Conclusions: In summary, QHTTF exerted a significant effect in improving glycolipid metabolism disorders of ZDF rats, which might show therapeutic effects by relieving insulin resistance, mitigating inflammation and oxidative damage, regulating related glucose, fatty acid, and amino acid metabolism, and increasing the expression of PPARα, PPARγ, and AMPK proteins by combining network analysis, metabolomics, and biological research. Full article

Rapidly proliferating tumor cells exhibit elevated demands for nutrients and energy to support their uncontrolled growth, with glucose serving as a key metabolic substrate. Glucose is transported into cells via facilitated diffusion mediated by glucose transporters (GLUTs), after which it undergoes a series of enzymatic reactions to generate energy. To accommodate their heightened metabolic needs, cancer cells frequently overexpress GLUTs, thereby enhancing glucose uptake. Notably, aerobic glycolysis—commonly referred to as the “Warburg effect”—has been identified as the predominant pathway of glucose metabolism within tumor tissues, even in the presence of adequate oxygen levels. Consequently, the conjugation of chemotherapeutic agents, including metallodrugs, to glucose-mimicking substrates holds significant potential for achieving tumor-specific intracellular drug delivery by exploiting the elevated glucose uptake characteristic of cancer cells. Moreover, in recent years, glycosylation of metal scaffolds has been extended to the development of bioactive metallodrugs for applications other than cancer treatment, such as potential tumor imaging, antiviral, antimicrobial, antiparasitic and anti-neurodegenerative agents. Accordingly, major advancements in the design of metal-based glycoconjugates for medicinal applications are here summarized and critically discussed, focusing on related results and discoveries published subsequently to our previous (2015) review article on the topic. Full article

Background: Premenopausal women typically exhibit superior glucose metabolism compared to males, but this metabolic advantage is lost after menopause. The primary cause is the sharp decline in estrogen levels post-menopause. Genistein, a natural compound predominantly derived from leguminous plants, possesses structural similarity to estrogen. This enables specific binding to estrogen receptors, allowing genistein to exert estrogen-mimicking effects under conditions of estrogen deficiency. The aim of this study was to investigate the effects and potential mechanisms of genistein on glucose metabolism in the liver and skeletal muscle of ovariectomized (OVX) mice fed a high-fat diet (HFD). Methods: Animal experiments were performed using 8-week-old mice that were OVX to construct a model of estrogen deficiency and impaired their glucose metabolism by a continuous HFD. Genistein was administered by gavage (50 mg/kg-day) for 10 weeks and 17β-estradiol was administered subcutaneously (50 μg/kg) every 4 days for 10 weeks as a positive control. Results: Genistein significantly improved glucose metabolism (including fasting glucose, postprandial glucose, serum glucose levels, and HOMA-IR index) but did not affect serum estrogen levels and uterine weights in OVX mice. Genistein promoted increased expression and translocation of glucose transporter 4 (GLUT4) in the gastrocnemius muscle, enhanced phosphorylation of the PI3K/AKT pathway, and upregulated expression of the G protein-coupled estrogen receptor (GPER). Concurrently, it stimulates hepatic glycogen accumulation and upregulates GLUT2 expression in the liver. Conclusions: GEN improves glucose metabolism in ovariectomized mice, and this improvement is primarily attributed to increased expression and membrane translocation of GLUT4 in the gastrocnemius muscle mediated by the GPER-PI3K/AKT pathway. Full article

Wheat is a crucial crop for human nutrition, and the demand for high-quality indicators within the “from farm to fork” concept is increasing. Based on this premise, this study examined how, at the farm level, the fertilization system can influence key quality indicators relevant to wheat production and final products. This research was conducted under specific conditions of the Western Plain of Romania at the Agricultural Research and Development Station (ARDS), Lovrin, during 2015–2017. Fertilization involved the autumn application of phosphorus (concentrated superphosphate; 0, 40, 80, 120, 160 kg ha⁻¹ active substance, a.s.) and potassium (potassium chloride; 0, 40, 80, 120 kg ha⁻¹ a.s.). Nitrogen (ammonium nitrate; 0, 30, 60, 90, 120 kg ha⁻¹ active substance) was applied in spring in two stages. The combination of these three fertilizers resulted in 18 fertilized variants (T2 to T19), tested alongside an unfertilized control (T1). The experimental variants were arranged in four randomized replications. Grain quality was assessed based on protein content (PRO, %), gluten (GLT, g 100 g⁻¹), gliadins (Gliad, %), glutenins (Glut, g 100 g⁻¹), high-molecular-weight glutenins (HMW, g 100 g⁻¹), low-molecular-weight glutenins (LMW, g 100 g⁻¹), and the gliadin/glutenin ratio (Gliad/Glut). Compared to the average values for each indicator across the experiment, certain variants produced values above the mean, with statistical significance. Variant T16 stood out by producing values above the mean for all indicators, with statistical confidence. Multivariate analysis showed that five indicators with very strong (PRO, GLT) and strong (HMW, Glut, LMW) influence grouped in PC1, while two indicators (Gliad, Gliad/Glut) with very strong and strong influence grouped in PC2. The analysis revealed varying levels of correlation between the applied fertilizers, with nitrogen (N) showing very strong and strong correlations with most indicators, while phosphorus and potassium showed moderate-to-weak correlations. Regression analysis generated mathematical models that statistically described how each indicator varied in relation to the fertilizers applied. Full article

Background: Post-myocardial infarction (MI) heart failure (HF) is characterized by myocardial energy metabolism disorder, with excessive glycolysis playing a key role in its progression. Silybin (SIL), a flavonoid derived from Silybum marianum, has demonstrated hepatoprotective and metabolic regulatory effects. However, the role of this flavonoid in ameliorating post-myocardial infarction heart failure (post-MI HF) by modulating energy metabolism remains unclear. Methods: This study employed an oxygen–glucose deprivation (OGD) model to induce myocardial cell injury in vitro, with YC-1 treatment used to inhibit hypoxia-inducible factor-1α (HIF-1α) for mechanistic validation. A myocardial infarction-induced HF mouse model was used for in vivo experiments. Results: In vitro, SIL enhanced cell viability, increased ATP levels, and decreased lactate production and reactive oxygen species (ROS) accumulation in OGD-treated myocardial cells. SIL downregulated the mRNA and protein expression of HIF-1α, 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3), glucose transporter 1 (GLUT1), and lactate dehydrogenase A (LDHA) while inhibiting HIF-1α nuclear translocation. Furthermore, SIL suppressed glycolytic proteins (PFKFB3, GLUT1, and LDHA) in a manner comparable to the HIF-1α inhibitor YC-1. This confirms that SIL’s inhibition of glycolysis is HIF-1α-dependent. In vivo, SIL treatment improved cardiac function parameters (LVEF and LVFS) and attenuated left ventricular remodeling (LVID;d and LVID;s) in post-MI HF mice. Additionally, myocardial fibrosis markers were significantly reduced, accompanied by a decrease in the myocardial mRNA and protein expression of glycolytic proteins, including HIF-1α, PFKFB3, GLUT1, and LDHA. Conclusions: Silybin effectively ameliorates post-myocardial infarction heart failure through the HIF-1α-mediated regulation of glycolysis, leading to improved myocardial energy metabolism and enhanced cardiac function. Full article

Objective: Insulin resistance (IR) is a complex and multifactorial disorder that contributes to type 2 diabetes and cardiovascular disease. MicroRNAs (miRNAs) play important roles in diverse developmental and disease processes. However, the molecular mechanisms of IR are unclear. This paper aims to explore the role of miRNA in regulating IR and to elucidate the mechanisms responsible for these effects. Methods: IR models were created by feeding a high-fat diet (HFD) to mice or stimulating 3T3-L1 cells with palmitate. Twelve weeks of HFD trigger weight gain, leading to lipid accumulation and insulin resistance in mice. The expression profiles of miRNAs in adipose tissues (AT) from the HFD-induced mouse models were analyzed. The relationship between miR-221-3p and SOCS1 was determined using dual luciferase reporter gene assays. Metabolic alterations in AT were investigated by real-time PCR and Western blot. Results: miR-221-3p was significantly increased in AT. HFD-induced disturbances in glucose homeostasis were aggravated by miR-221-3p upregulation. The inhibition of miR-221-3p promoted insulin sensitivity including reduced lipid accumulation and the disruption of glucose metabolism. Of note, the 3′-UTR of SOCS1 was found to be a direct target of miR-221-3p. The SOCS1 inhibitor attenuated miR-221-3p-induced increases in IRS-1 phosphorylation, AKT phosphorylation, and GLUT4. miR-221-3p was considered to be involved in the PI3K/AKT signaling pathway, thus leading to increased insulin sensitivity and decreased IR in HFD-fed mice and 3T3-L1 adipocytes. Conclusions: The miR-221-3p/SOCS1 axis in AT plays a pivotal role in the regulation of glucose metabolism, providing a novel target for treating IR and diabetes. Full article