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insulin glargine (Abasaglar / Basaglar / LY2963016)

✓ Approved

Cipla Inc · INSR · 重组蛋白

什么是 insulin glargine？

insulin glargine 是一种重组蛋白，由Cipla Inc研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)、Subcutaneous Injection。

药物档案

商品名Abasaglar, Basaglar, LY2963016
公司Cipla Inc
药物类别重组蛋白, 多肽类
分子靶点INSR
给药途径Injectable (Others), Subcutaneous Injection
状态Approved
来源： ClinicalTrials.gov, Cipla Inc

作用机制

分子靶点

insulin glargine 作用于 1 个分子靶点：

INSRinsulin receptor (CD220, HHF5)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

insulin glargine 针对 2 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Metabolism and nutrition disordersType 1 diabetes mellitus✓ Approved
Metabolism and nutrition disordersType 2 diabetes mellitus✓ Approved

相关研究文献

PubMedInternational journal of epidemiology2026-08-08

Mechanisms underlying the effect of adiposity on risk of post-menopausal oestrogen receptor-positive breast cancer: an interventional mediation analysis.

Albers Frances E M FEM, Dashti S Ghazaleh SG, Swain Christopher T V CTV, Rinaldi Sabina S et al.

Adiposity increases the risk of post-menopausal oestrogen receptor (ER)-positive breast cancer. Inflammation, insulin, and insulin-like growth factors and sex-steroid hormones may explain this effect. We performed interventional mediation analysis to estimate the effects of hypothetical interventions targeting these pathways in females with obesity on reducing their excess risk of post-menopausal ER-positive breast cancer relative to females with normal weight. The mediation analysis included 1260 post-menopausal females (352 with ER-positive breast cancer) from a case-cohort within the Melbourne Collaborative Cohort Study. A Monte Carlo g-computation approach with non-parametric bootstrapping was used to estimate the risk differences (RDs) and 95% confidence intervals (CIs) for interventional direct and indirect effects of hypothetical interventions that shift the joint distribution of inflammation, insulin, and sex-steroid hormone biomarkers in females with obesity to the levels observed in females with normal weight. The estimated RD for the total effect of obesity relative to normal weight on post-menopausal ER-positive breast cancer was 16.1 (95% CI: 3.3, 30.4) per 1000 females. The RDs for indirect effects through inflammation, insulin, and sex-steroid hormones were 16.4 (95% CI: 4.3, 27.2), -8.4 (95% CI: -23.4, 1.2), and 13.0 (95% CI: 3.3, 23.7) per 1000 females, respectively. The - RD for the direct effect not via any of these three pathways was -5.3 (95% CI: -17.4, 10.6) per 1000 females. Inflammation and sex-steroid hormones, but not insulin, contributed to the detrimental effect of adiposity on the risk of post-menopausal ER-positive breast cancer. Interventions targeting these pathways may reduce the risk for females with obesity.

PMID 42568039
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PubMedAppetite2026-08-08

An IP3R3-independent glucose-specific taste signaling pathway triggers an unconditioned cephalic insulin response in mice.

Glendinning John I JI, Ashkar Natalie N, Georgiou Kiriaki K, Guardado Ashley A et al.

The cephalic-phase insulin response (CPIR) is elicited by oral stimulation with sapid substances. It produces a rapid rise in plasma insulin that promotes glucose disposal during and after meals. Although some taste and food-related cues require conditioning to evoke a CPIR, oral stimulation with D-glucose elicits this response without prior conditioning in mice. Here, we investigated how D-glucose activates this unconditioned CPIR. First, we measured chorda tympani (CT) taste nerve responses in wild-type B6 mice and a strain lacking the type 3 inositol 1,4,5-trisphosphate receptor (IP3R3), a principal mediator of sweet-, bitter-, and umami-evoked taste signaling. Unexpectedly, the IP3R3 KO mice retained CT nerve responses to D-glucose while responses to all other sweeteners were abolished. Second, we tested whether this IP3R3-independent taste signaling pathway mediates the unconditioned CPIR by determining whether oral stimulation with D-glucose still evoked a CPIR in IP3R3 KO mice. Licking D-glucose elicited a normal CPIR, consistent with this hypothesis. Third, selective oral stimulation with D-glucose, but not fructose, triggered a CPIR in wild-type B6 mice. Finally, the unconditioned CPIR exhibited remarkable stimulus specificity in wild-type B6 mice: it was elicited by D-glucose but not by L-glucose, monosodium glutamate, soybean oil, saccharin, or isomaltulose, and was unaffected by olfactory loss. These findings provide evidence for a D-glucose-selective taste signaling pathway that initiates the unconditioned CPIR independently of canonical sweet taste transduction.

PMID 42567366
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PubMedActa physiologica (Oxford, England)2026-08-08

MicroRNA-Driven Regulation of β-Cell Function in Type 2 Diabetes: Molecular Mechanisms, Network Insights, and Translational Perspectives.

Eliasson Lena L, Karagiannopoulos Alexandros A, Nagao Mototsugu M, Wendt Anna A

MicroRNAs (miRNAs) have emerged as central regulators of pancreatic islet biology, influencing β-cell development, proliferation, and function. In type 2 diabetes (T2D), both adaptive and maladaptive miRNA responses shape β-cell compensation and progressive secretory dysfunction. Here, we review current insights into the regulation of insulin secretion, with a focus on exocytosis and the autocrine and paracrine regulation of β-cells, and discuss the involvement of miRNAs in these processes. We describe miRNA biogenesis and the regulation of miRNAs in β-cells, focusing on glucose- and cAMP-responsive miRNAs and epigenetic control. We summarize mechanistic evidence linking individual miRNAs to the regulation of β-cell function during T2D development, including effects on metabolic signaling and the exocytotic machinery, and compare results from humans, rodents, and cell lines, while emphasizing both the need for and difficulties of performing these investigations in β-cells from human donors. Moreover, recent network-level analyses reveal that T2D is characterized not by isolated miRNA changes but by coordinated changes in miRNA-mRNA regulatory pathways that converge on reduced and/or compensatory insulin secretion. Beyond cell-intrinsic actions, we discuss how circulating miRNAs transported via extracellular vesicles (EVs) mediate crosstalk between β-cells and peripheral tissues, influencing insulin resistance, β-cell function, and systemic glucose homeostasis. Finally, we highlight the potential of circulating miRNAs as diagnostic and predictive biomarkers, as well as the use of EVs and miRNAs for therapeutic applications, while underscoring the technical challenges that currently limit clinical translation. Nevertheless, advances in technical, network, and inter-organ analyses position miRNAs as promising biomarkers and therapeutic targets in T2D.

PMID 42568255
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PubMedFrontiers in endocrinology2026-08-08

Automated insulin delivery in war refugee children with type 1 diabetes: a 3-year follow-up.

Neuman Vit V, Plachy Lukas L, Pruhova Stepanka S, Kolouskova Stanislava S et al.

Following the war in Ukraine, Europe received a large influx of war refugees, including children with type 1 diabetes (CwD). The aim of this study was to describe their diabetes control during the first three years. A total of 143 (70 M, 73 F) CwD were recruited into this longitudinal observational study between March 2022 and June 2025 at 9 tertiary pediatric diabetes centers. The following data were collected yearly: treatment type, CGM use, anthropometrics, HbA1c, and CGM metrics. Statistical inference was performed using linear mixed models adjusting for age, sex, age at T1D onset, and therapy type. Additionally, the participants were compared to matched controls from a nationwide pediatric diabetes registry. The median HbA1c decreased significantly from 58.0 mmol/mol, 7.5% (IQR 49.0-73.0, 6.6-8.8%) to 52 mmol/mol, 6.9% (IQR 48-64 mmol/mol, 6.5-8.0%) over 3 years (P<0.001). We observed a significant increase in CGM use (46.4% to 95.5%) and insulin pump use, from 8.0% (no AID systems) to 63.6% (only AID systems) (both P<0.001). The trend in HbA1c decline depended on the therapy type, the estimated effect of AID initiation was -5.39 mmol/mol (95% CI -10.12 to -0.65 mmol/mol) (P = 0.003). The mean time in range (TIR) of CwD who initiated AID was not significantly different from that of matched non-migrant controls (73.4% vs. 71.0%, P = 0.420), while those using insulin pens had a lower TIR than controls (51.8% vs. 62.9%, P = 0.003). We observed a significant improvement in T1D control among refugee CwD, emphasizing the role of AID, regardless of socioeconomic background.

PMID 42568388
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PubMedFrontiers in pharmacology2026-08-08

Hepatoprotective effects of empagliflozin in metabolic dysfunction-associated steatotic liver disease: a systematic review and meta-analysis of preclinical studies.

Ali Lashin S LS, Mostafa Mohamed O MO, Alsharayiah Dana D, Elkholy Mohamed A MA et al.

The worldwide burden of metabolic dysfunction-associated steatotic liver disease (MASLD) is rising sharply, powered by high prevalence of obesity and its associated metabolic insults. Though urgent, definitive treatment is not yet available. Empagliflozin, a sodium glucose co-transporter inhibitor has been suggested in both human and animal studies to have diverse beneficial effects in MASLD by anti-inflammation and anti-oxidative stress effects, but many of the underlying mechanisms remain unexplained. The main aim of this systematic review and meta-analysis was to evaluate the effects of empagliflozin's in preclinical animal studies trying to view new horizons for future treatment of MASLD. we searched the related animal preclinical studies in databases including Scopus, Web of Science, Cochrane library, Wily online library and PubMed. The research team screened the literature and extracted data; any discrepancies were resolved by the research team leader through discussion. The quality of research methods was assessed by SYRCLE (systematic review center for laboratory animal experimentation) risk of bias tool. The meta-analysis was guided by the Cochrane Handbook; statistical analyses were conducted via RevMan 5.4 offline version and Comprehensive Met analysis V3 software. Our meta-analysis included 17 studies, involving 584 animals. In comparison with the model group, empagliflozin significantly reduced steatosis markers including hepatic burden of lipids, including triglycerides and cholesterol, NAFLD Activity Score (NAS) and total serum cholesterol (TC). It also significantly reduced hepatic fibrosis markers including fibrosis grade, transforming growth factor-β (TGF-β) and collagen type I alpha 1 chain) COL1A1). Beyond its anti-steatofibrotic effects, empagliflozin significantly downregulated hepatic expression of inflammatory and oxidative markers including tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and malondialdehyde (MDA). Moreover, empagliflozin significantly improved glycemic indices including Homeostatic Model Assessment for Insulin Resistance (HOMA-IR), serum insulin, and fasting blood sugar (FBS). Empagliflozin significantly protected the liver against steatosis and fibrosis by mitigating hepatic inflammation, oxidative stress and insulin resistance.

PMID 42568838
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PubMedFrontiers in endocrinology2026-08-08

Machine learning and bioinformatics identify and validate membrane protein biomarkers for type 2 diabetes mellitus.

Liu Tong T, Tang Zhaoyuan Z, Aierken Zulipikaer Z, Zhang Jie J et al.

Type 2 diabetes mellitus (T2DM) is among the most rapidly increasing metabolic disorders worldwide. Membrane proteins, integral components of biological membranes, are pivotal in insulin signal transduction and significantly contribute to the pathogenesis of T2DM. However, the systematic investigation of membrane proteins linked to T2DM remains insufficient. The T2DM dataset and membrane protein-related genes were sourced from the GEO database and the Uniprot website, respectively. Bioinformatics methodologies, including Gene Ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, and protein-protein interaction (PPI) network analysis, were employed to assess the differentially expressed membrane protein-related genes between the normal control group and the T2DM group. Subsequently, machine learning algorithms, including Gaussian Mixture Model (GMM), Random Forest (RF), and Support Vector Machine (SVM), were utilized to identify hub genes. Following this, a clinical diagnostic model was constructed, and the receiver operating characteristic (ROC) curve was plotted. Candidate genes were further examined in palmitic acid (PA)-induced NES2Y and HepG2 cell models and in high-fat diet/streptozotocin-induced T2DM mice. Finally, Functional effects were assessed by gene knockdown, reverse transcription quantitative PCR (RT-qPCR), western blotting (WB), immunofluorescence (IF), co-immunoprecipitation, histological examination, and lipid staining. A total of 1,856 DEGs were identified between T2DM and control samples, including 599 upregulated genes and 1,257 downregulated genes, among which 42 were membrane proteinrelated T2DM DEGs. Machine learning algorithms were then applied to pinpoint two target genes: ICAM1 and EZR, the latter of which encodes Ezrin, a membrane-cytoskeleton linker protein. The ROC curve analysis showed that the diagnostic model exhibited strong predictive capability, with an AUC value of 0.95. PA treatment increased lipid accumulation and EZR/ICAM1 mRNA and Ezrin/ICAM1 protein expression in the cell models. Ezrin co-immunoprecipitated with the insulin receptor. In PA-treated HepG2 cells, ICAM1 or EZR knockdown increased p85α and AKT phosphorylation and GLUT4 protein expression. Ezrin and ICAM1 were also elevated in the livers of T2DM mice. ICAM1 and EZR may serve as potential diagnostic biomarkers and candidate therapeutic targets associated with T2DM. Furthermore, ICAM1 and EZR may be associated with insulin resistance by reducing glucose transport efficiency, potentially through modulation of the PI3K-AKT signaling pathway.

PMID 42568355
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