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insulin glargine (Galactus / Glaricon / Basalog)

✓ Approved

Mylan · INSR · 重组蛋白

什么是 insulin glargine？

insulin glargine 是一种重组蛋白，由Mylan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Galactus, Glaricon, Basalog
公司Mylan
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, Mylan

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

PubMedJournal of diabetes science and technology2026-08-05

Real-World Outcomes of Automated Insulin Delivery Use in Hospitalized Adults With Diabetes.

Ruddiman Kathleen R KR, Evans Joni K JK, Aloi Joseph A JA, Usoh Chinenye C et al.

Automated insulin delivery (AID) systems are increasingly used by individuals living with diabetes in the outpatient setting, but data on their safety and effectiveness during hospitalizations remains limited. The objective is to evaluate the use and efficiency of AID systems in hospitalized adults with diabetes. We performed a retrospective cohort study based on electronic health record data from hospital admissions of 316 patients with diabetes using insulin pumps. Automated insulin delivery and continuous glucose monitor use, insulin pump continuation, length of stay (LOS), and glycemic outcomes among the cohort were analyzed. The primary aims of the study were to describe rates of insulin pump continuation and reasons associated with removal, and rates of pump reinitiation. Secondary outcomes included effects of insulin pump removal and prompt endocrinology consultation on inpatient glycemic outcomes and LOS. Insulin pumps were continued in 64.2% of all admissions. The most common reason for pump discontinuation was surgery (30.1%). Length of stay was longer when pumps were removed (8.3 vs 4.7 days, P < .001) and when endocrinology consultation occurred more than 24 hours after admission (P < .001). Insulin pump continuation was associated with lower hyperglycemia (glucose >180 mg/dL) rates without an increase in hypoglycemia (glucose <70 mg/dL) in both critical and noncritical care settings. Continuation of insulin pumps was associated with improvement in hyperglycemia without increased hypoglycemia risk and with shorter LOS in the hospital. Standardized institutional policies including prompt glycemic management team consultation may help expand safe continuation of AID during hospitalizations.

PMID 42554596
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PubMedPloS one2026-08-05

In vitro evaluation of microfluidic WS6-loaded Eudragit nanoparticles for improving insulin-producing cell differentiation.

Abuarqoub Duaa D, Mohammad Marwa M, Albarghouthi Rand R, Abuoun Mohammad M et al.

This study explores a stem-cell-based approach for diabetes treatment by enhancing the viability and functionality of insulin-producing cells (IPCs) derived from stem cells of the apical papilla (SCAP). Although SCAP can differentiate into IPCs, limited cell survival remains a challenge. To address this, the proliferation enhancer WS6 was incorporated into Eudragit RS100 nanoparticles (NPs) using microfluidics. The WS6-loaded NPs were characterized for size, charge, PDI, morphology, stability, and drug loading. An MTT assay was performed as a preliminary screening method to evaluate the cytocompatibility of blank-NPs and to optimize treatment concentration. SCAP cells were treated with free WS6 or WS6-loaded NPs, and cellular uptake of NPs was evaluated using flow cytometry and fluorescence imaging. Additionally, the viability of treated cells was determined by propidium iodide (PI) and trypan blue. Prior to differentiation, definitive endoderm formation was assessed through SOX17 and FOXA2 expressions. After differentiation into IPCs, maturation markers such as insulin, C-peptide, PDX-1, NKX2.2, and NKX6.1 were examined, and apoptosis assays measured cell viability. Functional insulin secretion was tested using an in vitro glucose-stimulated insulin secretion (GSIS) assay. Results showed that WS6-loaded NPs significantly improved SCAP viability, increased healthy cell percentages, and enhanced IPC maturation. Treated IPCs demonstrated functional insulin secretion and improved glucose regulation. Overall, WS6-loaded NPs represent a promising approach to enhance IPC proliferation and generation for diabetes therapy.

PMID 42550869
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PubMedFrontiers in immunology2026-08-05

Sucrose-free low-fat diet induces metabolic dysfunction through gut dysbiosis and colonic inflammation in mice.

Almansour Nourah N, Kochumon Shihab S, Al-Rashed Fatema F, Malik Md Zubbair MZ et al.

Low-fat diets are widely promoted as health-protective; however, the consequences of removing sucrose within a low-fat dietary framework remain unclear. Here, we investigated the effects of a sucrose-free low-fat diet (SF-LFD) compared with a sucrose-containing low-fat control diet (C-LFD) in mice (n=6/group) over 16 weeks. Despite unchanged body and liver weights, SF-LFD feeding resulted in impaired glucose tolerance, reduced insulin sensitivity, and broad alterations in circulating metabolic hormones, including elevated C-peptide, incretins, ghrelin, and resistin, as well as reduced fasting insulin. 16S rRNA sequencing revealed that SF-LFD markedly disrupted gut microbial diversity and composition, with depletion of short-chain fatty acid-producing commensals, including Lactobacillus murinus and members of the Lachnospiraceae family, and enrichment of taxa associated with inflammatory or stress-adapted states, including Helicobacter ganmani, Odoribacter splanchnicus, and Alistipes species. This dysbiosis was accompanied by pronounced colonic inflammation characterized by crypt architectural disruption, loss of goblet cells, submucosal expansion, increased CD3+ T-cell and F4/80+ macrophage infiltration, and robust upregulation of inflammatory mediators, including Il1b, Il6, Ccl2, Rorγt, and Tbx21. SF-LFD feeding induced hepatic microvesicular steatosis, lobular inflammation, recruitment of F4/80+ and CD11c+ immune cells and increased hepatic expression of IL1b and IL6. Together, these findings suggest that sucrose elimination from a low-fat diet disrupts gut microbiota, impairs metabolic homeostasis, and promotes gut and liver inflammation, revealing an unrecognized dietary trigger of metabolic dysfunction.

PMID 42553085
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PubMedReproductive sciences (Thousand Oaks, Calif.)2026-08-05

Accurate Measurement of Serum Free Testosterone Levels via Liquid Chromatography‒Tandem Mass Spectrometry (LC‒MS/MS) has Predictive Value in the Diagnosis of Polycystic Ovary Syndrome and Associated Metabolic Disorders.

Liu Yang Y, Li Cheng C, Li Jie J, Wei Zhaolian Z et al.

Polycystic ovary syndrome (PCOS), in which hyperandrogenism is a major feature, is the most prevalent endocrine disorder among women of reproductive age. Serum free testosterone (FT) reflects the biologically active fraction of circulating testosterone. Accurate assessment of FT allows for precise identification of hyperandrogenism and provides critical guidance for the diagnosis of PCOS. Women with PCOS and normal controls (NCs) were included in this study. Fasting serum samples were collected during the early follicular phase to evaluate key clinical parameters, and FT levels were quantified using liquid chromatography‒tandem mass spectrometry (LC‒MS/MS). The diagnostic value of FT for identifying PCOS was assessed using Spearman's correlation analysis and receiver operating characteristic curves. A total of 202 women were included in the PCOS group, 121 were included in the NC group. Total testosterone (TT), free androgen index (FAI), and FT levels were significantly greater in the PCOS group than in the NC group. Both FAI and FT were positively correlated with body mass index (BMI), triglycerides, low-density lipoprotein cholesterol, fasting insulin and the homeostasis model assessment for insulin resistance; and were negatively correlated with high-density lipoprotein cholesterol. Following age and BMI adjustments, the area under the curve (AUC) for FT (AUC = 0.886) was greater than that for TT (AUC = 0.856) or FAI (AUC = 0.864). Compared with conventional assessments of TT and FAI, LC-MS/MS-based measurements of FT demonstrate superior diagnostic performance for identifying PCOS. Both FT and FAI are associated with obesity and the features of metabolic syndrome in PCOS patients.

PMID 42552471
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PubMedPhysiological genomics2026-08-05

Transcriptome analysis reveals IGF-dependent and IGF-independent mechanisms affected by loss of IGF binding protein-2b in rainbow trout.

Cleveland Beth M BM, Radler Lisa L, Shimizu Munetaka M

In teleosts, insulin-like growth factor binding protein-2b (IGFBP-2b) is the major carrier of serum insulin-like growth factor (IGF). A line of gene edited rainbow trout (2bKO) was produced that lack a functional IGFBP-2b and associated phenotypes of reduced serum IGF-1, increased appetite, and faster growth compared to wild type controls (WT). Transcriptomic analysis was completed in liver and muscle from fed and feed deprived fish from the 2bKO and WT line; the DEG profiles were used to identify biological functions and pathways affected by the loss of IGFBP-2b and predict IGF-dependent and IGF-independent mechanisms regulated by IGFBP-2b. In general, DEGs reflected down-regulation of hepatic functions and signaling pathways in 2bkO liver, while an overall up-regulation was observed in muscle. A predicted increase in IGF-1 signaling in muscle of fed fish likely facilitated an up-regulation in myogenic mechanisms. IGF-independent responses in both liver and muscle are consistent with IGFBP-2b interacting with Type II, III, and IV nuclear receptors such as HNF4A, THR, LXR, and PXR, thus mediating changes in lipid, glucose, and sterol metabolism. In liver, immune and cytokine systems were inhibited (TNF-a, NF-kB, IL-1B), supporting that IGFBP-2b may play a central role to regulate the crosstalk between systems that modulate the balance of energy between growth and immune function. In summary, through both enhanced IGF-1 signaling and regulation of IGF-independent mechanisms, it is predicted that the loss of IGFBP-2b increased muscle growth and regulated nutrient metabolism and cytokine signaling, providing insight into the functional role of IGFBP-2b in rainbow trout.

PMID 42552781
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PubMedDiabetes, metabolic syndrome and obesity : targets and therapy2026-08-05

Prolonging Partial Remission in Type 1 Diabetes: The Role of Low-Carbohydrate Diet: A Literature Review.

Rittweger de Moor Margaux M, Gdoura Mariem M, Lysy Philippe A PA

Type 1 diabetes mellitus (T1DM) is an autoimmune disease characterized by progressive destruction of insulin-producing β-cells, resulting in lifelong insulin dependence and impaired quality of life. Although a transient phase of partial remission may occur after diagnosis, sustained preservation of β-cell function remains exceptional. Recently, low-carbohydrate diets (LCD) have gained attention among patients, partly driven by anecdotal reports describing prolonged remission. The aim of this review was to critically examine the existing clinical evidence for prolonged partial remission under LCD in patients with T1DM and to summarize the biological mechanisms proposed in the literature to explain such observations. A literature review was conducted focusing on reports of prolonged remission in individuals with T1DM adopting an LCD, as well as experimental studies exploring mechanistic pathways potentially modulated by carbohydrate restriction. Only six individual cases describing prolonged partial remission under LCD were identified in the literature. The diagnostic certainty of T1DM in these reports was variable, and misclassification (eg, latent autoimmune diabetes in adults or monogenic diabetes) cannot be excluded. The mechanistic hypotheses proposed-including reduction of glucotoxicity, modulation of inflammation, attenuation of oxidative stress, and possible β-cell regeneration-are derived predominantly from animal models, in vitro studies, and non-T1DM populations. Currently, no controlled clinical trial has demonstrated that LCDs prolong remission or preserve β-cell function in patients with T1DM. Evidence supporting prolonged partial remission under LCD in patients with T1DM remains based on rare case reports of uncertain diagnostic validity. Mechanistic data are largely indirect and extrapolated from heterogeneous experimental contexts. At present, LCD cannot be considered as a therapeutic strategy for inducing or maintaining remission in T1DM. This review highlights the need for well-designed longitudinal studies with stringent diagnostic criteria and mechanistic validation in authentic T1DM models.

PMID 42553879
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