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human insulin (Biohulin)

✓ Approved

Novo Nordisk A/S · INSR · 小分子

什么是 human insulin？

human insulin 是一种小分子，由Novo Nordisk A/S研发。该药已获批，用于治疗相关适应症。

药物档案

商品名Biohulin
公司Novo Nordisk A/S
药物类别小分子, 多肽类
分子靶点INSR
状态Approved
来源： ClinicalTrials.gov, Novo Nordisk A/S

作用机制

分子靶点

human insulin 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

human insulin 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
InvestigationsGlucose tolerance test abnormal✓ Approved

相关研究文献

PubMedDiabetes & metabolism journal2026-09-11

Mitochondrial Proteostasis Links Diabetes and Sarcopenia: Cross-Scale Convergence from Experimental Models to Human Multi-Omics.

Wei Shibo S, Shin Soyeon S, Ryu Dongryeol D, Oh Chang-Myung CM

Sarcopenia in type 2 diabetes mellitus is increasingly recognized as a mechanistic consequence of chronic metabolic stress rather than mere age-related comorbidity. This review synthesizes evidence demonstrating how insulin resistance, hyperglycemia, lipotoxicity, and inflammation converge on skeletal muscle mitochondrial proteostasis to drive progressive decline. We evaluate seven pathway modules-mitochondrial dynamics, mitophagy, biogenesis, oxidative phosphorylation, nicotinamide adenine dinucleotide (NAD+)/sirtuin (SIRT)-linked regulation, protein import, and the mitochondrial unfolded protein response (UPRmt)-across an evidence map encompassing basic, clinical, and multi-omics studies. Dynamics and mitophagy represent mechanistically central quality-control nodes; their impairment permits dysfunctional organelle accumulation and promotes atrophic cascades. Direct evidence density, however, remains weighted toward oxidative phosphorylation and mitochondrial biogenesis. NAD+/SIRT-linked regulation, protein import fidelity, and UPRmt represent mechanistically upstream but comparatively underinvestigated signals. We propose a diabetes-centered framework where mitochondrial proteostasis failure mediates atrophy and reinforces insulin resistance via a self-amplifying feed-forward loop, supported by pathway responsiveness to coherent interventions. Human multi-omics data highlight network-level dysregulation rather than isolated defects, underscoring module-based biomarker strategies. Translationally, exercise remains the mechanistic cornerstone, while pathway-directed adjuncts-NAD+ precursor repletion, mitophagy modulators, and emerging pharmacotherapeutics-are warranted for patients with identifiable module-specific failure patterns.

PMID 42722377
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PubMedSignal transduction and targeted therapy2026-09-11

Insulin-like growth factor receptor signaling in physiology and disease.

Dilawar Muhammad M, Malik Anoosha A, Liao Junguang J, Shen Panpan P et al.

The insulin-like growth factor (IGF) signaling pathway plays a pivotal role in regulating a myriad of cellular and physiological processes, including cell proliferation, differentiation, and the maintenance of redox homeostasis. This review provides a comprehensive overview of the IGF/IGF receptor (IGFR) signaling axis, outlining its historical milestones and delineating its evolution from foundational discoveries to contemporary advancements. We elucidate the structural components of pathway, including ligands, receptors, and IGF-binding proteins, and discuss how multilevel regulation integrates upstream signals with downstream effectors such as the PI3K-AKT and MAPK/ERK pathways. Particular emphasis is placed on the crosstalk between IGF signaling and other pathways, including insulin, EGFR, PDGFR, VEGF, Wnt/β-catenin, JAK-STAT, and TGF-β/BMP in homeostasis and pathophysiological processes. We further discuss the role of IGF signaling in pathological process, highlighting insights from animal models and its implication in a wide range of human diseases, including cancer, cardiovascular diseases, neurodegenerative conditions, metabolic syndromes, skeletal abnormalities, and autoimmune and rare genetic disorders. Finally, we examine the therapeutic potential of targeting the IGF/IGFR axis, current clinical research advancements, FDA-approved pharmacological agents, and ongoing clinical trials. By incorporating historical insights with up-to-date scientific breakthroughs, our review underscores the need for systems-level and context-specific approaches to better understand IGF signaling dynamics, thus paving the way for the development of precision and personalized therapeutic strategies.

PMID 42722676
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PubMedF1000Research2026-09-11

Green Tea and Decaffeinated Light Roasted Green Coffee Extract Combination Improved Cardiac Insulin Resistance through Free Fatty Acids and Adiponectin/FAS Pathways Amelioration in Metabolic Syndrome Rat Model.

Lukitasari Mifetika M, Rohman Mohammad Saifur MS, Nugroho Dwi Adi DA, Nur Kholis Mukhamad M et al.

Insulin resistance has been independently associated with cardiac diseases. Free fatty acids (FFAs) are known to induce cardiac insulin resistance via low-grade inflammation. Therefore, lowering FFA levels may improve cardiac insulin resistance. This study investigated the effects of a combination of green tea and decaffeinated light-roasted green coffee extract on free fatty acid-induced cardiac insulin resistance by modulating the adiponectin/FAS pathways. This study used 25 male Sprague-Dawley rats. Metabolic syndrome (MS) was induced using a high-fat, high-sucrose (HFHS) diet and a low-dose streptozotocin (STZ) injection, while a normal chow (NC) diet served as the healthy control. The MS rats were treated for 9 weeks with green tea (300 mg/kg b.w.), decaffeinated light-roasted green coffee (200 mg/kg b.w.), or a combination of both extracts. The experimental subjects were divided into five groups: 1) MS (HFHS diet + STZ), 2) NC (normal chow), 3) GT (green tea extract), 4) GC (decaffeinated light-roasted green coffee extract), and 5) CM (combination of both extracts). Adiponectin and HOMA-IR levels were analysed using ELISA, while the gene expression of Adipo-R1, FAS, PI3K, PDK1, Akt, and GLUT4 was measured using RT-PCR. The combination of green tea and decaffeinated light-roasted green coffee demonstrated synergistic effects in reducing FFA levels. The adiponectin/FAS pathways were attenuated in the CM group. Furthermore, the combination therapy improved cardiac insulin resistance marker expressions, including IRS-1/2, PI3K, PDK1, Akt, and GLUT4. The combination of green tea and decaffeinated light-roasted green coffee extract improved cardiac insulin resistance more effectively than the administration of either extract alone, by reducing FFA levels through the modulation of the adiponectin/FAS pathways.

PMID 42723777
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PubMedEuropean journal of pediatrics2026-09-11

Association between insulin resistance and obstructive sleep apnea in non-diabetic children with obesity.

Sunman Birce B, Alboğa Didem D, Akgül Erdal Meltem M, Demir Havva İpek Hİ et al.

Although several studies have demonstrated an independent association between obstructive sleep apnea (OSA) and insulin resistance, the evidence remains inconsistent. We aimed to investigate the relationship between the presence and severity of OSA and insulin resistance in non-diabetic children with obesity and to explore the potential role of homeostasis model assessment-insulin resistance index (HOMA-IR) in identifying children at higher risk for OSA. Children with obesity aged 6-18 years who underwent polysomnography were retrospectively analyzed. Patients with diabetes, neuromuscular disorders, craniofacial anomalies, or those receiving treatment affecting insulin sensitivity were excluded. Age, sex, BMI, and oral glucose tolerance test (OGTT) results were extracted from medical records, and HOMA-IR was calculated. Patients were divided into two groups based on their obstructive apnea-hypopnea index (OAHI): < 2 and ≥ 2 events/h. ROC analysis was performed for HOMA-IR to determine the optimal cutoff value for identifying patients with OSA. A total of 90 children with obesity were enrolled, among whom 39 (43.3%) had OSA. The groups were comparable in terms of age and sex. Median HOMA-IR values were significantly higher in the OSA group (p = 0.014). Total OAHI showed moderately positive correlation with HOMA-IR (ρ = 0.325, p = 0.002), and baseline insulin levels measured during OGTT (ρ = 0.323, p = 0.002). In multiple linear regression analysis, HOMA-IR remained independently associated with OSA severity after adjustment for age, sex, BMI z-score, sleep efficiency, and pubertal status (β = 0.691, p = 0.025). ROC analysis identified a HOMA-IR cutoff of 3.39, with 72% sensitivity and 59% specificity for OSA. HOMA-IR was independently associated with OSA severity in children with obesity, suggesting that insulin resistance may serve as a useful adjunct marker for identifying patients at higher risk and prioritizing PSG evaluation. • Childhood obesity is strongly associated with both obstructive sleep apnea (OSA) and insulin resistance. Whether insulin resistance contributes to OSA risk beyond the effect of obesity remains controversial. • Access to polysomnography (PSG) is limited, creating an unmet need for practical tools to identify children at greatest risk for OSA. • To our knowledge, this is the first pediatric study to evaluate HOMA-IR as a tool for identifying children with obesity at increased risk of obstructive sleep apnea and to propose a clinically applicable HOMA-IR threshold for prioritizing polysomnography referral. • In non-diabetic children with obesity, insulin resistance was independently associated with OSA severity, regardless of obesity, pubertal status, and other clinically relevant confounders. Children with HOMA-IR ≥ 3.39 had a substantially greater burden of obstructive sleep apnea. These findings support HOMA-IR as a simple, widely available biomarker that could help prioritize children with obesity for PSG evaluation and improve risk stratification in pediatric sleep medicine.

PMID 42722762
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PubMedFrontiers in endocrinology2026-09-11

A case report of young-onset type 2 diabetes patient with severe metabolic dysregulation carrying an LRP6 variant.

Xiang Dan D, Yuan Li L, Liao Shuaiju S, Wang Yangtian Y

The global epidemic of type 2 diabetes mellitus (T2D), along with its rising prevalence among younger populations, raises substantial public health concerns; severe hypertriglyceridemia (sHTG) is a major risk factor for acute pancreatitis. Insulin resistance in T2D often coincides with dyslipidemia, contributing to lipotoxicity, and insulin-resistant states may be linked to specific genetic variants. This report presents a 27-year-old man with poor glycemic control, recurrent dizziness, extreme hypertriglyceridemia (TG > 37.87 mmol/L), insulin resistance, pancreatic fat infiltration, and early-stage diabetic nephropathy. Despite a family history of T2D, his clinical presentation far exceeded that of typical T2D. High-throughput sequencing revealed a heterozygous LRP6 variant (c.3107A>G, p.Asn1036Ser). Multidisciplinary treatment-incorporating acute-phase plasma exchange, ω-3 fatty acid ethyl ester 90, inclisiran, subcutaneous insulin aspart pump therapy, metformin, insulin icodec, finerenone, and Huangkui capsules-led to improvements in the patient's metabolic indicators. This case report describes a patient with type 2 diabetes mellitus presenting with extreme metabolic disorders, in whom a variant in the LRP6 gene was detected. Although the variant co-occurs with the observed phenotype, its pathogenicity cannot currently be established in the absence of functional validation. This case emphasizes that genetic variant screening should be considered in patients with unexplained severe metabolic disturbances, particularly those with early-onset disease. This case also provides a foundation for future functional studies and genetic confirmation.

PMID 42723884
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PubMedTranslational pediatrics2026-09-11

Early-onset type 1 diabetes mellitus in a child with a pathogenic CTLA4 variant complicated by generalized lipodystrophy and severe insulin resistance: a case report and literature review.

Ding Yu Y, Li Qun Q, Zhang Qianwen Q, Gao Shiyang S et al.

The co-occurrence of early-onset type 1 diabetes mellitus (T1DM), acquired generalized lipodystrophy (AGL), and severe insulin resistance (SIR) is extremely rare, poses significant therapeutic challenges and no cases associated with pathogenic Cytotoxic T-lymphocyte-associated 4 (CTLA4) variants have been previously documented. We performed genetic testing, flow cytometric immunophenotyping, leptin measurement and a 4.5-year clinical follow-up in a 3-year-3-month-old boy with early-onset T1DM, insulin allergy following initial insulin therapy, progressive lipodystrophy, SIR and mild hepatic dysfunction. We additionally conducted a systematic literature review to summarize CTLA4 variant-related autoimmune endocrine disorders and fat metabolism abnormalities. Pathological biopsy of subcutaneous adipose tissue revealed scattered lymphocytes and histiocytes infiltrating the fat septa and perivascular areas. A heterozygous pathogenic c.151C>T (p.Arg51*) variant in the CTLA4 gene was identified by whole-exome sequencing (WES) analysis. His father and sister carried the same variant with incomplete penetrance. The patient showed markedly reduced CTLA4 expression on regulatory T cells and undetectable serum leptin. Treatment with abatacept normalized liver function but did not improve glycemic control or insulin resistance. During the follow-up, the patient's growth consistently exceeded the 97th percentile for age and gender. This report established the first association between a pathogenic CTLA4 variant and AGL, which expands the known clinical phenotypic spectrum of CTLA4-related immune dysregulation disorders. CTLA4 genetic testing should be considered in patients presenting with early-onset T1DM and unexplained lipodystrophy to enable early diagnosis and guide personalized management.

PMID 42724548
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