Human Skeletal Muscle Cells, HSkMC-T2D
Human Skeletal Muscle Cells: Type 2 Diabetes: HSkMC-T2D
Human Skeletal Muscle Cells from donors with type 2 diabetes (HSkMC-T2D) are specialized primary cells isolated from adult skeletal muscle tissue, retaining characteristics of the in vivo donor state.
Description
Human Skeletal Muscle Cells from donors with type 2 diabetes (HSkMC-T2D) are specialized primary cells isolated from adult skeletal muscle tissue, retaining characteristics of the in vivo donor state. Because skeletal muscle represents the primary site for insulin-stimulated glucose disposal, these primary cells provide a valuable in vitro model for studying the pathophysiology of metabolic dysfunction. Skeletal muscle plays an instrumental role in systemic metabolism, systemic glucose homeostasis, and diabetes, particularly in conditions where chronic hyperglycemia and impaired glucose tolerance contribute to disease progression.
In healthy tissue, insulin binding initiates a complex signaling pathway that translocates the primary glucose transporter (such as GLUT4) to the plasma membrane, driving robust glucose uptake. In contrast, cells derived from type 2 diabetic subjects (or obese subjects) often exhibit hallmark metabolic defects associated with type 2 diabetes (or type 2 diabetes mellitus and broader diabetes mellitus pathology). Researchers utilize these disease-state primary models to investigate how molecular alterations impair insulin sensitivity, often show reduced markers of mitochondrial function (such as altered expression of mitochondrial genes) and diminished mitochondrial mass, and can exhibit increased oxidative stress in response to metabolic challenge during glucose transport.
Studies using Human Skeletal Muscle Cells (HSkMC) from donors with type 2 diabetes allow scientists to dissect the molecular mechanisms underlying metabolic disease complications, tracking how altered oxidative metabolism and oxidative phosphorylation link to metabolic and proteostasis pathways. Under pathological conditions or chronic metabolic stress, a dysregulated balance between protein synthesis and protein degradation can contribute to pathological reductions in skeletal muscle mass (including muscle mass and skeletal muscle atrophy). Furthermore, researchers examine how therapeutic compounds — such as activators of the amp activated protein kinase pathway — or modulators of autophagy can rescue impaired metabolic signaling and restore proper cellular function.
While certain comparative studies or foundational physiological principles have historically been established using models like rat skeletal muscle (with notable contributions from researchers such as Hirshman, MF), utilizing primary human cells derived directly from a diagnosed patient can improve translational relevance compared with non-human models. These cultures enable rigorous investigation into how genetic and environmental risk factors disrupt cellular metabolic networks, offering a robust platform for drug discovery and the identification of novel therapeutic targets for metabolic disorders.
Human Skeletal Muscle Cells (HSkMC), isolated from adult or fetal donor limbs are positive for sarcomere myosin and can undergo differentiation to exhibit actin and myosin myofilaments. Our HSkMC provide a useful model system to study many aspects of muscular function and disease. Skeletal Muscle Cells play an instrumental role in the glucose metabolism and diabetes.
Select HSkMC lots have been additionally tested to demonstrate stimulation-dependent AMPK signaling and responsiveness to insulin stimulation. More information about pre-screened skeletal muscle cells can be found on the Pre-Screened Skeletal Muscle Cell Product Page.
HSkMC from Cell Applications, Inc. have been used to:
- Serve as a differentiated control in a study of developmental regulator genes in hESC
- Characterize statin-induced gene expression changes and demonstrate cytotoxic effect of statins in skeletal muscle cells
- Identify molecular mechanisms of mitochondrial myopathy and sideroblastic anemia resulting from a missense mutation in the PUS1 gene
- Investigate chemokine-like factor expression in the idiopathic inflammatory myopathies
- Demonstrate that fasting activates AceCS2 gene expression by inducing KLF15 transcription factor
- Characterize human FGFR3-positive sarcoma-initiating stem cells
- Identify trans-Golgi network proteins and Notch and Hedgehog pathways as putative targets for rhabdomyosarcoma therapy
- Show that riluzole muscle relaxant effects are mediated by inhibition of INa and stimulation of BKC-channel activity
- Develop nitric esters that combine the pharmacological functions of NO and muscle relaxation properties for treatment of muscular diseases
- Develop biodegradable polymer-based transgene delivery vectors for muscular dystrophy treatment
- Design optimal coating for orthopedic metallic implants
Type 2 Diabetes (T2D) Cellular Disease Models For T2D research and drug discovery, Cell Applications offers multiple cell types, isolated from donors where genetics and lifestyle factors contributed to insulin resistance and high blood sugar levels.
Details
| Tissue | Human limb skeletal muscle from donor with Type 2 Diabetes (T2D) | |
|---|---|---|
| QC | No bacteria, yeast, fungi, mycoplasma, virus | |
| Character | Multinucleated myotubes form after culture in fusion medium | |
| Bioassay | Attach, spread, proliferate in Growth Med | |
| Cryovial | 500,000 HSkMC-T2D (2nd passage) frozen in Basal Medium w/ 10% FBS, 10% DMSO | |
| Kit | Cryovial frozen HSkMC-T2D (150T2D-05a), Growth Medium (151-500), Subcltr Rgnt Kit (090K) | |
| Proliferating | Shipped in Tsfr Med, psg 3, flasks or plates | |
| Doublings | At least 15 | |
| Applications | Laboratory research use only (RUO). Not for human, clinical, diagnostic or veterinary use. |
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