Human iPS Cell Line (Type 2 Diabetes)

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Cat.No.

CSC-00849L

Description

Human iPS Cell Line (Type 2 Diabetes) is derived from the human somatic cells from patients with Type 2 Diabetes. The pertinent donor information is available upon request. These iPS cells are established from a single clone and expanded in feeder-free conditions. The cells have been fully characterized for their self-renewal and pluripotency.

Species

Human

Culture Properties

Adherent

Application

For Research Use Only

Shipping

Dry Ice

Storage and Shipping

Remove cryovials (dry ice packaging) and place the vial into liquid nitrogen for storage. Alternatively, thaw and use the cells immediately.

Citation Guidance

If you use this products in your scientific publication, it should be cited in the publication as: Creative Bioarray cat no. If your paper has been published, please click here to submit the PubMed ID of your paper to get a coupon.

Human iPS Cell Line (Type 2 Diabetes) is a disease-specific induced pluripotent stem cell (iPSC) line generated from somatic cells obtained from individuals diagnosed with Type 2 Diabetes Mellitus (T2DM). Through biological reprogramming, these cells acquire pluripotency, but preserve the genetic background and disease susceptibilities of the donor. They thus represent a great platform to explore the genetic and cellular pathways underlying the pathophysiology of T2DM.

These cells have high self-renewal potential and, in addition, can be differentiated into a wide range of metabolically relevant cell types including pancreatic β cells, hepatocytes, adipocytes, skeletal muscle cells, endothelial cells and other tissues involved in glucose homeostasis. The human iPS cell lines produced from T2DM patients are commonly utilized to study the insulin resistance, β-cell malfunction, poor glucose metabolism, and genetic variables contributing to the disease progression.

Besides disease modeling, these cells are important instruments for drug discovery, toxicity testing, biomarker finding and personalized medicine studies. Also enabling the construction of patient-specific in vitro models for researching diabetic consequences such as retinopathy, nephropathy, neuropathy and cardiovascular disease. Moreover, T2DM-derived iPSCs are rapidly being used in the field of regenerative medicine and cell therapy research to generate functional insulin-producing cells. They are an important resource for diabetes research and therapy development, as they are able to replicate patient-specific disease characteristics.

Phosphoproteomic Analysis of Cell-Intrinsic Insulin Resistance in Type 2 Diabetes–Derived iPSC-Hepatocytes

Hepatic insulin resistance is a hallmark of type 2 diabetes (T2D), but distinguishing cell-intrinsic defects from systemic metabolic influences is challenging in vivo. Gattu et al. differentiated induced pluripotent stem cells (iPSCs) from control and T2D donors into hepatocyte-like cells (iHeps) to model intrinsic hepatic insulin signaling defects.

T2D iHeps exhibited pathway-selective insulin resistance: insulin failed to suppress gluconeogenic genes (PCK1, G6PC) but retained the ability to induce lipogenic enzymes (FASN, ACACA) and showed a 1.5‑fold increase in de novolipogenesis (Fig. 1). Insulin-stimulated phosphorylation of IRβ(Y1150/1151), AKT(T308), GSK3α/β, and FOXO1/3a was reduced by 30–50% in T2D iHeps. Unbiased LC‑MS/MS phosphoproteomics identified 1,710 insulin-regulated phosphosites (|FC| > 1.5, adj. p< 0.05): 43% showed impaired insulin regulation in T2D, whereas 57% displayed emergent (gain-of-function) insulin-regulated phosphorylation. Impaired signaling involved the IRS→AKT cascade, Rho‑GTPase, Notch‑HLH, and IFN‑stimulated gene pathways, linked to reduced AKT2/3, PKCθ, CHK2, PHKG2, and STK32C activity. Emergent signaling involved Rho‑GTPase components, RNA metabolism, membrane trafficking, and chromatin modifiers, associated with increased ROCK1/2, MST4, and BCKDK activity.

These findings reveal a bipartite phosphoproteomic signature of hepatic insulin resistance—combined loss and paradoxical gain of insulin-regulated phosphorylation—driven by altered upstream kinase activities. This cell‑intrinsic model provides mechanistic insight into T2D pathophysiology and nominates new kinase targets for therapeutic intervention.

Directed differentiation of iHeps. (A) Schematic of iPS cell differentia... — Fig. 1. Directed differentiation of iHeps (Gattu A K, Tanzer M, et al., 2025).

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For research use only. Not for any other purpose.