Rat Preadipocyte Cells

Cat.No.: CSC-C5126S

Species: Rat

Source: Adipose

Cell Type: Preadipocyte

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Cat.No.
CSC-C5126S
Description
Preadipocytes are fat cell precursors. They exhibit adipose fat depot specificity, and differentiate and proliferate from distinct progenitor cells.
Rat Preadipocyte Cells from Creative Bioarray are isolated from the rat adipose tissue. The method we use to isolate Rat Preadipocyte Cells was developed based on a combination of established and our proprietary methods. The Rat Preadipocyte Cells are characterized by immunofluorescence with antibodies specific to preadipocyte factor 1 (Pref-1). Each vial contains 0.5x10^6 cells per ml and is delivered frozen.
Species
Rat
Source
Adipose
Recommended Medium
SuperCult® Rat Preadipocyte Cell Medium
Cell Type
Preadipocyte
Disease
Normal
Quality Control
Rat Preadipocyte Cells are negative for HIV-1, HBV, HCV, mycoplasma, bacteria, yeast and fungi.
Storage and Shipping
Creative Bioarray ships frozen cells on dry ice. On receipt, immediately transfer frozen cells to liquid nitrogen (-180 °C) until ready for experimental use. Never can cells be kept at -20 °C.
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.

Rat preadipocytes are mesenchymal progenitor cells isolated from the stromal vascular fraction of rat adipose tissue. Committed to the adipocyte lineage, they undergo synchronous differentiation into mature, functional adipocytes in vitro, offering a physiologically authentic primary culture system. Their attributes provide distinct advantages over immortalized murine lines such as 3T3-L1. First, as non-transformed cells, they retain a normal diploid karyotype and intact cell-cycle regulation, ensuring that adipogenic signaling and metabolic outputs faithfully recapitulate in vivo biology without the confounding effects of aneuploidy or aberrant growth pathways. Second, rat preadipocytes preserve species-specific hormonal and pharmacological responses, which is critical because the rat is a dominant translational model for obesity, insulin resistance, and cardiovascular disease. Third, the system permits depot-specific investigation: cells can be harvested from distinct visceral, subcutaneous, and brown fat pads, each retaining intrinsic developmental and metabolic programs, thereby enabling dissection of regional differences in adipogenesis and adipokine secretion. Fourth, by modulating the induction cocktail, the same precursors can be directed toward either white or beige/brown adipocyte phenotypes, allowing parallel study of energy storage and thermogenesis. Fifth, they are amenable to genetic manipulation via lentiviral transduction and siRNA, facilitating mechanistic gene-function analyses in a relevant cellular context. Differentiated adipocytes robustly exhibit insulin-stimulated glucose uptake, lipolysis, and secretion of adipokines such as leptin and adiponectin. Collectively, rat preadipocytes combine physiological fidelity, depot specificity, phenotypic plasticity, and experimental tractability, establishing them as an indispensable tool for dissecting adipocyte biology, screening metabolic therapeutics, and elucidating the pathogenesis of metabolic disorders.

Rno-miR-130b Attenuates Lipid Accumulation Through Promoting Apoptosis and Inhibiting Differentiation in Rat Intramuscular Adipocytes

This study aims to investigate the effect of miR-130b on lipid accumulation at early-stage (24 and 48 h) and late-stage (7 d) adipogenic differentiation and to clarify potential mechanisms using primary rat intramuscular preadipocytes (IMAs).

Results showed that at 24 h and 48 h, miR-130b overexpression significantly reduced lipid deposition by inhibiting proliferation and inducing apoptosis. Furthermore, miR-130b overexpression significantly inhibited the expression of cell cycle and apoptosis marker genes. Specifically, the mRNA expression of Ccnd1 tended to decrease, while the BCL2 protein level was significantly decreased at 48 h. In contrast, miR-130b inhibition significantly increased the BCL2 protein level. At 7 d, the miR-130b mimic significantly decreased intracellular TG content and tended to decrease Hsd11b1 mRNA expression while significantly promoting Lpl mRNA expression. Additionally, the miR-130b mimic significantly increased the CASP3 protein level and tended to decrease the BCL2 protein level.

In conclusion, these data indicated for the first time that miR-130b could reduce lipid deposition in rat IMAs through different mechanisms: at the early stage of differentiation by inhibiting proliferation and promoting apoptosis and at the late stage by inhibiting adipogenic differentiation, promoting lipid hydrolysis, and promoting apoptosis.

Overexpression of MiR-130b Significantly Inhibited Lipid Deposition in Rat IMAs.

Fig. 1. Overexpression of miR-130b significantly inhibited lipid deposition in rat IMAs at early adipogenic differentiation stages (both 24 h and 48 h) (Yu, Yichen, et al., 2025).

Overexpression of MiR-130b Promoted Apoptosis by Inhibiting BCL2 and Increasing CASP3 Expression in Rat IMAs.

Fig. 2. Effect of miR-130b overexpression on adipogenesis, lipid hydrolysis, and apoptosis in rat IMAs at the late stage of differentiation (7 d) (Yu, Yichen, et al., 2025).

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