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Source: Cell Biology International
Drug: Insulin

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Total 5 results found since Jan 2013.

GPR120 is not required for ω-3 PUFAs-induced cell growth inhibition and apoptosis in breast cancer cells.
Abstract Intake of ω-3 PUFAs reduces the frequency of breast cancer, and GPR120 receptor transduces ω-3 PUFAs signaling to increase insulin sensitivity in mice, but whether GPR120 mediates ω-3 PUFAs signaling to inhibit breast carcinogenesis is currently unknown. In the present study, we found that GPR120 is highly expressed in human breast cancerous tissues but not adjacent normal tissue. Knockdown of GPR120 by siRNA in breast cancer cells significantly reduced cell growth, and dramatically increased ω-3 FFA-induced cell growth inhibition and apoptosis. Thus, these observations indicated that GPR120 promotes ...
Source: Cell Biology International - October 5, 2017 Category: Cytology Authors: Zhu S, Jiang X, Jiang S, Lin G, Gong J, Chen W, He Z, Chen YQ Tags: Cell Biol Int Source Type: research

Geniposide protects pancreatic β cells from high glucose-mediated injury by activation of AMP-activated protein kinase.
Abstract Our previous works indicated that geniposide could regulate glucose-stimulated insulin secretion (GSIS), and improved chronic high glucose-induced dysfunctions in pancreatic β cells, but the molecular mechanisms remain largely unknown. In the present study, we investigated the role of 5 -AMP-activated protein kinase (AMPK) in high glucose induced cell injury and explored the associated molecular mechanisms in rat INS-1 pancreatic β cells. Data suggested that geniposide obviously prevented the cell damage induced by high (25 mM) glucose in INS-1 cells, which increased the protein levels of cell apoptos...
Source: Cell Biology International - February 27, 2017 Category: Cytology Authors: Liu C, Cui Y, Hao S, Yin F, Zhang Y, Liu J Tags: Cell Biol Int Source Type: research

Nuclear co-repressor (NCoR) is required to maintain insulin sensitivity in C2 C12 myotubes.
Abstract Nuclear co-repressor (NCoR) regulate peripheral insulin sensitivity, however its role in modulating insulin sensitivity in skeletal muscle remains elusive. Present study investigated protein expression and effect of NCoR on insulin sensitivity in murine skeletal muscle cell line C2 C12 . Myotubes as compared to myoblasts of C2 C12 cells was found to be more sensitive in response to insulin as increase in insulin stimulated phosphorylation of AKT at serine 473 residue (pAKT(S473) ) was significantly higher in myotubes. Incidentally, reduced protein level of NCoR coincided with differentiation of myoblasts ...
Source: Cell Biology International - December 8, 2016 Category: Cytology Authors: Choudhary AK, Dey CS Tags: Cell Biol Int Source Type: research

AMPK activation by prolonged stimulation with interleukin-1 β contributes to the promotion of GLUT4 translocation in skeletal muscle cells.
AMPK activation by prolonged stimulation with interleukin-1β contributes to the promotion of GLUT4 translocation in skeletal muscle cells. Cell Biol Int. 2016 Aug 29; Authors: Takaguri A, Inoue S, Kubo T, Satoh K Abstract Impaired insulin signaling in skeletal muscle cells causes insulin resistance associated with the onset of type 2 diabetes. Although interleukin (IL)-1β has been considered to be implicated in the pathogenesis of type 2 diabetes, the action of prolonged stimulation with IL-1β on the insulin signaling pathway in skeletal muscle cells remains poorly understood. In the current study,...
Source: Cell Biology International - August 28, 2016 Category: Cytology Authors: Takaguri A, Inoue S, Kubo T, Satoh K Tags: Cell Biol Int Source Type: research

IRE1α and TRB3 do not contribute to the disruption of proximal insulin signaling caused by palmitate in C2C12 myotubes.
Abstract Endoplasmic reticulum (ER) stress is a central actor in the physiopathology of insulin resistance (IR) in various tissues. The subsequent unfolded protein response (UPR) interacts with insulin signaling through inositol-requiring 1α (IRE1α) activation and tribbles homolog 3 (TRB3) expressions. IRE1α impairs insulin actions through the activation of c-Jun N-terminal kinase (JNK) and TRB3 is a pseudokinase inhibiting Akt. In muscle cells, the link between ER stress and IR has only been demonstrated by using chemical ER stress inducers or overexpression techniques. However, the involvement of ER stress in...
Source: Cell Biology International - September 4, 2015 Category: Cytology Authors: Pierre N, Fernández-Verdejo R, Regnier P, Vanmechelen S, Demeulder B, Francaux M Tags: Cell Biol Int Source Type: research