Faculty Opinions recommendation of Overexpression of vesicle-associated membrane protein (VAMP) 3, but not VAMP2, protects glucose transporter (GLUT) 4 protein translocation in an in vitro model of cardiac insulin resistance.

2013 ◽  
Author(s):  
Y Peng Loh ◽  
Joshua J Park
Keyword(s):  
Insulin Resistance ◽  
Membrane Protein ◽  
In Vitro Model ◽  
Glucose Transporter ◽  
Protein Translocation ◽  
Glut 4 ◽  
Vitro Model

scholarly journals Studies of insulin resistance in adipocytes induced by macrophage mediator.

1983 ◽  
Vol 157 (4) ◽  
pp. 1360-1365 ◽  
Author(s):  
P Pekala ◽  
M Kawakami ◽  
W Vine ◽  
M D Lane ◽  
A Cerami
Keyword(s):  
Insulin Resistance ◽  
Fatty Acid ◽  
Insulin Receptor ◽  
Functional Ability ◽  
Molecular Basis ◽  
In Vitro Model ◽  
Fatty Acid Synthetase ◽  
Storage Lipid ◽  
Vitro Model

An apparent insulin resistance is noted in 3T3-L1 adipocytes after the addition of an endotoxin-induced mediator from macrophages. Examination at the level of the insulin receptor has revealed that the mediator does not effect either the functional ability of the cells to bind insulin or the ability of insulin to stimulate the uptake of glucose. The resistance appears to reflect a post-receptor interference with the insulin-induced biosynthesis of the anabolic enzymes, acetyl Co-A carboxylase and fatty acid synthetase, which are required for the conversion of glucose into storage lipid. These studies offer a new in vitro model for investigating the molecular basis of insulin resistance.

scholarly journals The insulin-sensitizing mechanism of myo-inositol is associated with AMPK activation and GLUT-4 expression in human endometrial cells exposed to a PCOS environment

2020 ◽  
Vol 318 (2) ◽  
pp. E237-E248 ◽  
Author(s):  
Heidy Cabrera-Cruz ◽  
Lorena Oróstica ◽  
Francisca Plaza-Parrochia ◽  
Ignacio Torres-Pinto ◽  
Carmen Romero ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
In Vitro Model ◽  
Normal Weight ◽  
Endometrial Cells ◽  
Insulin Resistant ◽  
Protein Levels ◽  
Glut 4 ◽  
Vitro Model ◽  
Dependent Mechanism

Polycystic ovary syndrome (PCOS) is an endocrine-metabolic disorder characterized by hyperandrogenism and ovulatory dysfunction but also obesity and hyperinsulinemia. These characteristics induce an insulin-resistant state in tissues such as the endometrium, affecting its reproductive functions. Myo-inositol (MYO) is an insulin-sensitizing compound used in PCOS patients; however, its insulin-sensitizing mechanism is unclear. To understand the relationship of MYO with insulin action in endometrial cells, sodium/myo-inositol transporter 1 (SMIT-1) (MYO-transporter), and MYO effects on protein levels related to the insulin pathway were evaluated. SMIT-1 was assessed in endometrial tissue from women with normal weight, obesity, insulin resistance, and PCOS; additionally, using an in vitro model of human endometrial cells exposed to an environment resembling hyperinsulinemic-obese-PCOS, MYO effect was evaluated on p-AMPK and GLUT-4 levels and glucose uptake by Western blot, immunocytochemistry, and confocal microscopy, respectively. SMIT-1 was detected in endometrial tissue from all groups and decreased in PCOS and obesity ( P < 0.05 vs. normal weight ). In the in vitro model, PCOS conditions decreased p-AMPK levels, while they were restored with MYO ( P < 0.05). The diminished GLUT-4 protein levels promoted by PCOS environment were restored by MYO through SMIT-1 and p-AMPK-dependent mechanism ( P < 0.05). Also, MYO restored glucose uptake in cells under PCOS condition through a p-AMPK-dependent mechanism. Finally, these results were similar to those obtained with metformin treatment in the same in vitro conditions. Consequently, MYO could be a potential insulin sensitizer through its positive effects on insulin-resistant tissues as PCOS-endometrium, acting through SMIT-1, provoking AMPK activation and elevated GLUT-4 levels and, consequently, increase glucose uptake by human endometrial cells. Therefore, MYO may be used as an effective treatment option in insulin-resistant PCOS women.

Insulin resistance in uremia: In vitro model in the rat liver using human serum to study mechanisms

Metabolism ◽  
1986 ◽  
Vol 35 (11) ◽  
pp. 989-998 ◽  
Author(s):  
Franco Folli ◽  
Madhur K. Sinha ◽  
Diego Brancaccio ◽  
Jose F. Caro
Keyword(s):  
Insulin Resistance ◽  
Human Serum ◽  
Rat Liver ◽  
In Vitro Model ◽  
Vitro Model

scholarly journals Human embryonic stem cell-derived cardiomyocytes as an in vitro model to study cardiac insulin resistance

2018 ◽  
Vol 1864 (5) ◽  
pp. 1960-1967 ◽  
Author(s):  
Ilvy M.E. Geraets ◽  
Dipanjan Chanda ◽  
Florence H.J. van Tienen ◽  
Arthur van den Wijngaard ◽  
Rick Kamps ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Stem Cell ◽  
Embryonic Stem Cell ◽  
Human Embryonic Stem Cell ◽  
In Vitro Model ◽  
Embryonic Stem ◽  
Vitro Model

An in vitro model for investigation of vitamin A effects on wound healing

2021 ◽  
pp. 1-6
Author(s):  
Hoda Keshmiri Neghab ◽  
Mohammad Hasan Soheilifar ◽  
Gholamreza Esmaeeli Djavid
Keyword(s):  
Wound Healing ◽  
Endothelial Cell ◽  
Vitamin A ◽  
In Vitro Model ◽  
Cellular Proliferation ◽  
Endothelial Cell Migration ◽  
Normal Fibroblast ◽  
Anti Inflammatory ◽  
Vitro Model

Abstract. Wound healing consists of a series of highly orderly overlapping processes characterized by hemostasis, inflammation, proliferation, and remodeling. Prolongation or interruption in each phase can lead to delayed wound healing or a non-healing chronic wound. Vitamin A is a crucial nutrient that is most beneficial for the health of the skin. The present study was undertaken to determine the effect of vitamin A on regeneration, angiogenesis, and inflammation characteristics in an in vitro model system during wound healing. For this purpose, mouse skin normal fibroblast (L929), human umbilical vein endothelial cell (HUVEC), and monocyte/macrophage-like cell line (RAW 264.7) were considered to evaluate proliferation, angiogenesis, and anti-inflammatory responses, respectively. Vitamin A (0.1–5 μM) increased cellular proliferation of L929 and HUVEC (p < 0.05). Similarly, it stimulated angiogenesis by promoting endothelial cell migration up to approximately 4 fold and interestingly tube formation up to 8.5 fold (p < 0.01). Furthermore, vitamin A treatment was shown to decrease the level of nitric oxide production in a dose-dependent effect (p < 0.05), exhibiting the anti-inflammatory property of vitamin A in accelerating wound healing. These results may reveal the therapeutic potential of vitamin A in diabetic wound healing by stimulating regeneration, angiogenesis, and anti-inflammation responses.

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