Glucose Transporter 4 (GLUT 4) Is Highly Expressed in Mitochondria-rich Oxyphil Cells

1998 ◽  
Vol 6 (4) ◽  
pp. 224-227 ◽  
Author(s):  
J. M??ller-H??cker ◽  
A. Sch??fer ◽  
T. Strowitzki
Keyword(s):  
Glucose Transporter ◽  
Glucose Transporter 4 ◽  
Glut 4

scholarly journals Adipocytes Exhibit Abnormal Subcellular Distribution and Translocation of Vesicles Containing Glucose Transporter 4 and Insulin-Regulated Aminopeptidase in Type 2 Diabetes Mellitus: Implications Regarding Defects in Vesicle Trafficking

2001 ◽  
Vol 86 (11) ◽  
pp. 5450-5456 ◽  
Author(s):  
Lidia Maianu ◽  
Susanna R. Keller ◽  
W. Timothy Garvey
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Body Mass Index ◽  
Body Mass ◽  
Glucose Transporter ◽  
Diabetic Patients ◽  
Low Density ◽  
Glucose Transporter 4 ◽  
Glut 4

Insulin resistance in type 2 diabetes is due to impaired stimulation of the glucose transport system in muscle and fat. Different defects are operative in these two target tissues because glucose transporter 4 (GLUT 4) expression is normal in muscle but markedly reduced in fat. In muscle, GLUT 4 is redistributed to a dense membrane compartment, and insulin-mediated translocation to plasma membrane (PM) is impaired. Whether similar trafficking defects are operative in human fat is unknown. Therefore, we studied subcellular localization of GLUT4 and insulin-regulated aminopeptidase (IRAP; also referred to as vp165 or gp160), which is a constituent of GLUT4 vesicles and also translocates to PM in response to insulin. Subcutaneous fat was obtained from eight normoglycemic control subjects (body mass index, 29 ± 2 kg/m2) and eight type 2 diabetic patients (body mass index, 30 ± 1 kg/m2; fasting glucose, 14 ± 1 mm). In adipocytes isolated from diabetics, the basal 3-O-methylglucose transport rate was decreased by 50% compared with controls (7.1 ± 2.9 vs. 14.1 ± 3.7 mmol/mm2 surface area/min), and there was no increase in response to maximal insulin (7.9 ± 2.7 vs. 44.5 ± 9.2 in controls). In membrane subfractions from controls, insulin led to a marked increase of IRAP in the PM from 0.103 ± 0.04 to 1.00± 0.33 relative units/mg protein, concomitant with an 18% decrease in low-density microsomes and no change in high-density microsomes (HDM). In type 2 diabetes, IRAP overall expression in adipocytes was similar to that in controls; however, two abnormalities were observed. First, in basal cells, IRAP was redistributed away from low-density microsomes, and more IRAP was recovered in HDM (1.2-fold) and PM (4.4-fold) from diabetics compared with controls. Second, IRAP recruitment to PM by maximal insulin was markedly impaired. GLUT4 was depleted in all membrane subfractions (43–67%) in diabetes, and there was no increase in PM GLUT4 in response to insulin. Type 2 diabetes did not affect the fractionation of marker enzymes. We conclude that in human adipocytes: 1) IRAP is expressed and translocates to PM in response to insulin; 2) GLUT4 depletion involves all membrane subfractions in type 2 diabetes, although cellular levels of IRAP are normal; and 3) in type 2 diabetes, IRAP accumulates in membrane vesicles cofractionating with HDM and PM under basal conditions, and insulin-mediated recruitment to PM is impaired. Therefore, in type 2 diabetes, adipocytes express defects in trafficking of GLUT4/IRAP-containing vesicles similar to those causing insulin resistance in skeletal muscle.

scholarly journals Tsg101 Is Involved in the Sorting and Re-Distribution of Glucose Transporter-4 to the Sarcolemma Membrane of Cardiac Myocytes

Cells ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 1936
Author(s):  
Kobina Essandoh ◽  
Shan Deng ◽  
Xiaohong Wang ◽  
Yutian Li ◽  
Qianqian Li ◽  
...  
Keyword(s):  
Cardiac Myocytes ◽  
Glucose Transporter ◽  
Ischemia Reperfusion ◽  
Susceptibility Gene ◽  
Cardiac Cells ◽  
Acid Oxidation ◽  
Glucose Transporter 4 ◽  
Loss Of Function ◽  
Glut 4 ◽  
Insulin Dependent

Cardiac cells can adapt to pathological stress-induced energy crisis by shifting from fatty acid oxidation to glycolysis. However, the use of glucose-insulin-potassium (GIK) solution in patients undergoing cardiac surgery does not alleviate ischemia/reperfusion (I/R)-induced energy shortage. This indicates that insulin-mediated translocation of glucose transporter-4 (Glut-4) is impaired in ischemic hearts. Indeed, cardiac myocytes contain two intracellular populations of Glut-4: an insulin-dependent non-endosomal pool (also referred to as Glut-4 storage vesicles, GSVs) and an insulin-independent endosomal pool. Tumor susceptibility gene 101 (Tsg101) has been implicated in the endosomal recycling of membrane proteins. In this study, we aimed to examine whether Tsg101 regulated the sorting and re-distribution of Glut-4 to the sarcolemma membrane of cardiomyocytes under basal and ischemic conditions, using gain- and loss-of-function approaches. Forced overexpression of Tsg101 in mouse hearts and isolated cardiomyocytes could promote Glut-4 re-distribution to the sarcolemma, leading to enhanced glucose entry and adenosine triphosphate (ATP) generation in I/R hearts which in turn, attenuation of I/R-induced cardiac dysfunction. Conversely, knockdown of Tsg101 in cardiac myocytes exhibited opposite effects. Mechanistically, we identified that Tsg101 could interact and co-localize with Glut-4 in the sarcolemma membrane of cardiomyocytes. Our findings define Tsg101 as a novel regulator of cardiac Glut-4 trafficking, which may provide a new therapeutic strategy for the treatment of ischemic heart disease.

scholarly journals Golden sea cucumber extract revives glucose transporter-4 and interleukin-6 protein level in diabetic mouse muscle

2019 ◽  
Vol 12 (5) ◽  
pp. 684-688
Author(s):  
Bambang Purwanto ◽  
Sundari Indah Wiyasihati ◽  
Putri Ayu Masyitha ◽  
Kristanti Wanito Wigati ◽  
Irfiansyah Irwadi
Keyword(s):  
Free Radical ◽  
Interleukin 6 ◽  
Protein Level ◽  
Sea Cucumber ◽  
Muscle Wasting ◽  
Glucose Transporter ◽  
Diabetic Mouse ◽  
Glucose Transporter 4 ◽  
Mouse Muscle ◽  
Glut 4

Background: Streptozotocin (STZ)-induced free radical oxidant activity resulted in muscle wasting due to protein carbonyl (PC), glucose transporter-4 (Glut-4), and interleukin-6 (IL-6) protein alteration. Antioxidant ingredient in the golden sea cucumber extract was found in promising level to inhibit free radical activity. Aim: This study was aimed to investigate the effect of golden sea cucumber extract on PC, IL-6, and Glut-4 level of STZ-induced diabetes mouse. Materials and Methods: This study was performed using mice, which were grouped into non-diabetes, diabetes, and diabetes-treated extract groups. The golden sea cucumber was extracted using 70% ethanol, which was administered by oral gavage twice a day for 5 consecutive days. Results: The extract reduced PC level and improved muscle Glut-4 and IL-6 protein level of diabetic mouse. Conclusion: The extract of golden sea cucumber revived muscle Glut-4 and IL-6 protein level in protection against muscle wasting.

scholarly journals Davidones F and G, Two Novel Flavonoids from Sophora davidii (Franch.) Skeels

Molecules ◽  
2021 ◽  
Vol 26 (14) ◽  
pp. 4182
Author(s):  
Ping Song ◽  
Xuecui Li ◽  
Tongxi Zhou ◽  
Yu Peng ◽  
Ho-Young Choi ◽  
...  
Keyword(s):  
Glucose Transporter ◽  
Ethyl Acetate Fraction ◽  
2D Nmr ◽  
Side Chain ◽  
Glucose Transporter 4 ◽  
Glut 4 ◽  
Planar Structures ◽  
Nmr Data ◽  
Glut 4 Translocation ◽  
Sophora Davidii

An unprecedented novel flavanone davidone F (1) with a seven-membered ring side chain, and a novel flavanonol davidone G (2), along with 11 known flavonoids, were isolated from the ethyl acetate fraction of Sophora davidii (Franch.) Skeels. Their planar structures were established by UV, IR, HRESIMS, 1D and 2D NMR data. The relative configurations of 1 and 2 were determined by calculation of NMR chemical shift values, the absolute configuration of 1 and 2 were assigned by comparing their experimental and calculated electronic circular dichroism (ECD) spectra. Moreover, compounds 1–13 were screened for the translocation activity of glucose transporter 4 (GLUT-4), and the fluorescence intensity was increased to the range of 1.56 and 2.79 folds. Compounds 1 and 2 showed moderate GLUT-4 translocation activity with 1.64 and 1.79 folds enhancement, respectively, at a concentration of 20 μg/mL.

scholarly journals Pengaruh Latihan Fisik terhadap Perbaikan Resistensi Insulin

2021 ◽  
Vol 2 (2) ◽  
pp. 110-114
Author(s):  
Devitya Angielevi Sukarno
Keyword(s):  
Insulin Resistance ◽  
Blood Glucose ◽  
Protein Kinase ◽  
Cell Membrane ◽  
Blood Glucose Level ◽  
Insulin Signaling ◽  
Glucose Transporter ◽  
Insulin Receptor Substrate ◽  
Glucose Transporter 4 ◽  
Glut 4

Abstract--Insulin resistance underlies the pathogenesis of chronic disease, such as diabetes mellitus which has high morbidity and mortality rate. Insulin resistance is a pathological condition when cells fail to respond normally to the insulin hormone, because of insulin signaling pathway disruption. Bound between insulin and insulin’s receptor cannot phosphorylate tyrosine and fail to activate insulin receptor substrate-1 (IRS-1). This failure decrease Glucose transporter-4 (GLUT-4) expression on the skeletal muscle’s cell membrane, that leads to decrease glucose influx and increase blood glucose level. A routine physical training which does according to adequate training dose, will activate adenosin 5’monophosphate-activated protein kinase (AMPK) and lead to the translocation of GLUT-4 vesicles without insulin and insulin’s receptor bonding.GLUT-4 expression on the skeletal muscle’s cell membrane which is stimulated by muscle contraction will increase glucose influx and decrease blood glucose level. Keywords: insulin resistance; physical training; insulin signaling pathway   Abstrak--Resistensi insulin merupakan penyebab yang mendasari terjadinya penyakit kronis seperti diabetes melitus yang memiliki angka morbiditas dan mortalitas tinggi.Resistensi insulin merupakan keadaan patologis dimana terjadi kegagalan respon seluler terhadap hormon insulin akibat gangguan pada jalur sinyal insulin.Ikatan insulin pada reseptornya tidak dapat menyebabkan fosforilasi tirosin sehingga tidak dapat mengaktivasi insulin receptor substrate-1 (IRS-1). Kegagalan aktivasi tersebut akan menyebabkan penurunan ekspresi Glucose transporter-4 (GLUT-4) pada membran sel otot rangka sehingga ambilan glukosa oleh sel menurun dan glukosa darah meningkat. Latihan fisik yang dilakukan secara rutin, teratur dan sesuai dengan dosis latihan yang tepat dapat mengaktivasi adenosin 5’monophosphate-activated protein kinase (AMPK), sehingga menyebabkan translokasi vesikel berisi GLUT-4, tanpa melalui ikatan insulin dengan reseptornya. Ekspresi GLUT-4 pada membran sel yang dirangsang oleh kontraksi otot akan meningkatkan ambilan glukosa dan menurunkan glukosa darah. Kata kunci: resistensi insulin; latihan fisik; jalur sinyal insulin

scholarly journals Potential Role of Protein Kinase B in Glucose Transporter 4 Translocation in Adipocytes*

Endocrinology ◽  
1997 ◽  
Vol 138 (5) ◽  
pp. 2005-2010 ◽  
Author(s):  
Jean-François Tanti ◽  
Sophie Grillo ◽  
Thierry Grémeaux ◽  
Paul J. Coffer ◽  
Emmanuel Van Obberghen ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Cell Surface ◽  
Okadaic Acid ◽  
Potential Role ◽  
Glucose Transporter ◽  
Protein Kinase B ◽  
Glucose Transporter 4 ◽  
Glut 4 ◽  
Glut 4 Translocation

Abstract Phosphatidylinositol 3-kinase (PI 3-kinase) activation promotes glucose transporter 4 (Glut 4) translocation in adipocytes. In this study, we demonstrate that protein kinase B, a serine/threonine kinase stimulated by PI 3-kinase, is activated by both insulin and okadaic acid in isolated adipocytes, in parallel with their effects on Glut 4 translocation. In 3T3-L1 adipocytes, platelet-derived growth factor activated PI 3-kinase as efficiently as insulin but was only half as potent as insulin in promoting protein kinase B (PKB) activation. To look for a potential role of PKB in Glut 4 translocation, adipocytes were transfected with a constitutively active PKB (Gag-PKB) together with an epitope tagged transporter (Glut 4 myc). Gag-PKB was associated with all membrane fractions, whereas the endogenous PKB was mostly cytosolic. Expression of Gag-PKB led to an increase in Glut 4 myc amount at the cell surface. Our results suggest that PKB could play a role in promoting Glut 4 appearance at the cell surface following exposure of adipocytes to insulin and okadaic acid stimulation.

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