scholarly journals PHOSPHATIDYLINOSITOL -3KINASE (PI3K) DI PERBENIHAN ADIPOSIT YANG DIPAJAN GLUKOSA TINGGI DENGAN RETINOL

2018 ◽  
Vol 22 (2) ◽  
pp. 109
Author(s):  
Novi Khila Firani ◽  
Bambang Prijadi
Keyword(s):  
High Glucose ◽  
Glucose Transporter ◽  
Determination Method ◽  
Glucose Transporter 4 ◽  
Phosphatidylinositol 3 Kinase ◽  
Elisa Method ◽  
Glucose Levels ◽  
Glucose Exposure ◽  
The Mean

Retinol is one of the active forms of vitamin A. In the previous study, it was known that retinol level in serum of DM patient waslower than in healthy people, which correlated with an increase of the glucose levels in these patients. The importance of retinol in insulinsignaling mechanisms that play a role in the pathogenesis of DM is still unknown. One of the components that play a role in insulinsignaling on adipocytes is phosphatidylinositol-3 kinase (PI3K), which encourages the translocation of glucose transporter-4 (GLUT4) tothe cell surface. The aim of this study was to know the importance of retinol therapy in the levels of PI3K enzyme on visceral adipocyteculture with high glucose exposure (25 mM) as a model of DM in vitro by determination method. Retinol therapy was given at a doseof 0.1 μM, 1 μM , and 10 μM. Measurement of PI3K level was done by ELISA method. The mean (SD) levels of PI3K enzyme were 1.91(0.27), 0.94 (0.15), 1.98 (0.22), 1.69 (0.81), 2.04 (0.16) ng/mL respectively, for adipocyte cultures exposed to 5mM glucose (as aphysiological condition), 25mM glucose, and 25mM glucose concentration with doses of retinol therapy 0.1 μM, 1 μM and10 μM. Theresults of this study indicated that high glucose exposure (25 mM) decreased the level of PI3K compared with adipocyte’s culture on5 mM glucose exposure. Retinol therapy with a dose of 0.1μM, 1μM and10 μM on adipocyte culture exposed with high glucose couldincrease the levels of PI3K.

Normal Ca2+ extrusion by the Ca2+ pump of intact red blood cells exposed to high glucose concentrations

2001 ◽  
Vol 280 (6) ◽  
pp. C1449-C1454 ◽  
Author(s):  
Julia E. Raftos ◽  
Amanda Edgley ◽  
Robert M. Bookchin ◽  
Zipora Etzion ◽  
Virgilio L. Lew ◽  
...  
Keyword(s):  
High Glucose ◽  
Diabetic Rats ◽  
Maximal Velocity ◽  
Glucose Levels ◽  
Normal Human ◽  
Streptozotocin Diabetic Rats ◽  
The Mean ◽  
Human Rbcs

The ATPase activity of the plasma membrane Ca2+ pump (PMCA) has been reported to be inhibited by exposure of red blood cell (RBC) PMCA preparations to high glucose concentrations. It has been claimed that this effect could have potential pathophysiological relevance in diabetes. To ascertain whether high glucose levels also affect PMCA transport function in intact RBCs, Ca2+extrusion by the Ca2+-saturated pump [PMCA maximal velocity ( V max)] was measured in human and rat RBCs exposed to high glucose in vivo or in vitro. Preincubation of normal human RBCs in 30–100 mM glucose for up to 6 h had no effect on PMCA V max. The mean V max of RBCs from 15 diabetic subjects of 12.9 ± 0.7 mmol · 340 g Hb−1 · h−1 was not significantly different from that of controls (14.3 ± 0.5 mmol · 340 g Hb−1 · h−1). Similarly, the PMCA V max of RBCs from 11 streptozotocin-diabetic rats was not affected by plasma glucose levels more than three times normal for 6–8 wk. Thus exposure to high glucose concentrations does not affect the ability of intact RBCs to extrude Ca2+.

scholarly journals Live imaging of GLUT2 glucose-dependent trafficking and its inhibition in polarized epithelial cysts

Open Biology ◽  
2014 ◽  
Vol 4 (7) ◽  
pp. 140091 ◽  
Author(s):  
Merav Cohen ◽  
Daniel Kitsberg ◽  
Sabina Tsytkin ◽  
Maria Shulman ◽  
Benjamin Aroeti ◽  
...  
Keyword(s):  
Subcellular Localization ◽  
Glucose Transporter ◽  
Critical Role ◽  
Live Imaging ◽  
Glucose Absorption ◽  
Recycling Endosome ◽  
Physiological Importance ◽  
Glucose Levels ◽  
Glucose Reabsorption ◽  
Glucose Exposure

GLUT2 is a facilitative glucose transporter, expressed in polarized epithelial cells of the liver, intestine, kidney and pancreas, where it plays a critical role in glucose homeostasis. Together with SGLT1/2, it mediates glucose absorption in metabolic epithelial tissues, where it can be translocated apically upon high glucose exposure. To track the subcellular localization and dynamics of GLUT2, we created an mCherry–hGLUT2 fusion protein and expressed it in multicellular kidney cysts, a major site of glucose reabsorption. Live imaging of GLUT2 enabled us to avoid the artefactual localization of GLUT2 in fixed cells and to confirm the apical GLUT2 model. Live cell imaging showed a rapid 15 ± 3 min PKC-dependent basal-to-apical translocation of GLUT2 in response to glucose stimulation and a fourfold slower basolateral translocation under starvation. These results mark the physiological importance of responding quickly to rising glucose levels. Importantly, we show that phloretin, an apple polyphenol, inhibits GLUT2 translocation in both directions, suggesting that it exerts its effect by PKC inhibition. Subcellular localization studies demonstrated that GLUT2 is endocytosed through a caveolae-dependent mechanism, and that it is at least partly recovered in Rab11A-positive recycling endosome. Our work illuminates GLUT2 dynamics, providing a platform for drug development for diabetes and hyperglycaemia.

scholarly journals The Intracellular Growth of M. tuberculosis Is More Associated with High Glucose Levels Than with Impaired Responses of Monocytes from T2D Patients

2019 ◽  
Vol 2019 ◽  
pp. 1-10
Author(s):  
Martha Torres ◽  
María Teresa Herrera ◽  
Guadalupe Fabián-San-Miguel ◽  
Yolanda Gonzalez
Keyword(s):  
High Glucose ◽  
Healthy Subjects ◽  
Intrinsic Factor ◽  
Growth Control ◽  
Intracellular Growth ◽  
Glucose Levels ◽  
Basal Expression ◽  
Ligand Stimulation

Diabetes mellitus, a metabolic disease characterized by hyperglycemia and poor glucose control, is a risk factor for Mycobacterium tuberculosis (M. tuberculosis) infection and the development of active tuberculosis. To evaluate whether M. tuberculosis infection susceptibility is associated with an intrinsic factor in monocytes from type 2 diabetes (T2D) patients or it is associated with hyperglycemia per se, we analyzed TLR-2 and TLR-4 expression by flow cytometry and the cytokines IL-1β, IL-6, IL-8, IL-10, and TNF-α by cytometric bead array assays, either stimulated with TLR-2 and TLR-4 ligands or infected with M. tuberculosis in the whole blood from T2D patients (n=43) and healthy subjects (n=26) or in CD14+ monocytes from healthy subjects cultured in high glucose (HG) (30 mM). The intracellular growth of M. tuberculosis was evaluated by CFU counts at 0, 1, and 3 days in both monocytes from T2D patients and monocytes from healthy subjects cultured in HG. We did not find significant differences in TLR expression, cytokine production, or growth of M. tuberculosis in monocytes from T2D patients compared with those in monocytes from healthy subjects. Despite these results, in vitro assays of monocytes cultured with 30 mM glucose led to significantly increased TLR-2 and TLR-4 basal expression compared to those of monocytes cultured with 11 mM glucose (P<0.05). Conversely, the production of IL-6 by TLR-2 ligand stimulation, of IL-1β, IL-6, and IL-8 by TLR-4 ligand stimulation, and of IL-8 by M. tuberculosis infection significantly decreased in monocytes cultured in HG (P<0.05). Additionally, the intracellular survival of M. tuberculosis increased in monocytes in HG after day 3 of culture (P<0.05). In conclusion, HG decreased IL-8 production and the intracellular growth control of M. tuberculosis by monocytes, supporting the hypothesis that hyperglycemia plays an important role in the impaired immune responses to M. tuberculosis in patients with T2D.

scholarly journals Elevated glucose acts directly on osteocytes to increase sclerostin expression in diabetes

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Donna M. Pacicca ◽  
Tammy Brown ◽  
Dara Watkins ◽  
Karen Kover ◽  
Yun Yan ◽  
...  
Keyword(s):  
Bone Quality ◽  
High Glucose ◽  
Negative Impact ◽  
Negative Regulator ◽  
Diabetic Rat ◽  
Diabetic Patients ◽  
Bone Homeostasis ◽  
Glucose Levels ◽  
Elevated Glucose

AbstractBone quality in diabetic patients is compromised, leading to weaker bones and increased fracture risk. However, the mechanism by which this occurs in diabetic bone remains to be fully elucidated. We hypothesized that elevated glucose and glucose variation would affect the function of osteocytes, essential regulators of bone homeostasis and quality. To first test this hypothesis, we used the IDG-SW3 osteocyte-like cell line to examine the effects of glucose levels on osteocyte function and viability in vitro. We confirmed our in vitro findings using the in vivo streptozotocin-induced (STZ) diabetic rat model and ex-vivo cultured osteocytes from these rats. IDG-SW3 cells cultured under high glucose conditions displayed significantly increased Sost mRNA(100-fold) and sclerostin protein, a negative regulator of bone formation(5000-fold), compared to cells in control media. mRNA expression of osteoblast markers such as Osx, Ocn and Col1a1 was unaffected by glucose. Factors associated with osteoclast activation were affected by glucose, with Rankl being upregulated by low glucose. Opg was also transiently upregulated by high glucose in mature IDG-SW3 cells. Induction of diabetes in Sprague-Dawley rats via a single dose of STZ (70 mg/kg) resulted in elevated maximum glucose and increased variability compared to control animals (670/796 vs. 102/142 mg/dL). This was accompanied by increased Sost/sclerostin expression in the osteocytes of these animals. These results show that glucose levels directly regulate osteocyte function through sclerostin expression and suggest a potential mechanism for the negative impact of diabetes on bone quality.

scholarly journals Gene expression of epithelial glucose transporters: the role of diabetes mellitus.

1994 ◽  
Vol 5 (5) ◽  
pp. S29
Author(s):  
J H Dominguez ◽  
B Song ◽  
L Maianu ◽  
W T Garvey ◽  
M Qulali
Keyword(s):  
Gene Expression ◽  
Diabetes Mellitus ◽  
Small Intestine ◽  
High Glucose ◽  
Glucose Transporter ◽  
Basolateral Membrane ◽  
Glucose Levels ◽  
Uncontrolled Diabetes ◽  
Extracellular Level

The functions of absorption of dietary glucose by the small intestine and reabsorption of filtered glucose by the renal proximal tubule are strikingly similar in their organization and in the way they adapt to uncontrolled diabetes mellitus. In both cases, transepithelial glucose and Na+ fluxes are augmented. The epithelial adaptations to hyperglycemia of uncontrolled diabetes are accomplished by increasing the glucose transport surface area and the number of the efflux glucose transporter GLUT2 located in the basolateral membrane. The signals that modify the size of the epithelium and the overexpression of basolateral GLUT2 are not known. It was speculated that high glucose levels and enhanced Na+ flux may be important factors in the signaling event that culminates in a renal and intestinal epithelium that is modified to transport higher rates of glucose against a higher extracellular level of glucose.

scholarly journals SENP3 regulates high glucose-induced endothelial dysfunction via ROS dependent signaling

2020 ◽  
Vol 17 (6) ◽  
pp. 147916412097089
Author(s):  
Fuheng Chen ◽  
Dongdong Ma ◽  
Aizhong Li
Keyword(s):  
Endothelial Dysfunction ◽  
High Glucose ◽  
Type I Diabetes ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Type I ◽  
Dependent Manner ◽  
Glucose Levels ◽  
And Migration

Background: The current study aimed to explore the role of SENP3 in endothelial cell dysfunction in a high-glucose setting. Methods: The gene and protein expressions of SENP3 in high-glucose cultured HAECs were examined using quantitative PCR and western blotting. The effects of SENP3 on HAEC viability, apoptosis, migration, and endothelial–monocyte adhesion were evaluated in vitro by knockdown. Moreover, a mouse streptozotocin-induced type I diabetes model was established for SENP3 expression assessment. In addition, the effects of SENP3 on ROS-related signaling pathways were investigated in high-glucose cultured HAECs. Results: Significantly increased levels of SENP3 mRNA and protein were found in high-glucose cultured HAECs in a time-dependent manner. SENP3 knockdown reversed high glucose-induced HAEC viability, apoptosis, and migration reduction. SENP3 knockdown attenuated the high glucose-induced intercellular adhesion of THP-1 monocytic cells and HAECs via downregulation of ICAM-1 and VCAM-1 expression. Increased levels of SENP3, ICAM-1, and VCAM-1 expression were observed in the aorta tissue of mice with type I diabetes. Downregulation of SENP3 expression was observed in HAECs cultured with high glucose levels using the free radical scavenger N-acetyl-L-cysteine or NOX4 siRNA. Conclusions: SENP3 was involved in high glucose-induced endothelial dysfunction, and ROS-dependent signaling served as the mechanism.

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