Sodium‐glucose co‐transporter ( SGLT ) and glucose transporter ( GLUT ) expression in the kidney of type 2 diabetic subjects

2017 ◽  
Vol 19 (9) ◽  
pp. 1322-1326 ◽  
Author(s):  
Luke Norton ◽  
Christopher E. Shannon ◽  
Marcel Fourcaudot ◽  
Cheng Hu ◽  
Niansong Wang ◽  
...  
Keyword(s):  
Glucose Transporter ◽  
Type 2 Diabetic ◽  
Glut Expression

scholarly journals Serum from Jiao-Tai-Wan treated rats increases glucose consumption by 3T3-L1 adipocytes through AMPK pathway signaling

2019 ◽  
Vol 39 (4) ◽  
Author(s):  
Lin Yuan ◽  
Peng Tang ◽  
Hui-Jiao Li ◽  
Na Hu ◽  
Xiao-Yu Zhong ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Glucose Transporter ◽  
Glucose Consumption ◽  
Diabetic Mouse ◽  
Rat Serum ◽  
Insulin Resistant ◽  
Ampk Pathway ◽  
Compound C ◽  
Type 2 Diabetic

Abstract Type 2 diabetes (T2DM) is characterized by hyperglycemia resulting from insulin resistance. Jiao-Tai-Wan (JTW), a traditional Chinese medicine consisting of a 10:1 formulation of Rhizoma Coptidis (RC) and Cortex Cinnamomi (cinnamon) was shown to have hypoglycemic efficacy in a type 2 diabetic mouse model. Here we investigated whether glucose consumption by insulin-resistant adipocytes could be modulated by serum from JTW-treated rats, and if so, through what mechanism. JTW-medicated serum was prepared from rats following oral administration of JTW decoction twice a day for 4 days. Fully differentiated 3T3-L1 adipocytes – rendered insulin resistance by dexamethasone treatment – were cultured in medium containing JTW-medicated rat serum. JTW-medicated serum treatment increased glucose uptake, up-regulated levels of phosphorylated adenosine 5′-monophoshate-activated protein kinase (p-AMPK), and stimulated expression and translocation of glucose transporter 4 (GLUT4). JTW-medicated serum induced significantly greater up-regulation of p-AMPK and GLUT4 than either RC or cinnamon-medicated serum. JTW-medicated serum induced effects on 3T3-L1 adipocytes could be partially inhibited by treatment with the AMPK inhibitor compound C. In conclusion, JTW-medicated serum increased glucose consumption by IR adipocytes partially through the activation of the AMPK pathway, and JTW was more effective on glucose consumption than either RC or cinnamon alone.

scholarly journals Effect of β-sitosterol on Insulin Receptor, Glucose Transporter 4 Protein Expression and Glucose Oxidation in the Gastrocnemius Muscle of High Fat Diet Induced Type -2 Diabetic Experimental Rats

2021 ◽  
Vol 55 (2s) ◽  
pp. s479-s491
Author(s):  
Madhan Krishnan ◽  
Shyamaladevi Babu ◽  
Ponnulakshmi Rajagopal ◽  
Sohara Parveen Nazar ◽  
Mayilvanan Chinnaiyan ◽  
...  
Keyword(s):  
Protein Expression ◽  
Insulin Receptor ◽  
High Fat Diet ◽  
Glucose Oxidation ◽  
Gastrocnemius Muscle ◽  
Glucose Transporter ◽  
Glucose Transporter 4 ◽  
High Fat ◽  
Type 2 Diabetic

scholarly journals Magnesium upregulates insulin receptor and glucose transporter-4 in streptozotocin-nicotinamide-induced type-2 diabetic rats

2018 ◽  
Vol 52 (1) ◽  
pp. 6-16 ◽  
Author(s):  
Ayodele Olufemi Morakinyo ◽  
Titilola Aderonke Samuel ◽  
Daniel Abiodun Adekunbi
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Glucose Transporter ◽  
Diabetic Rats ◽  
Glucose Transporter 4 ◽  
Magnesium Supplementation ◽  
Glucose Levels ◽  
Type 2 Diabetic

Abstract Objective. We investigated the effects of magnesium supplementation on glucose tolerance, insulin sensitivity, oxidative stress as well as the concentration of insulin receptor and glucose transporter-4 in streptozotocin-nicotinamide induced type-2 diabetic (T2D) rats. Methods. Rats were divided into four groups designated as: 1) control (CTR); 2) diabetic untreated (DU); 3) diabetic treated with 1 mg of Mg/kg diet (Mg1-D); and 4) diabetic treated with 2 mg of Mg/kg diet (Mg2-D). T2D was induced with a single intraperitoneal (i.p.) injection of freshly prepared streptozotocin (55 mg/kg) aft er an initial i.p. injection of nicotinamide (120 mg/kg). Glucose tolerance, insulin sensitivity, lipid profile, malondialdehyde (MAD) and glutathione content, insulin receptors (INSR) and glucose transporter-4 (GLUT4), fasting insulin and glucose levels were measured, and insulin resistance index was calculated using the homeostatic model assessment of insulin resistance (HOMA-IR). Results. Magnesium supplementation improved glucose tolerance and lowered blood glucose levels almost to the normal range. We also recorded a noticeable increase in insulin sensitivity in Mg-D groups when compared with DU rats. Lipid perturbations associated T2D were significantly attenuated by magnesium supplementation. Fasting glucose level was comparable to control values in the Mg-D groups while the HOMA-IR index was significantly lower compared with the DU rats. Magnesium reduced MDA but increased glutathione concentrations compared with DU group. Moreover, INSR and GLUT4 levels were elevated following magnesium supplementation in T2D rats. Conclusion. These findings demonstrate that magnesium may mediate effective metabolic control by stimulating the antioxidant defense, and increased levels of INSR and GLUT4 in diabetic rats.

Daidzein promotes glucose uptake through glucose transporter 4 translocation to plasma membrane in L6 myocytes and improves glucose homeostasis in Type 2 diabetic model mice

2014 ◽  
Vol 25 (2) ◽  
pp. 136-143 ◽  
Author(s):  
Sun Hee Cheong ◽  
Keisuke Furuhashi ◽  
Katsuki Ito ◽  
Masato Nagaoka ◽  
Takayuki Yonezawa ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Glucose Uptake ◽  
Glucose Homeostasis ◽  
Glucose Transporter ◽  
Glucose Transporter 4 ◽  
Diabetic Model ◽  
Type 2 Diabetic ◽  
L6 Myocytes

scholarly journals Activation of the cardiac non-neuronal cholinergic system prevents the development of diabetes-associated cardiovascular complications

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Eng Leng Saw ◽  
James T. Pearson ◽  
Daryl O. Schwenke ◽  
Pujika Emani Munasinghe ◽  
Hirotsugu Tsuchimochi ◽  
...  
Keyword(s):  
Vascular Function ◽  
Cholinergic System ◽  
Glucose Transporter ◽  
Immunoblot Analysis ◽  
Diabetic Heart ◽  
Mouse Heart ◽  
Glucose Content ◽  
Glut 4 ◽  
Type 2 Diabetic

Abstract Background Acetylcholine (ACh) plays a crucial role in the function of the heart. Recent evidence suggests that cardiomyocytes possess a non-neuronal cholinergic system (NNCS) that comprises of choline acetyltransferase (ChAT), choline transporter 1 (CHT1), vesicular acetylcholine transporter (VAChT), acetylcholinesterase (AChE) and type-2 muscarinic ACh receptors (M2AChR) to synthesize, release, degrade ACh as well as for ACh to transduce a signal. NNCS is linked to cardiac cell survival, angiogenesis and glucose metabolism. Impairment of these functions are hallmarks of diabetic heart disease (DHD). The role of the NNCS in DHD is unknown. The aim of this study was to examine the effect of diabetes on cardiac NNCS and determine if activation of cardiac NNCS is beneficial to the diabetic heart. Methods Ventricular samples from type-2 diabetic humans and db/db mice were used to measure the expression pattern of NNCS components (ChAT, CHT1, VAChT, AChE and M2AChR) and glucose transporter-4 (GLUT-4) by western blot analysis. To determine the function of the cardiac NNCS in the diabetic heart, a db/db mouse model with cardiac-specific overexpression of ChAT gene was generated (db/db-ChAT-tg). Animals were followed up serially and samples collected at different time points for molecular and histological analysis of cardiac NNCS components and prosurvival and proangiogenic signaling pathways. Results Immunoblot analysis revealed alterations in the components of cardiac NNCS and GLUT-4 in the type-2 diabetic human and db/db mouse hearts. Interestingly, the dysregulation of cardiac NNCS was followed by the downregulation of GLUT-4 in the db/db mouse heart. Db/db-ChAT-tg mice exhibited preserved cardiac and vascular function in comparison to db/db mice. The improved function was associated with increased cardiac ACh and glucose content, sustained angiogenesis and reduced fibrosis. These beneficial effects were associated with upregulation of the PI3K/Akt/HIF1α signaling pathway, and increased expression of its downstream targets—GLUT-4 and VEGF-A. Conclusion We provide the first evidence for dysregulation of the cardiac NNCS in DHD. Increased cardiac ACh is beneficial and a potential new therapeutic strategy to prevent or delay the development of DHD.

Sign in / Sign up

Export Citation Format

Share Document