495-P: Kidney May Regulate SGLT2-Dependent Glucose Reabsorption through Sweet Taste Receptors: Implications for Diabetes

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 495-P
Author(s):  
LUPING ZHOU ◽  
WEI HUANG ◽  
NAN LIU ◽  
XIU M. MA ◽  
MAN GUO ◽  
...  
2013 ◽  
Vol 183 (2) ◽  
pp. 606-611 ◽  
Author(s):  
Rizwan M. Chaudhry ◽  
Alok Garg ◽  
Mohamed M. Abdelfatah ◽  
Judith A. Duenes ◽  
Michael G. Sarr

Cell ◽  
2001 ◽  
Vol 106 (3) ◽  
pp. 381-390 ◽  
Author(s):  
Greg Nelson ◽  
Mark A. Hoon ◽  
Jayaram Chandrashekar ◽  
Yifeng Zhang ◽  
Nicholas J.P. Ryba ◽  
...  

Nutrients ◽  
2017 ◽  
Vol 9 (7) ◽  
pp. 653 ◽  
Author(s):  
Allen Lee ◽  
Chung Owyang

Obesity Facts ◽  
2019 ◽  
Vol 12 (2) ◽  
pp. 190-198 ◽  
Author(s):  
Ri Lu Feng ◽  
Cheng Qian ◽  
Lian Yong Liu ◽  
Qian Jing Liu ◽  
Yun Qiu Jin ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Menizibeya O. Welcome ◽  
Nikos E. Mastorakis ◽  
Vladimir A. Pereverzev

Sweet taste receptors are transmembrane protein network specialized in the transmission of information from special “sweet” molecules into the intracellular domain. These receptors can sense the taste of a range of molecules and transmit the information downstream to several acceptors, modulate cell specific functions and metabolism, and mediate cell-to-cell coupling through paracrine mechanism. Recent reports indicate that sweet taste receptors are widely distributed in the body and serves specific function relative to their localization. Due to their pleiotropic signaling properties and multisubstrate ligand affinity, sweet taste receptors are able to cooperatively bind multiple substances and mediate signaling by other receptors. Based on increasing evidence about the role of these receptors in the initiation and control of absorption and metabolism, and the pivotal role of metabolic (glucose) regulation in the central nervous system functioning, we propose a possible implication of sweet taste receptor signaling in modulating cognitive functioning.


Endocrinology ◽  
2014 ◽  
Vol 155 (6) ◽  
pp. 2112-2121 ◽  
Author(s):  
George A. Kyriazis ◽  
Kathleen R. Smith ◽  
Björn Tyrberg ◽  
Tania Hussain ◽  
Richard E. Pratley

β-Cells rapidly secrete insulin in response to acute increases in plasma glucose but, upon further continuous exposure to glucose, insulin secretion progressively decreases. Although the mechanisms are unclear, this mode of regulation suggests the presence of a time-dependent glucosensory system that temporarily attenuates insulin secretion. Interestingly, early-stage β-cell dysfunction is often characterized by basal (ie, fasting) insulin hypersecretion, suggesting a disruption of these related mechanisms. Because sweet taste receptors (STRs) on β-cells are implicated in the regulation of insulin secretion and glucose is a bona fide STR ligand, we tested whether STRs mediate this sensory mechanism and participate in the regulation of basal insulin secretion. We used mice lacking STR signaling (T1R2−/− knockout) and pharmacologic inhibition of STRs in human islets. Mouse and human islets deprived of STR signaling hypersecrete insulin at short-term fasting glucose concentrations. Accordingly, 5-hour fasted T1R2−/− mice have increased plasma insulin and lower glucose. Exposure of isolated wild-type islets to elevated glucose levels reduced STR expression, whereas islets from diabetic (db/db) or diet-induced obese mouse models show similar down-regulation. This transcriptional reprogramming in response to hyperglycemia correlates with reduced STR function in these mouse models, leading to insulin hypersecretion. These findings reveal a novel mechanism by which insulin secretion is physiologically regulated by STRs and also suggest that, during the development of diabetes, STR function is compromised by hyperglycemia leading to hyperinsulinemia. These observations further suggest that STRs might be a promising therapeutic target to prevent and treat type 2 diabetes.


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