scholarly journals Disordered Control of Intestinal Sweet Taste Receptor Expression and Glucose Absorption in Type 2 Diabetes

Diabetes ◽  
2013 ◽  
Vol 62 (10) ◽  
pp. 3532-3541 ◽  
Author(s):  
R. L. Young ◽  
B. Chia ◽  
N. J. Isaacs ◽  
J. Ma ◽  
J. Khoo ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Taste Receptor ◽  
Sweet Taste ◽  
Glucose Absorption ◽  
Receptor Expression ◽  
Sweet Taste Receptor

Disordered Control of Intestinal Sweet Taste Receptor Expression in Type 2 Diabetes

2011 ◽  
Vol 140 (5) ◽  
pp. S-99-S-100
Author(s):  
Richard L. Young ◽  
Bridgette Chia ◽  
Jing Ma ◽  
Tongzhi Wu ◽  
Joan Khoo ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Taste Receptor ◽  
Sweet Taste ◽  
Receptor Expression ◽  
Sweet Taste Receptor

scholarly journals Sweet taste receptor expression in ruminant intestine and its activation by artificial sweeteners to regulate glucose absorption

2014 ◽  
Vol 97 (8) ◽  
pp. 4955-4972 ◽  
Author(s):  
A.W. Moran ◽  
M. Al-Rammahi ◽  
C. Zhang ◽  
D. Bravo ◽  
S. Calsamiglia ◽  
...  
Keyword(s):  
Taste Receptor ◽  
Sweet Taste ◽  
Glucose Absorption ◽  
Receptor Expression ◽  
Artificial Sweeteners ◽  
Sweet Taste Receptor

Expression of sweet taste receptor and gut hormone secretion in modelled type 2 diabetes

2017 ◽  
Vol 252 ◽  
pp. 142-149 ◽  
Author(s):  
Rilu Feng ◽  
Cheng Qian ◽  
Qianjing Liu ◽  
Yunqiu Jin ◽  
Lianyong Liu ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Hormone Secretion ◽  
Taste Receptor ◽  
Sweet Taste ◽  
Sweet Taste Receptor ◽  
Gut Hormone

scholarly journals Sweet Taste Is Complex: Signaling Cascades and Circuits Involved in Sweet Sensation

2021 ◽  
Vol 15 ◽  
Author(s):  
Elena von Molitor ◽  
Katja Riedel ◽  
Michael Krohn ◽  
Mathias Hafner ◽  
Rüdiger Rudolf ◽  
...  
Keyword(s):  
Alternative Pathway ◽  
Taste Receptor ◽  
Physiological Role ◽  
Primary Source ◽  
Sweet Taste ◽  
Receptor Expression ◽  
Taste Bud ◽  
Sweet Taste Receptor ◽  
The Brain ◽  
Taste Bud Cells

Sweetness is the preferred taste of humans and many animals, likely because sugars are a primary source of energy. In many mammals, sweet compounds are sensed in the tongue by the gustatory organ, the taste buds. Here, a group of taste bud cells expresses a canonical sweet taste receptor, whose activation induces Ca2+ rise, cell depolarization and ATP release to communicate with afferent gustatory nerves. The discovery of the sweet taste receptor, 20 years ago, was a milestone in the understanding of sweet signal transduction and is described here from a historical perspective. Our review briefly summarizes the major findings of the canonical sweet taste pathway, and then focuses on molecular details, about the related downstream signaling, that are still elusive or have been neglected. In this context, we discuss evidence supporting the existence of an alternative pathway, independent of the sweet taste receptor, to sense sugars and its proposed role in glucose homeostasis. Further, given that sweet taste receptor expression has been reported in many other organs, the physiological role of these extraoral receptors is addressed. Finally, and along these lines, we expand on the multiple direct and indirect effects of sugars on the brain. In summary, the review tries to stimulate a comprehensive understanding of how sweet compounds signal to the brain upon taste bud cells activation, and how this gustatory process is integrated with gastro-intestinal sugar sensing to create a hedonic and metabolic representation of sugars, which finally drives our behavior. Understanding of this is indeed a crucial step in developing new strategies to prevent obesity and associated diseases.

311 Altered Duodenal Sweet Taste Receptor Expression in Diabetic Hyperglycemia

2008 ◽  
Vol 134 (4) ◽  
pp. A-44
Author(s):  
Kate Sutherland ◽  
Stuart M. Brierley ◽  
Chris Rayner ◽  
Michael Horowitz ◽  
L. Ashley Blackshaw ◽  
...  
Keyword(s):  
Taste Receptor ◽  
Sweet Taste ◽  
Receptor Expression ◽  
Sweet Taste Receptor

scholarly journals Critically evaluating sweet taste receptor expression and signaling through a molecular pharmacology lens

FEBS Journal ◽  
2021 ◽  
Vol 288 (8) ◽  
pp. 2660-2672 ◽  
Author(s):  
Nicola J. Smith ◽  
Jennifer N. Grant ◽  
Justin I. Moon ◽  
Sean S. So ◽  
Angela M. Finch
Keyword(s):  
Taste Receptor ◽  
Sweet Taste ◽  
Receptor Expression ◽  
Molecular Pharmacology ◽  
Sweet Taste Receptor

scholarly journals 3-Deoxyglucosone Induces Glucagon-Like Peptide-1 Secretion from STC-1 Cells via Upregulating Sweet Taste Receptor Expression under Basal Conditions

2019 ◽  
Vol 2019 ◽  
pp. 1-10
Author(s):  
Xiudao Song ◽  
Fei Wang ◽  
Heng Xu ◽  
Guoqiang Liang ◽  
Liang Zhou ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Transient Receptor Potential ◽  
Taste Receptor ◽  
Sweet Taste ◽  
Receptor Expression ◽  
Oral Glucose ◽  
Intragastric Administration ◽  
Sweet Taste Receptor ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

3-Deoxyglucosone (3DG) is derived from D-glucose during food processing and storage and under physiological conditions. We reported that glucagon-like peptide-1 (GLP-1) secretion in response to an oral glucose load in vivo and high-glucose stimulation in vitro was decreased by acute 3DG administration. In this study, we determined the acute effect of 3DG on GLP-1 secretion under basal conditions and investigated the possible mechanisms. Normal fasting rats were given a single acute intragastric administration of 50 mg/kg 3DG. Plasma basal GLP-1 levels and duodenum 3DG content and sweet taste receptor expression were measured. STC-1 cells were acutely exposed to 3DG (80, 300, and 1000 ng/ml) for 1 h under basal conditions (5.6 mM glucose), and GLP-1 secretion, intracellular concentrations of cyclic adenosine monophosphate (cAMP) and Ca2+, and molecular expression of STR signaling pathway were measured. Under the fasted state, plasma GLP-1 levels, duodenum 3DG content, and duodenum STR expression were elevated in 3DG-treated rats. GLP-1 secretion was increased in 3DG-treated cells under either 5.6 mM glucose or glucose-free conditions. 3DG-induced acute GLP-1 secretion from STC-1 cells under 5.6 mM glucose was inhibited in the presence of the STR inhibitor lactisole, which was consistent with the observation under glucose-free conditions. Moreover, acute exposure to 3DG increased the protein expression of TAS1R2 and TAS1R3 under either 5.6 mM glucose or glucose-free conditions, with affecting other components of STR signaling pathway, including the upregulation of transient receptor potential channel type M5 TRPM5 and the increment of intracellular Ca2+ concentration. In summary, the glucose-free condition was used to first demonstrate the involvement of STR in 3DG-induced acute GLP-1 secretion. These results first showed that acute 3DG administration induces basal GLP-1 secretion in part through upregulation of STR expression.

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