Mount Sinai researchers have identified sweet-sensing taste receptors T1R3 and G protein gustducin in the human intestine. The discovery may lead to new treatments for obesity and diabetes.
The two taste receptors, which are critical to sweet taste in the tongue, are also expressed in specialized taste cells of the gut where they sense glucose within the intestine.
Advertisement
The small intestine is the major site where dietary sugars are absorbed into the body to provide energy, and maintain normal metabolism and homeostasis. If glucose is absorbed in excess obesity may occur.
As part of the studies titled 'T1R3 and gustducin in gut sense sugars to regulate expression of Na+-glucose cotransporter 1' and 'Gut-expressed gustducin and taste receptors regulate secretion of glucagon-like peptide-1', Robert F. Margolskee and colleagues reasoned that the sugar sensors of the tongue's taste buds might also be there in the gut.
The study found that T1R3 and gustducin, critical to sweet taste in the tongue, were also expressed in specialized taste cells of the gut where they sensed glucose within the intestine.
Researchers noted that carbohydrate ingested from meals and beverages broke down into glucose, which stimulated the sweet-sensing proteins in these gut taste cells. Activating the sweet-sensing proteins of the gut taste cells promoted secretion of glucagon-like peptide-1 (GLP-1), an intestinal hormone that plays a key role in promoting insulin secretion and regulating appetite.
"We now know that the receptors that sense sugar and artificial sweeteners are not limited to the tongue. Our work is an important advance for the new field of gastrointestinal chemosensation - how the cells of the gut detect and respond to sugars and other nutrients. Cells of the gut taste glucose through the same mechanisms used by taste cells of the tongue.
The gut taste cells regulate secretion of insulin and hormones that regulate appetite. Our work sheds new light on how we regulate sugar uptake from our diets and regulate blood sugar levels," Margolskee said.
The findings of the study were published online in the August ' "Early Edition' of the Proceedings of the National Academy of Sciences.
Source: ANI
LIN/J
Advertisement
The study found that T1R3 and gustducin, critical to sweet taste in the tongue, were also expressed in specialized taste cells of the gut where they sensed glucose within the intestine.
Researchers noted that carbohydrate ingested from meals and beverages broke down into glucose, which stimulated the sweet-sensing proteins in these gut taste cells. Activating the sweet-sensing proteins of the gut taste cells promoted secretion of glucagon-like peptide-1 (GLP-1), an intestinal hormone that plays a key role in promoting insulin secretion and regulating appetite.
"We now know that the receptors that sense sugar and artificial sweeteners are not limited to the tongue. Our work is an important advance for the new field of gastrointestinal chemosensation - how the cells of the gut detect and respond to sugars and other nutrients. Cells of the gut taste glucose through the same mechanisms used by taste cells of the tongue.
The gut taste cells regulate secretion of insulin and hormones that regulate appetite. Our work sheds new light on how we regulate sugar uptake from our diets and regulate blood sugar levels," Margolskee said.
The findings of the study were published online in the August ' "Early Edition' of the Proceedings of the National Academy of Sciences.
Source: ANI
LIN/J
Advertisement
Advertisement
|
Advertisement
Latest Research News
South Korea's total fertility rate, averaging the number of children a woman aged 15-49 has in her lifetime, dropped to 0.81.
Scientists identified mechanisms governing immune cells, selectively removing troublemakers to reshape skin immunity. Benefits those with psoriasis, vitiligo.
By 2050, an anticipated increase from 494 million cases in 2020 to 1.06 billion people with musculoskeletal disabilities is expected.
Experts consulted by GlobalData anticipate a significant overhaul in the Gaucher disease scenario because of forthcoming gene therapies in development.
Within the seven major markets, 12% to 20% of diagnosed prevalent NASH cases present severe liver damage (stage 4 liver fibrosis), denoting cirrhosis.