In a 2017 study, researchers investigated the role of sweet taste receptors in the tongue and gastrointestinal system in the regulation of blood sugar. The study found that blocking sweet taste receptors increases insulin and C-peptide levels after sugar consumption.
It is currently unclear how sweet taste receptor (STR) activation influences blood sugar through regulation of hormones such as insulin, which lowers blood sugar levels, and glucagon, which raises it. As STRs in the tongue and small intestine are sensitive to the basic sugar glucose and to non-caloric artificial sweeteners (NCAS), an improved understanding of the role STR activation plays in the control of blood sugar may have significant implications for the treatment and management of conditions such as diabetes and obesity.
In a 2017 study published in the American Journal of Clinical Nutrition, researchers investigated the role of STRs in the regulation of sugar and hormone levels after sugar consumption. Young, lean, healthy, non-diabetic individuals who consumed less than a spoonful of NCAS or a can of a diet beverage weekly were recruited for the study. Pregnant or nursing women, those who had smoked within the last 3 months, on medications known to affect heart, immune, or metabolic function, who were hypersensitive to the study treatments, or who had medical complications making blood collection difficult were excluded.
Participants were given 60 mL of water alone, 60 mL of water with 300 ppm of the NCAS saccharin (which stimulates STRs), or 60 mL of water with 300 ppm saccharin and 500 ppm lactisole (which inhibits STRs). Ten minutes later, participants were then administered 75 g of a glucose solution with or without 500 ppm lactisole. The glucose solution also contained 3.0 g of 3-O-methylglucose (3OM) and 1.4 g of acetaminophen (Tylenol) to allow estimation of glucose absorption and stomach emptying, respectively. As such, there were 4 treatment groups: water plus glucose(treatment 1), water with lactisole plus glucose with lactisole(treatment 2), water with saccharin plus glucose (treatment 3), and water with saccharin and lactisole plus glucose with lactisole. Participants were instructed not to ingest any NCAS or Tylenol other than what was provided to them for the duration of the study. Blood samples were collected 15, 10, and 2 minutes before and 30, 45, 60, 90, 120, 150, and 180 minutes after glucose ingestion in order to measure blood levels of sugar, 3OM, acetaminophen, glucagon, insulin, the insulin precursor C-peptide, and the incretinsGLP-1, GLP-2, and gastric inhibitory peptide (GIP), which are associated with increased insulin secretion.
Overall, 10 participants completed the study. Treatment with the STR-inhibitor lactisole was found to increase levels of insulin and C-peptide after consumption of the glucose solution, except in those also given saccharin. Treatment with lactisole also reduced insulin sensitivity after consuming the glucose solution according to Stumvoll’s insulin sensitivity index, regardless of whether saccharin was taken beforehand. The insulinogenic, β-cell glucose-stimulated insulin dose response, and β-cell potentiation of insulin secretion indexes did not register any significant changes in the activity of the insulin-producing β-cells of the pancreas. Further, no effects on glucagon, GLP-1, GLP-2, or GIP levels were observed. The rate of glucose absorption, measured by changes in 3OM levels, and stomach emptying, measured by changes in acetaminophen levels, remained unaffected by treatment.
The findings suggest that sweet taste receptors in the tongue and small intestine are involved in the regulation of blood sugar control. Blocking sweet taste receptors increased insulin and C-peptide levels, without affecting the activity of β-cells, rate of stomach emptying or glucose absorption, and glucagon or incretins levels. These results suggest that STRs may suppress insulin through an unknown mechanism. Further research with a larger study population examined over a longer period of time, exploring the relative contributions of STR input from different sources – i.e. STRs in the tongue versus the small intestine – and with different degrees of stimulation and inhibition may provide important insight into their value as therapeutic targets for the treatment of conditions such as obesity and diabetes.
Written By: Raishard Haynes, MBS