Leptin Levels and Gene Variants: Unraveling Their Impact on Sweet Sensitivity

Study on Sweet Taste Sensitivity, Leptin Levels, and Food Intake

Introduction

A recent study investigated the roles of salivary leptin levels and genetic variations in sweet taste receptors on sweet taste sensitivity and satiety. Taste is a critical factor influencing food preferences and consumption levels, with sensitivity varying among individuals. For example, those with heightened sensitivity to fatty acids typically consume lower amounts of fats and energy-dense foods. However, the impact of sweet taste sensitivity on the intake of sweet foods and its effect on sensory-specific satiety—defined as the loss of appetite for previously consumed foods—remains poorly understood.

Objectives of the Study

The study aimed to clarify the relationship between sweet taste sensitivity and food intake while assessing whether serum leptin levels influence this relationship. Leptin, a hormone that helps regulate hunger and satiety, was a focal point of the research. Additionally, the study examined how polymorphisms in sweet taste receptor genes might impact food intake, with findings published in the *British Journal of Nutrition*.

Methodology

A total of 30 adults, including students and staff from the University of Queensland, participated in the research. Participants completed an eating questionnaire to provide insights into their eating habits. To assess sweet taste sensitivity, they were presented with three samples: two with pure water and one containing 9 millimolar of sucrose. Those who accurately identified the sucrose solution across three sessions were classified as highly sensitive, while the others were deemed low sensitivity.

Eating Behavior Assessment

Participants underwent an eating behavior test where they were randomly assigned one of three soups during three separate sessions: sweet, umami (as a control), or a no-taste energy soup (also a control). Following the soup consumption, they were given access to a buffet meal that included four food categories: high-fat sweet food, low-fat sweet food, high-fat non-sweet food, and low-fat non-sweet food.

Sweet sensory-specific satiety was measured by asking participants to rate their liking and wanting for the soups before and after consumption. Other assessed parameters included perceived appetite, desire to eat, and prospective consumption at various intervals before and after soup and meal consumption. Additionally, saliva samples were collected at different times to measure salivary leptin levels, along with buccal cell samples to identify variants within the TAS1R2 and TAS1R3 genes, which are associated with sweet taste sensitivity and sugar intake.

Findings

From the taste sensitivity test, 19 participants were identified as having high sensitivity, while the remainder exhibited low sensitivity. Notably, leptin levels were significantly higher in the low sensitivity group compared to the high sensitivity group.

Regarding sweet sensitivity and food intake, the high sensitivity group consumed greater amounts of non-sweet foods, including more protein and fewer carbohydrates as a percentage of their total energy intake compared to the low sensitivity group. Additionally, the high sensitivity group reported higher sweet sensory-specific satiety scores. However, parameters such as perceived appetite, desire to eat, and prospective consumption did not vary with sweet sensitivity.

No correlations were found between variations in the TAS1R2 and TAS1R3 genes and sweet taste sensitivity. Nonetheless, one specific allele in the TAS1R2 gene was linked to a higher carbohydrate intake, while another allele was associated with increased consumption of sweet foods. No associations were noted for different alleles of the TAS1R3 gene with food intake.

Conclusion

In summary, the study identified a connection between sweet taste sensitivity and the intake of carbohydrates and sweet foods. Lower sensitivity to sugars correlated with higher levels of the satiety hormone leptin, which signals the brain to reduce food intake. The findings also suggest a genetic component influencing food consumption behaviors. Further long-term studies with a broader participant demographic, including diverse ethnic groups, are necessary to enhance our understanding of these relationships.

Author Information

Written by Usha B. Nair, Ph.D.

References

(1) Running CA, Craig BA, Mattes RD. Oleogustus: The Unique Taste of Fat. Chem Senses. 2015 Sep;40(7):507-16. doi: 10.1093/chemse/bjv036. Epub 2015 Jul 3. PubMed PMID: 26142421.
(2) Stewart JE, Feinle-Bisset C, Golding M, Delahunty C, Clifton PM, Keast RS. Oral sensitivity to fatty acids, food consumption and BMI in human subjects. Br J Nutr. 2010 Jul;104(1):145-52. doi: 10.1017/S0007114510000267. Epub 2010 Mar 3. PubMed PMID: 20196892.
(3) Stewart JE, Newman LP, Keast RS. Oral sensitivity to oleic acid is associated with fat intake and body mass index. Clin Nutr. 2011 Dec;30(6):838-44. doi: 10.1016/j.clnu.2011.06.007. Epub 2011 Jul 14. PubMed PMID: 21757270.
(4) Keast RS, Azzopardi KM, Newman LP, Haryono RY. Impaired oral fatty acid chemoreception is associated with acute excess energy consumption. Appetite. 2014 Sep;80:1-6. doi: 10.1016/j.appet.2014.04.022. Epub 2014 Apr 28. PubMed PMID: 24787499.
(5) Han P, Keast RSJ, Roura E. Salivary leptin and TAS1R2/TAS1R3 polymorphisms are related to sweet taste sensitivity and carbohydrate intake from a buffet meal in healthy young adults. Br J Nutr. 2017 Nov 7:1-8. doi: 10.1017/S0007114517002872. [Epub ahead of print] PubMed PMID: 29110749.