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How do Leptin Levels and Gene Variants affect Sensitivity to Sweets?

A study examined if salivary leptin levels and variations in sweet taste-receptor genes were involved in sweet taste sensitivity and satiety.

Taste plays an important role in the preference for certain foods and the magnitude of food intake. Moreover, taste sensitivity can vary widely among individuals. For instance, people who have high oral sensitivity to fatty acids tend to consume fewer fats and energy dense foods.1-4 However, little is known about the effects of sweet taste sensitivity on sweet food intake. Also not known is whether sweet food sensitivity influences the loss of appetite for previously eaten foods (called sensory-specific satiety).

A recent study attempted to delineate the relationship between sweet taste sensitivity and food intake.5 The study also checked if the relationship between sweet taste sensitivity and food intake was influenced by serum leptin levels. Leptin is a hormone that regulates hunger and satiety. Finally, it examined if polymorphisms or variations in sweet taste receptor genes influenced food intake. The researchers published their results in the British Journal of Nutrition.

Sweet Taste Sensitivity Test

A total of 30 adults recruited from the students and staff at the University of Queensland participated in the study. Researchers used an eating questionnaire to obtain information about the participants’ eating behaviors. The sweet taste sensitivity of the participants was judged by providing them with three samples: two samples with pure water and a third containing 9 millimolar of sucrose. The participants who correctly identified the sucrose solution out of the three samples in three independent sessions were deemed highly sensitive, whereas the rest were grouped as having low sensitivity.

Eating Behavior Test

The participants were also subjected to an eating behavior test. This involved the participants being randomly offered one of three soups during three independent sessions: sweet, umami taste (control), or no-taste energy (also control). After consuming soup, the participants ate a buffet meal, which 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 calculated by asking the participants to score their liking and wanting for the sweet and non-sweet soups before and after soup consumption. Other parameters that were scored included perceived appetite, desire to eat, and prospective consumption: these were determined at various times before and after soup consumption and after meal consumption.

The researchers also collected samples of saliva at various time points to determine salivary leptin levels. They also collected buccal cell samples, which were used to determine the variants within TAS1R2 and TAS1R3, the two genes associated with sweet taste sensitivity and sugar intake.

Based on the taste sensitivity test, 19 participants were highly sensitive, while the rest had low sensitivity. Additionally, leptin levels were significantly higher in the low sensitivity group compared to the high sensitivity group.

Study Results

With regards to sweet sensitivity and food intake, the high sensitivity group consumed more non-sweet foods, and more protein and fewer carbohydrates as a percentage of total energy intake compared to the low sensitivity group. Moreover, the high sensitivity group had higher sweet sensory-specific satiety scores compared to the low sensitivity group. However, parameters such as perceived appetite, desire to eat, and prospective consumption were not affected by sweet sensitivity.

No correlations were observed between variations in the TAS1R2 and TAS1R3 genes and sweet taste sensitivity. However, one allele (variant) at a specific site in the TAS1R2 gene was associated with a higher consumption of carbohydrates as a percentage of the total energy intake, whereas another allele at a different site in the same gene was associated with higher consumption of sweet foods. No associations were found between different alleles of the TAS1R3 gene and food intake.

In summary, this study found an association between sweet taste sensitivity and carbohydrate and sweet food intake. Low sensitivity to sugars was associated with higher levels of the satiety hormone leptin, which then tells the brain to suppress food intake. The results also indicate a genetic basis underlying food consumption. Additional long-term studies involving more participants from diverse ethnic groups would be required to further our understanding of these processes.

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.

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