During the last decades, obesity has become one of the major health issues for our civilization with its increasing prevalence in all age groups. According to WHO, there are more than 1.9 billion obese adults and 42 million overweight young children worldwide [1
]. It is generally accepted that obesity is influenced by environmental and genetic factors [2
]. However, one of the key factors is also an excess of fat in our diet which, associated with the lack of physical activity, leads to an increase in body mass index (BMI) [3
]. Dietary fat provides more than twofold energy compared to proteins and carbohydrates, thus high consumption of lipids would worsen obesity and result into several pathologies like atherosclerosis, hypertension, and some other diseases [3
Dietary fat is mainly perceived by its textural properties [5
]. Nevertheless, growing evidences indicate the existence of another factor, i.e
., taste for fat, which could play a role in the attraction for dietary lipids [6
]. There are two main long-chain fatty acid receptors, i.e.
, CD36 and GPR120, which play a role in the gustatory detection of lipids. The CD36 (also known as FAT, fatty acid translocase) belongs to the scavenger receptor family, and is known to bind to various ligands such as thrombospondin-1, oxidized low-density lipoproteins, growth hormone (GH)-releasing peptides and also dietary fatty acids [7
]. The GPR120 belongs to the G-protein-coupled receptor (GPCR) family and is expressed in human and rodent taste bud cells [8
]. Recent studies conducted on animal models and in vitro
cell cultures showed possible alternative roles of GPR120 and CD36 in oral fat sensing. Hence, GPR120 seems to play a role in post-prandial regulation, whereas CD36 serves as a primary fat taste sensor in the lingual epithelium [6
It has been previously shown that a single nucleotide polymorphism (SNP) rs1761667 of CD36
gene, located in the 5’ flanking exon 1A area [10
], is associated with the decreased expression of CD36 protein [12
]. This CD36
gene polymorphism has been associated with some pathologies like coronary artery disease [10
] and type 2 diabetes mellitus [14
]. Besides, rs1761667 polymorphism has been shown to influence gustatory perception of dietary lipids in humans. The first evidence of the impact of rs1761667 polymorphism on oral fat sensing was reported by Pepino et al.
] who showed that A-allele is associated with decreased oro-gustatory detection of oleic acid in some Afro-American obese subjects. We recently conducted a study on obese Tunisian women and showed that the participants with A-allele of rs1761667 polymorphism exhibited decreased oral sensitivity (high thresholds) to oleic acid [16
]. In another study conducted on young Algerian children age seven to eight, we have observed higher A-allele frequency of rs1761667 polymorphism in obese children compared to leans [17
]. As expected, the obese young children exhibited higher detection threshold for oleic acid than lean participants [17
]. Moreover, in the recent study Melis et al.
] have shown that high expression of CD36
(influenced by rs1761667) may by the determining factor for oral detecting of dietary fat predominantly in subjects with the low density of taste papillae.
The early period of childhood and adolescence is critical for the development of obesity in the later stage of life. It has been shown that young obese teenagers, predominantly males, are unable to return to the normal healthy state [19
]. Risk factors for childhood obesity include parental fatness, social status, birth weight, timing or rate of growth, physical activity, dietary factors, and other behavioral or psychological factors [20
]. Childhood obesity has been shown to result into high central adiposity and high blood pressure including high carotid extra-medial thickness in adulthood [21
]. Janssen et al
] have clearly shown that overweight and obesity during childhood are strong predictors of obesity and risk for coronary heart disease in young adults. Longitudinal studies have demonstrated that the transition from childhood to adulthood should be taken into account to build obesity prediction models [23
]. Hence, it seems imperative to know better the predictive factors of childhood obesity to avoid the obesity-associated complications in adulthood.
As mentioned above, there seems a relationship between decreased oral fat sensing and CD36 SNP in adult and young obese subjects; however, no such study is available in teenagers. We, therefore, conducted the present study to investigate the relationship between rs1761667 polymorphism of CD36 gene, oral fatty acid detection thresholds in young lean and obese Algerian teenagers.
It has been previously shown that the subjects which are obese at a young age became severely obese in adulthood [25
]. Excess of caloric intake, largely contributed by fat overconsumption, seems to be one of the factors implicated in this pathology [6
]. Moreover, altered oro-gustatory perception of lipids has been associated with obesity [6
]. It, therefore, seems mandatory to shed light on oral fat sensing that might take part in the regulation of feeding behavior in obese subjects.
As regards blood parameters, we observed higher glycemia, LDL-C, triglycerides, and insulin concentrations in obese children than the lean participants. It has been previously shown that the teenagers with a high degree of obesity exhibited high blood concentrations of LDL-C, glucose and insulin [27
]. Similar results were also obtained in an American population, where the prevalence of hyperinsulinemia and hypertriglyceridemia was significantly higher in severely obese children and adolescents, compared to the less obese individuals [28
]. We noticed low HDL-C concentrations in the obese group. Indeed, Ruel et al
] have reported that low HDL is associated with high BMI and waist circumference. Jiang et al
] have also shown that insulin levels were positively correlated with serum triglyceride, and negatively with HDL-C levels in all age group obese children including 12–17 years old participants. These investigators concluded that these changes in obese children might have adverse consequences for cardiovascular diseases in adulthood. Furthermore, in obese children, we also observed a high HOMA index, an indicator of insulin-resistance (IR) which is directly associated with the aggravation of obesity [31
As regards the gustatory detection of lipids, we noticed that obese participants exhibited a significantly higher detection threshold (lower sensitivity) compared to lean participants. Whilst the “High tasters” group is composed mainly of controls, in “Low tasters” group we can find predominantly obese teenagers. Previous studies performed on Australian [32
] and Tunisian [16
] adults also showed that the obese subjects exhibited reduced oleic acid sensitivity. Low fatty acid oro-sensory detection in obesity has been attributed to low expression of CD36 protein in the mouse [33
] or to AA genotype of rs1761667 polymorphism of CD36 in human beings [12
]. However, we did not observe a relationship between CD36 gene AA genotype and fatty acid detection thresholds. The reason for this failure might be the less developed papillae which might not have expressed sufficiently the truncated CD36 protein, transduced by CD36 rs1761667 AA genotype [12
], in the young Algerian children. In fact, it has been shown that fungiform papillae attain full size at the age of 8–10 years, and the circumvallate papillae, located in the posterior region, continue to grow until the age of 15–16 years [34
]. This argument is pertinent as the circumvallate papillae have been shown to express nine-time higher CD36 mRNA than fungiform papillae [35
]. Alternatively, it is also possible that a variant of GPR120, another lipido-receptor that is associated with obesity in a European study [36
], might be involved in low oro-sensory sensitivity in obese Algerian teenagers; however, further studies are required to confirm this hypothesis. We also noted higher A-allele frequency compared to G-allele in our study, and this kind of distribution has been, so far, reported in Arabic populations, namely in Tunisia [16
] and Algeria [17
]. Interestingly, previous studies conducted on different populations, namely Caucasians [18
], Indians [14
], and Asians [13
] showed a high frequency of G-allele.
Nonetheless, A-allele frequency of rs1761667 polymorphism of CD36 gene was higher in obese children than lean participants. A-allele was found to be associated with the intake of soda and French fries in obese children, suggesting that fat-containing products might influence, in the long-term, the fatty acid oro-sensory detection capacity. Our hypothesis is supported by the observations of Stewart et al
] who have reported that feeding a high-fat diet significantly increased oleic acid oral detection threshold in lean subjects. Similarly, feeding a high-fat diet in mice resulted in high oro-sensory threshold for linoleic acid [11
Ours is the first study to show an association between high oro-sensory threshold for a fatty acid and obesity in 13–14 year old teenagers. These results might be confirmed in other young population with different cultural and eating habits. Though the obese participants had CD36 A-allele, it was not associated with high oro-detection threshold for the fatty acid. Besides, we cannot rule out an influence of altered levels of sex hormones in obese teenagers on fat taste perception and other parameters. It is also difficult to determine whether oral fat perception sensitivity affects fat intake or body weight regulation. Future studies are required to address these questions.