Fat is one of the six types of taste. Perceived taste intensity could affect the preference for a food and whether or not it is consumed. Cluster of differentiation 36 (CD36) translocates fatty acids on the cellular membrane and is involved in the oral fat-sensing mechanism. Therefore, genetic variation rs1761667 in CD36 is known to be associated with the perception of fat taste and, hence, its dietary intake. This study examined whether CD36 rs1527479 T>C, a proxy of rs1761667, is associated with fat intake and related dietary behaviour in Koreans. Using the data of the Ansan/Ansung Study, a part of the Korean Genome Epidemiology Study, the association of rs1527479 with the intake of macronutrients, including fat and selected foods, and fat-related dietary behaviours were investigated in 3194 males and 3425 females grouped by their degree of obesity. The findings suggested that rs1527479 did not have a meaningful effect on the intake of fat or other macronutrients or on the selection of food among non-obese females and males. However, in males with obesity, the genetic variation showed a significant association with vegetable intake. Obese males with the mutant CC genotype had substantially lower cruciferous vegetable consumption (adjusted P = 0·0015) than individuals with the TT and CT genotypes. Rs1527479 had no significant effect on the frequency of consuming fried foods or commonly used types of seasoning and cooking oils. In conclusion, CD36 genetic variation was associated with the intake of cruciferous vegetables but not fat intake in obese Korean males.

Obese subjects have shown a preference for dietary lipids. A recent collection of evidence has proposed that a variant in the CD36 gene plays a significant role in this pathway. We assessed the association between the orosensory detection of a long-chain fatty acid, i.e. oleic acid (OA), and genetic polymorphism of the lipid taste sensor CD36 in obese and normal-weight subjects. Adult participants were recruited in the fasting condition. They were invited to fat taste perception sessions, using emulsions containing OA and according to the three-alternative forced-choice (3-AFC) method. Genomic DNA was used to determine the polymorphism (SNP rs 1761667) of the CD36 gene. Obese (n 50; BMI 34⋅97 (sd 4⋅02) kg/m2) exhibited a significantly higher oral detection threshold for OA (3⋅056 (sd 3⋅53) mmol/l) than did the normal-weight (n 50; BMI 22⋅16 (sd 1⋅81) kg/m2) participants (1⋅20 (sd 3⋅23) mmol/l; P = 0⋅007). There was a positive correlation between OA detection thresholds and BMI in all subjects; evenly with body fat percentage (BF%). AA genotype was more frequent in the obese group than normal-weight group. OA detection thresholds were much higher for AA and AG genotypes in obese subjects compared with normal-weight participants. Higher oral detection thresholds for fatty acid taste are related to BMI, BF% and not always to CD36 genotype.

Currently, the prevention and treatment of CVD have been a global focus since CVD is the number one cause of mortality and morbidity. In the pathogenesis of CVD, it was generally thought that impaired cholesterol homeostasis might be a risk factor. Cholesterol homeostasis is affected by exogenous factors (i.e. diet) and endogenous factors (i.e. certain receptors, enzymes and transcription factors). In this context, the number of studies investigating the potential mechanisms of dietary fatty acids on cholesterol homeostasis have increased in recent years. As well, the cluster of differentiation 36 (CD36) receptor is a multifunctional membrane receptor involved in fatty acid uptake, lipid metabolism, atherothrombosis and inflammation. CD36 is proposed to be a crucial molecule for cholesterol homeostasis in various mechanisms including absorption/reabsorption, synthesis, and transport of cholesterol and bile acids. Moreover, it has been reported that the amount of fatty acids and fatty acid pattern of the diet influence the CD36 level and CD36-mediated cholesterol metabolism principally in the liver, intestine and macrophages. In these processes, CD36-mediated cholesterol and lipoprotein homeostasis might be impaired by dietary SFA and trans-fatty acids, whereas ameliorated by MUFA in the diet. The effects of PUFA on CD36-mediated cholesterol homeostasis are controversial depending on the amount of n-3 PUFA and n-6 PUFA, and the n-3:n-6 PUFA ratio. Thus, since the CD36 receptor is suggested to be a novel nutrient-sensitive biomarker, the role of CD36 and dietary fatty acids in cholesterol metabolism might be considered in medical nutrition therapy in the near future. Therefore, the novel nutritional target of CD36 and interventions that focus on dietary fatty acids and potential mechanisms underlying cholesterol homeostasis are discussed in this review.

A major challenge in taste research is to overcome the flavour imperfections in food products and to build nutritious strategies to combat against obesity as well as other related metabolic syndromes. The field of molecular taste research and chemical senses has contributed to an enormous development in understanding the taste receptors and mechanisms of taste perception. Accordingly, the development of taste-modifying compounds or taste modulators that alter the perception of basic taste modalities has gained significant prominence in the recent past. The beneficial aspects of these substances are overwhelming while considering their potential taste-modifying properties. The objective of the present review is to provide an impression about the taste-modulating compounds and their distinctive taste-modifying properties with reference to their targets and proposed mechanisms of action. The present review also makes an effort to discuss the basic mechanism involved in oro-gustatory taste perception as well as on the effector molecules involved in signal transduction downstream to the activation of taste receptors.

Cluster of differentiation 36 (CD36) is a membrane receptor expressed on a wide variety of human cells. CD36 polymorphisms are reportedly associated with oral fat perception, dietary intake and metabolic disorders. The present study examined associations of two CD36 polymorphisms (rs1761667 and rs1527483) and dietary fat intake, and metabolic phenotypes in a Japanese population. This cross-sectional study was conducted based on clinical information collected from health check-ups in Japan (n 495). Dietary nutrient intake was estimated from a validated short FFQ and adjusted for total energy intake using the residual method. Mean blood pressure was calculated from systolic blood pressure (SBP) and diastolic blood pressure (DBP). Hypertension was defined as SBP ≥ 130 mmHg and/or DBP ≥ 85 mmHg, or use of antihypertensive drugs. Genotyping was performed using PCR with confronting two-pair primers method. Mean age was 63·4 (sd 9·9) years. Individuals with the AA genotype showed higher total fat and MUFA intake (standardised β = 0·110 and 0·087, P = 0·01 and 0·05, respectively) compared with the GG and GA genotypes. For metabolic phenotypes, the AA genotype of rs1761667 had a lower blood pressure compared with the GG genotype (standardised β = –0·123, P = 0·02). Our results suggested that the AA genotype of rs1761667 in the CD36 gene was associated with higher intake of total fat and MUFA and lower risk of hypertension in a Japanese population.

Recent evidence has raised the possibility of the existence of a sixth taste modality – that is, taste for fat – which is mediated by lingual CD36 and plays a role in obesity. Consequently, the genetic polymorphism of CD36 has been shown to be associated with altered oro-sensory detection of dietary lipids. In the present study, we investigated the relationship between oro-sensory perception of linoleic acid (LA), two CD36 polymorphisms (rs1527483 and rs3212018), obesity parameters and craving habits for dietary lipids in young Czech adults. We also sequenced 5 and 6 exons of CD36 to trace out any new mutation that might be responsible for the difference in taste perception. We observed that craving for dietary lipids was correlated with anthropometric parameters (P<0·05) and LA detection threshold (P=0·033). The participants with the CC genotype of the rs1527483 polymorphism had lower BMI (P=0·011), waist circumference (P=0·005), waist:height ratio (P=0·010) and higher sensitivity for LA (P=0·037) than the participants with the CT and TT genotypes. Interestingly, we did not observe any association between the rs3212018 polymorphism and the studied parameters. Moreover, we did not observe any mutation in exons 5 and 6 of the CD36 gene in these subjects. Finally, we can state that rs1527483, but not rs3212018, is associated with high body weight in young Czech subjects.

Recently, it has been remarked that dietary fatty acids and fatty acid receptors might be involved in the aetiology of diabetes. Therefore, this study was conducted to determine the relationship between dietary fatty acid pattern, fatty food preferences and soluble CD36 (sCD36) and insulin resistance in type 2 diabetes mellitus (DM). The study was carried out with thirty-eight newly diagnosed type 2 DM patients and thirty-seven healthy volunteers, aged 30–65 years. In the study, socio-demographic characteristics, dietary fat type and fatty acid pattern of individuals were recorded. After anthropometric measurements were taken, blood CD36, glucose, TAG and insulin levels were analysed. The results showed that although the type of fatty acid intake did not differ between the groups (P>0·05), the consumption of olive oil in the type 2 DM group was lower than the control group (P<0·05). Mean blood glucose, insulin, insulin resistance, TAG and sCD36 levels were determined to be higher in the type 2 DM group (P<0·05). However, there was no correlation between sCD36 levels and homeostatic model assessment of insulin resistance (HOMA-IR) value, blood insulin and TAG levels, waist circumference, dietary fatty acid pattern and food preferences in the type 2 DM group (P>0·05). Crucially, elevated sCD36 levels increased the type 2 DM risk (OR 1·21, P<0·05). In conclusion, sCD36 level may be a possible biomarker, independent from the dietary fatty acid pattern, for type 2 DM owing to its higher levels in these patients. Therefore, the new insights make CD36 attractive as a therapeutic target for diabetes.

Epitope mapping of a murine monoclonal antibody (mAb), 5H12, prepared against live Plasmodium falciparum-intected red blood cells indicated that the epitope consisted of amino acid residues 474–487 of the human anion transport protein, band 3. mAb 5H12 enhanced cytoadherence, but inhibited the CD36-like mediated resetting. A synthetic peptide based on the sequence of the epitope (FSFCETNGLE) blocked both resetting and cytoadherence, suggesting that this amino acid sequence may form the CD36-like receptor. The CD36-like region of band 3 was antigenically distinct from platelet or endothelial CD36.

Mammary epithelial cells, which express and secrete leptin into milk, accumulate triacylglycerol (TAG). We examined effects on the accumulation of cytosolic TAG of addition of short- (acetate and butyrate) or medium- (octanoate) chain fatty acids to the medium bathing bovine mammary epithelial cells (bMEC). Octanoate stimulated the accumulation of TAG in a concentration-dependent manner from 1 to 10 mM and increased lipid droplet formation and mRNA expression of CD36 (a fatty acid translocase). Additionally, expression of a peroxisome proliferator activated receptor (PPAR) γ 2 protein that is a lipid-activated transcription factor, was increased by the addition of acetate or octanoate. However, leptin mRNA expression was significantly reduced by addition of acetate or butyrate. Both short- and medium-chain fatty acids inhibited acetyl coenzyme A carboxylase (ACC) activities, which is pivotal in lipid synthesis, but elevated expression of uncoupling protein 2 (UCP2) mRNA, which is important in energy expenditure. These results suggest that octanoate induces cytosolic TAG accumulation and the formation of lipid droplets, and that acetate and butyrate inhibit leptin expression and lipid synthesis in bMEC.