Fat provides important sensory properties to baked food products, such as colour, taste, texture and odour, all of which contribute to overall consumer acceptance. Baked food products, such as crackers, cakes and biscuits, typically contain high amounts of fat. However, there is increasing demand for healthy snack foods with reduced fat content. In order to maintain consumer acceptance whilst simultaneously reducing the total fat content, fat replacers have been employed. There are a number of fat replacers that have been investigated in baked food products, ranging from complex carbohydrates, gums and gels, whole food matrices, and combinations thereof. Fat replacers each have different properties that affect the quality of a food product. In this review, we summarise the literature on the effect of fat replacers on the quality of baked food products. The ideal fat replacers for different types of low-fat baked products were a combination of polydextrose and guar gum in biscuits at 70% fat replacement (FR), oleogels in cake at 100% FR, and inulin in crackers at 75% FR. The use of oatrim (100% FR), bean puree (75% FR) or green pea puree (75% FR) as fat replacers in biscuits were equally successful.
Taste is the chemical sense responsible for the detection of non-volatile chemicals in potential foods. For fat to be considered as one of the taste primaries in humans, certain criteria must be met including class of affective stimuli, receptors specific for the class of stimuli on taste bud cells (TBC), afferent fibres from TBC to taste-processing regions of the brain, perception independent of other taste qualities and downstream physiological effects. The breakdown products of the macronutrients carbohydrates (sugars) and proteins (amino acids) are responsible for the activation of sweet and umami tastes, respectively. Following the same logic, the breakdown products of fat being fatty acids are the likely class of stimuli for fat taste. Indeed, psychophysical studies have confirmed that fatty acids of varying chain length and saturation are orally detectable by humans. The most likely fatty acid receptor candidates located on TBC are CD36 and G protein-coupled receptor 120. Once the receptors are activated by fatty acids, a series of transduction events occurs causing the release of neurotransmitters towards afferent fibres signalling the brain. Whether fatty acids elicit any direct perception independent of other taste qualities is still open to debate with only poorly defined perceptions for fatty acids reported. Others suggest that the fatty acid taste component is at detection threshold only and any perceptions are associated with either aroma or chemesthesis. It has also been established that oral exposure to fat via sham feeding stimulates increases in blood TAG concentrations in humans. Therefore, overall, with the exception of an independent perception, there is consistent emerging evidence that fat is the sixth taste primary. The implications of fatty acid taste go further into health and obesity research, with the gustatory detection of fats and their contributions to energy and fat intake receiving increasing attention. There appears to be a coordinated bodily response to fatty acids throughout the alimentary canal; those who are insensitive orally are also insensitive in the gastrointestinal tract and overconsume fatty food and energy. The likely mechanism linking fatty acid taste insensitivity with overweight and obesity is development of satiety after consumption of fatty foods.
Evidence suggests individuals less sensitive to fat taste (high fat taste thresholds (FTT)) may be overweight or obese and consume greater amounts of dietary fat than more sensitive individuals. The aims of this study were to assess associations between FTT, anthropometric measurements, fat intake, and liking of fatty foods. FTT was assessed in 69 Australian females (mean age 41.3 (15.6) (SD) years and mean body mass index 26.3 (5.7) kg/m2) by a 3-alternate forced choice methodology and transformed to an ordinal scale (FT rank). Food liking was assessed by hedonic ratings of high-fat and reduced-fat foods, and a 24-h food recall and food frequency questionnaire was completed. Linear mixed regression models were fitted. FT rank was associated with dietary % energy from fat ( = 0.110 [95% CI: 0.003, 0.216]), % energy from carbohydrate ( = −0.112 [−0.188, −0.035]), and frequency of consumption of foods per day from food groups: high-fat dairy ( = 1.091 [0.106, 2.242]), meat & meat alternatives ( = 0.669 [0.168, 1.170]), and grain & cereals ( = 0.771 [0.212, 1.329]) (adjusted for energy and age). There were no associations between FT rank and anthropometric measurements or hedonic ratings. Therefore, fat taste sensitivity appears to be associated with short-term fat intake, but not body size in this group of females.
1 May 2018 in The American Journal of Clinical Nutrition
Individuals with impaired fat taste (FT) sensitivity have reduced satiety responses after consuming fatty foods, leading to increased dietary fat intake. Habitual consumption of dietary fat may modulate sensitivity to FT, with high consumption decreasing sensitivity [increasing fatty acid taste threshold (FATT)] and low consumption increasing sensitivity (decreasing FATT). However, some individuals may be less susceptible to diet-mediated changes in FATT due to variations in gene expression. The objective of this study was to determine the effect of an 8-wk low-fat or high-fat diet on FATT while maintaining baseline weight (35% of energy from fat) diet. FATT was assessed by a 3-alternate forced choice methodology and transformed to an ordinal scale (FT rank) at baseline and at 4 and 8 wk. Linear mixed models were fit to assess diet effect on FT rank and diet effect modification due to zygosity. A variance components model was fit to calculate baseline heritability. There was a significant time × diet interaction for FT rank after the 8-wk trial (P < 0.001), with the same conclusions for the subset of participants maintaining baseline weight (low-fat; n = 32; high-fat: n = 35). There was no evidence of zygosity effect modification (interaction of time × diet × zygosity: P = 0.892). Heritability of baseline FT rank was 8%. There appears to be little to no genetic contribution on heritability of FATT or diet-mediated changes to FATT. Rather, environment, specifically dietary fat intake, is the main influencer of FT sensitivity, regardless of body weight. This trial was registered with the Australian New Zealand Clinical Trials Registry at http://www.anzctr.org.au/ as ACTRN12613000466741.
Significant experimental evidence supports fat as a taste modality; however, the associated peripheral mechanisms are not well established. Several candidate taste receptors have been identified, but their expression pattern and potential functions in human fungiform papillae remain unknown. The aim of this study is to identify the fat taste candidate receptors and ion channels that were expressed in human fungiform taste buds and their association with oral sensory of fatty acids. For the expression analysis, quantitative RT-PCR (qRT-PCR) from RNA extracted from human fungiform papillae samples was used to determine the expression of candidate fatty acid receptors and ion channels. Western blotting analysis was used to confirm the presence of the proteins in fungiform papillae. Immunohistochemistry analysis was used to localise the expressed receptors or ion channels in the taste buds of fungiform papillae. The correlation study was analysed between the expression level of the expressed fat taste receptors or ion channels indicated by qRT-PCR and fat taste threshold, liking of fatty food and fat intake. As a result, qRT-PCR and western blotting indicated that mRNA and protein of CD36, FFAR4, FFAR2, GPR84 and delayed rectifying K+ channels are expressed in human fungiform taste buds. The expression level of CD36 was associated with the liking difference score (R −0·567, β=−0·04, P=0·04) between high-fat and low-fat food and FFAR2 was associated with total fat intake (ρ=−0·535, β=−0·01, P=0·003) and saturated fat intake (ρ=−0·641, β=−0·02, P=0·008).