Is fat the sixth taste primary? Evidence and implications

Explores our tongue\u27s ability to detect fat as a distinct taste similar to our ability to sense sweet, sour, bitter, acid and savory. Abstract 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

The influence of diet and genes in fat taste

This thesis assessed the role of genes and diet on fat taste sensitivity through a co-twin randomised controlled trial. It found individuals become more sensitive to fat taste when consuming a low-fat diet, with little influence from genes. This has potential implications for reducing obesity via fat taste sensitivity mediation

High fat diet causes depletion of intestinal eosinophils associated with intestinal permeability.

The development of intestinal permeability and the penetration of microbial products are key factors associated with the onset of metabolic disease. However, the mechanisms underlying this remain unclear. Here we show that, unlike liver or adipose tissue, high fat diet (HFD)/obesity in mice does not cause monocyte/macrophage infiltration into the intestine or pro-inflammatory changes in gene expression. Rather HFD causes depletion of intestinal eosinophils associated with the onset of intestinal permeability. Intestinal eosinophil numbers were restored by returning HFD fed mice to normal chow and were unchanged in leptin-deficient (Ob/Ob) mice, indicating that eosinophil depletion is caused specifically by a high fat diet and not obesity per se. Analysis of different aspects of intestinal permeability in HFD fed and Ob/Ob mice shows an association between eosinophil depletion and ileal paracelullar permeability, as well as leakage of albumin into the feces, but not overall permeability to FITC dextran. These findings provide the first evidence that a high fat diet causes intestinal eosinophil depletion, rather than inflammation, which may contribute to defective barrier integrity and the onset of metabolic disease

Seasonality of Freeze Tolerance in a Subarctic Population of the Wood Frog, Rana sylvatica

We compared physiological characteristics and responses to experimental freezing and thawing in winter and spring samples of the wood frog, Rana sylvatica, indigenous to Interior Alaska, USA. Whereas winter frogs can survive freezing at temperatures at least as low as −16°C, the lower limit of tolerance for spring frogs was between −2.5°C and −5°C. Spring frogs had comparatively low levels of the urea in blood plasma, liver, heart, brain, and skeletal muscle, as well as a smaller hepatic reserve of glycogen, which is converted to glucose after freezing begins. Consequently, following freezing (−2.5°C, 48 h) tissue concentrations of these cryoprotective osmolytes were 44–88% lower than those measured in winter frogs. Spring frogs formed much more ice and incurred extensive cryohemolysis and lactate accrual, indicating that they had suffered marked cell damage and hypoxic stress during freezing. Multiple, interactive stresses, in addition to diminished cryoprotectant levels, contribute to the reduced capacity for freeze tolerance in posthibernal frogs

Identification and expression of a putative facilitative urea transporter in three species of true frogs (Ranidae): implications for terrestrial adaptation.

Urea transporters (UTs) help mediate the transmembrane movement of urea and therefore are likely important in amphibian osmoregulation. Although UTs contribute to urea reabsorption in anuran excretory organs, little is known about the protein’s distribution and functions in other tissues, and their importance in the evolutionary adaptation of amphibians to their environment remains unclear. To address these questions, we obtained a partial sequence of a putative UT and examined relative abundance of this protein in tissues of the wood frog (Rana sylvatica), leopard frog (R. pipiens), and mink frog (R. septentrionalis), closely related species that are adapted to different habitats. Using immunoblotting techniques, we found the protein to be abundant in the osmoregulatory organs but also present in visceral organs, suggesting that UTs play both osmoregulatory and nonosmoregulatory roles in amphibians. UT abundance seems to relate to the species’ habitat preference, as levels of the protein were higher in the terrestrial R. sylvatica, intermediate in the semiaquatic R. pipiens, and quite low in the aquatic R. septentrionalis. These findings suggest that, in amphibians, UTs are involved in various physiological processes, including solute and water dynamics, and that they have played a role in adaptation to the osmotic challenges of terrestrial environments

Seasonality of Freeze Tolerance in a Subarctic Population of the Wood Frog, Rana sylvatica

We compared physiological characteristics and responses to experimental freezing and thawing in winter and spring samples of the wood frog, Rana sylvatica, indigenous to Interior Alaska, USA. Whereas winter frogs can survive freezing at temperatures at least as low as −16°C, the lower limit of tolerance for spring frogs was between −2.5°C and −5°C. Spring frogs had comparatively low levels of the urea in blood plasma, liver, heart, brain, and skeletal muscle, as well as a smaller hepatic reserve of glycogen, which is converted to glucose after freezing begins. Consequently, following freezing (−2.5°C, 48 h) tissue concentrations of these cryoprotective osmolytes were 44–88% lower than those measured in winter frogs. Spring frogs formed much more ice and incurred extensive cryohemolysis and lactate accrual, indicating that they had suffered marked cell damage and hypoxic stress during freezing. Multiple, interactive stresses, in addition to diminished cryoprotectant levels, contribute to the reduced capacity for freeze tolerance in posthibernal frogs

Cryoprotectants and extreme freeze tolerance in a subarctic population of the wood frog.

Wood frogs (Rana sylvatica) exhibit marked geographic variation in freeze tolerance, with subarctic populations tolerating experimental freezing to temperatures at least 10-13 degrees Celsius below the lethal limits for conspecifics from more temperate locales. We determined how seasonal responses enhance the cryoprotectant system in these northern frogs, and also investigated their physiological responses to somatic freezing at extreme temperatures. Alaskan frogs collected in late summer had plasma urea levels near 10 μmol ml-1, but this level rose during preparation for winter to 85.5 ± 2.9 μmol ml-1 (mean ± SEM) in frogs that remained fully hydrated, and to 186.9 ± 12.4 μmol ml-1 in frogs held under a restricted moisture regime. An osmolality gap indicated that the plasma of winter-conditioned frogs contained an as yet unidentified osmolyte(s) that contributed about 75 mOsmol kg-1 to total osmotic pressure. Experimental freezing to –8°C, either directly or following three cycles of freezing/thawing between –4 and 0°C, or –16°C increased the liver’s synthesis of glucose and, to a lesser extent, urea. Concomitantly, organs shed up to one-half (skeletal muscle) or two-thirds (liver) of their water, with cryoprotectant in the remaining fluid reaching concentrations as high as 0.2 and 2.1 M, respectively. Freeze/thaw cycling, which was readily survived by winter-conditioned frogs, greatly increased hepatic glycogenolysis and delivery of glucose (but not urea) to skeletal muscle. We conclude that cryoprotectant accrual in anticipation of and in response to freezing have been greatly enhanced and contribute to extreme freeze tolerance in northern R. sylvatica

Fat taste sensitivity is associated with short-term and habitual fat intake

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 ( β ^ = 0.110 [95% CI: 0.003, 0.216]), % energy from carbohydrate ( β ^ = -0.112 [-0.188, -0.035]), and frequency of consumption of foods per day from food groups: high-fat dairy ( β ^ = 1.091 [0.106, 2.242]), meat & meat alternatives ( β ^ = 0.669 [0.168, 1.170]), and grain & cereals ( β ^ = 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

Effect of dietary fat intake and genetics on fat taste sensitivity: a co-twin randomized controlled trial

Background: 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. Objective: 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 (&lt;2.0 kg variation) to assess heritability and to explore the effect of genetics on diet-mediated changes in FATT. Design: A co-twin randomized controlled trial including 44 pairs (mean &plusmn; SD age: 43.7 &plusmn; 15.4 y; 34 monozygotic, 10 dizygotic; 33 women, 10 men, 1 gender-discordant) was conducted. Twins within a pair were randomly allocated to an 8-wk low-fat (&lt;20% of energy from fat) or high-fat (&gt;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. Results: There was a significant time &times; diet interaction for FT rank after the 8-wk trial (P&nbsp;&lt;&nbsp;0.001), with the same conclusions for the subset of participants maintaining baseline weight (low-fat; n&nbsp;=&nbsp;32; high-fat: n&nbsp;=&nbsp;35). There was no evidence of zygosity effect modification (interaction of time &times; diet &times; zygosity: P&nbsp;=&nbsp;0.892). Heritability of baseline FT rank was 8%. Conclusions: 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. <br /

The Lysozyme Inhibitor Thionine Acetate Is Also an Inhibitor of the Soluble Lytic Transglycosylase Slt35 from Escherichia coli

Lytic transglycosylases such as Slt35 from E. coli are enzymes involved in bacterial cell wall remodelling and recycling, which represent potential targets for novel antibacterial agents. Here, we investigated a series of known glycosidase inhibitors for their ability to inhibit Slt35. While glycosidase inhibitors such as 1-deoxynojirimycin, castanospermine, thiamet G and miglitol had no effect, the phenothiazinium dye thionine acetate was found to be a weak inhibitor. IC50 values and binding constants for thionine acetate were similar for Slt35 and the hen egg white lysozyme. Molecular docking simulations suggest that thionine binds to the active site of both Slt35 and lysozyme, although it does not make direct interactions with the side-chain of the catalytic Asp and Glu residues as might be expected based on other inhibitors. Thionine acetate also increased the potency of the beta-lactam antibiotic ampicillin against a laboratory strain of E. coli