Sweet Taste Of Sugar Research Articles

GUAVA LEAVES, CORN COBS, AND MANGOSTEEN PEELS AS ANTIOXIDANTS AND NATIONAL STANDARDIZED NATURAL PRESERVATIVES FOR COCONUT BROWN SUGAR

Objective: Below standard brown sugar is a sugar that cannot be made or resembles dodol (a traditional and sticky confection) because the sap is damaged. Although the sap is made into brown sugar, the product will not last long and become soft-textured sugar. The aim of this research is to prevent below standard sap and produces coconut sugar in accordance with Indonesian National Standard (SNI) using natural preservatives were formulated from guava leaves, corn cobs, and mangosteen peels.
 Methods: The formulation of guava leaves, corn cobs, and mangosteen peels was designed through several stages by testing the composition of the materials. The first step was measuring the pH value of each material with concentration 4.5%, which were 4.5 g per material and it was compared to the composition of the formula after the concentration of each material was combined to get the basis pH. The second step was formulation to get the natural preservatives by applying the formulas on the tap process of sap until the manufacturing process to get the coconut sugar. Quality of coconut sugar was conducted SNI 01-3743-1995 which included oven method for testing water content and insoluble parts, Luff schoorl method for reducing sugar content and sucrose, and atomic absorption spectroscopy method for testing the contamination of Cu metal.
 Results: Guava leaves, corn cobs, and mangosteen peels with each material 4.5% were the optimal concentrations as natural preservatives to inhibit fermentation process of sap. Coconut sugars were obtained using these natural preservatives. Coconut sugar that obtained had the moisture content was 0.2402%, the ash content was 1.3%, reducing sugar content was 0.39%, the sucrose level was 69.99%, and the metal contamination was 0.201 mg/kg Cu. While the results of organoleptic tests indicated the brownish-yellow sugar, a typical sweet taste of sugar, and the normal smell of coconut sugar. All of the coconut sugar properties were meet with SNI.
 Conclusion: Guava leaves, corn cobs, and mangosteen peels were effective as natural preservatives and antioxidants to produce the best quality of coconut sugar according to the SNI.

Flavor Preferences in Animals: Role of Mouth and Gut Nutrient Sensors

Flavor Preferences in Animals: Role of Mouth and Gut Nutrient Sensors

The makings of a powerful sweet tooth

The main attraction of nectar, a hummingbird favorite, is the sweet taste of sugar. Oddly, though, birds lack the main vertebrate receptor for sweet taste, T1R2. Baldwin et al. show that a related receptor, T1R1-T1R3, which generally controls savory taste in vertebrates, adapts in hummingbirds to detect sweet (see the Perspective by Jiang and Beauchamp). This repurposing probably allowed hummingbirds to specialize in nectar feeding and may have assisted the evolution of the many and varied hummingbird species seen today. M. W. Baldwin, Y. Toda, T. Nakagita, M. J. O’Connell, K. C. Klasing, T. Misaka, S. V. Edwards, S. D. Liberles, Evolution of sweet taste perception in hummingbirds by transformation of the ancestral umami receptor. Science 345 , 929–933 (2014). [Abstract][Full Text] P. Jiang, G. K. Beauchamp, Sensing nectar’s sweetness. Science 345 , 878–879 (2014). [Abstract][Full Text]

Effect of dopamine D1 and D2 receptor antagonism in the lateral hypothalamus on the expression and acquisition of fructose-conditioned flavor preference in rats

The attraction to sugar-rich foods is influenced by conditioned flavor preferences (CFP) produced by the sweet taste of sugar (flavor–flavor learning) and the sugar's post-oral actions (flavor–nutrient) learning. Brain dopamine (DA) circuits are involved in both types of flavor learning, but to different degrees. This study investigated the role of DA receptors in the lateral hypothalamus (LH) on the flavor–flavor learning produced the sweet taste of fructose. In an acquisition study, food-restricted rats received bilateral LH injections of a DA D1 receptor antagonist (SCH23390), a D2 antagonist (RAC, raclopride) or vehicle prior to 1-bottle training sessions with a flavored 8% fructose+0.2% saccharin solution (CS+/F) and a less-preferred flavored 0.2% saccharin solution (CS−). Drug-free 2-bottle tests were then conducted with the CS+ and CS− flavors presented in saccharin. The fructose-CFP did not differ among groups given vehicle (76%), 12nmol SCH (78%), 24nmol (82%) or 24nmol RAC (90%) during training. In an expression study with rats trained drug-free, LH injections of 12 or 24nmol SCH or 12–48nmol RAC prior to 2-bottle tests did not alter CS+ preferences (77–90%) relative to vehicle injection (86%). Only a 48nmol SCH dose suppressed the CS+ preference (61%). The minimal effect of LH DA receptor antagonism upon fructose flavor–flavor conditioning differs with the ability of LH SCH injections to block the acquisition of glucose flavor–nutrient learning.

Sucrose taste but not Polycose taste conditions flavor preferences in rats

Rats have an inborn preference for sweet taste and learn to prefer flavors associated with sweetness. They are also strongly attracted to the taste of glucose polymers (e.g., Polycose). This “poly” taste differs in quality from the sweet taste of sugar. To determine if poly taste, like sweet taste, conditions flavor preferences rats were trained with a distinctive flavor (CS+) added to 2% Polycose solution and a different flavor (CS−) added to plain water. In a subsequent two-bottle test the rats did not prefer the CS+ to CS− when both flavors were presented in water. In contrast, other rats significantly preferred a CS+ flavor that had been paired with 2% sucrose. Adding saccharin to a flavored Polycose solution did not improve CS+ flavor learning; rather, Polycose appeared to overshadow saccharin-induced conditioning. Flavor conditioning by a 16% Polycose solution was assessed using a sham-feeding procedure to prevent post-oral reinforcement. Although the rats sham-fed substantial amounts of the CS+ flavored Polycose solution, they failed to prefer the CS+ to the CS− flavor. This contrasts with the preference other rats displayed for a CS+ paired with sham-fed sucrose. Why attractive sweet and poly tastes differ in their ability to condition flavor preferences is not certain, although some findings suggest that they differentially activate dopamine and/or serotonin circuits involved in flavor learning.

Sweet taste signaling in the gut

The taste system plays a critical role in determining whether a food is nutritious and should be ingested or is potentially toxic and should be rejected (1). Considerable attention has focused on the sweet taste of sugar because it is such a potent stimulator of eating in humans and many other animal species. A major advance in our understanding of sweetness perception was the discovery of two G-coupled receptor proteins, T1R2 and T1R3, which dimerize to form a broadly tuned sweet taste receptor (1). Stimulation of the T1R2+T1R3 taste receptor by sugars or artificial sweeteners activates intracellular signaling elements, including α-gustducin, which stimulate peripheral gustatory nerves and, in turn, brain gustatory pathways. The central processing of the sweet taste signal typically activates feeding circuits as well as brain reward systems that promote sweet appetite (2). Brain autonomic centers may also relay information via the vagus nerve to prepare the digestive system for the incoming carbohydrate-rich food (2). Digestive and absorptive processing of the ingested food is further coordinated by sugar sensing in the intestinal tract, which modulates nutrient absorption, hormone release, and gastrointestinal motility, and generates satiation signals to the brain that terminate the meal (3, 4). In this issue of PNAS, Margolskee et al. (5) report that the same T1R2+T1R3 sweet taste receptor that initiates sugar ingestion in the mouth also detects sugar in the intestinal lumen and triggers physiological responses that promote sugar absorption and metabolism.