4.3 Article

Fat and carbohydrate preferences in mice:: the contribution of α-gustducin and Trpm5 taste-signaling proteins

出版社

AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpregu.00364.2007

关键词

soybean oil; Polycose; starch; Sefa Soyate oil; postoral conditioning

资金

  1. Intramural NIH HHS [Z01 DK031135] Funding Source: Medline
  2. NIDCD NIH HHS [DC-03055, R01 DC003055, DC-03155, R01 DC003155] Funding Source: Medline
  3. NIDDK NIH HHS [DK-031135, R37 DK031135-24, R01 DK031135, R37 DK031135] Funding Source: Medline

向作者/读者索取更多资源

Trpm5 and alpha-gustducin are key to the transduction of tastes of sugars, amino acids, and bitter compounds. This study investigated the role of these signaling proteins in the preference for fat, starch, and starch-derived polysaccharides (Polycose), using Trpm5 knockout (Trpm5 KO) and alpha-gustducin knockout (Gust KO) mice. In initial two-bottle tests (24 h/day), Trpm5 KO mice showed no preference for soybean oil emulsions (0.313-2.5%), Polycose solutions (0.5-4%), or starch suspensions (0.5-4%). Gust KO mice displayed an attenuated preference for Polycose, but their preferences for soybean oil and starch were comparable to those of C57BL/6J wild-type (WT) mice. Gust KO mice preferred starch to Polycose, whereas WT mice had the opposite preference. After extensive experience with soybean oil emulsions (Intralipid) and Polycose solutions, the Trpm5 KO mice developed preferences comparable to the WT mice, although their absolute intakes remained suppressed. Similarly, Gust KO mice developed a strong Polycose preference with experience, but they continued to consume less than the WT mice. These results implicate alpha-gustducin and Trpm5 as mediators of polysaccharide taste and Trpm5 in fat taste. The disruption in Polycose, but not starch, preference in Gust KO mice indicates that distinct, sensory signaling pathways mediate the response to these carbohydrates. The experience-induced rescue of fat and Polycose preferences in the KO mice likely reflects the action of a postoral-conditioning mechanism, which functions in the absence of a-gustducin and Trpm5.

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