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1.
Am J Clin Nutr ; 90(3): 764S-769S, 2009 Sep.
Article in English | MEDLINE | ID: mdl-19625681

ABSTRACT

The unique taste induced by monosodium glutamate is referred to as umami taste. The umami taste is also elicited by the purine nucleotides inosine 5'-monophosphate and guanosine 5'-monophosphate. There is evidence that a heterodimeric G protein-coupled receptor, which consists of the T1R1 (taste receptor type 1, member 1, Tas1r1) and the T1R3 (taste receptor type 1, member 3, Tas1r3) proteins, functions as an umami taste receptor for rodents and humans. Splice variants of metabotropic glutamate receptors, mGluR(1) (glutamate receptor, metabotropic 1, Grm1) and mGluR(4) (glutamate receptor, metabotropic 4, Grm4), also have been proposed as taste receptors for glutamate. The taste sensitivity to umami substances varies in inbred mouse strains and in individual humans. However, little is known about the relation of umami taste sensitivity to variations in candidate umami receptor genes in rodents or in humans. In this article, we summarize current knowledge of the diversity of umami perception in mice and humans. Furthermore, we combine previously published data and new information from the single nucleotide polymorphism databases regarding variation in the mouse and human candidate umami receptor genes: mouse Tas1r1 (TAS1R1 for human), mouse Tas1r3 (TAS1R3 for human), mouse Grm1 (GRM1 for human), and mouse Grm4 (GRM4 for human). Finally, we discuss prospective associations between variation of these genes and umami taste perception in both species.


Subject(s)
Genetic Variation , Receptors, G-Protein-Coupled/genetics , Receptors, Metabotropic Glutamate/genetics , Taste Perception/genetics , Taste/genetics , Animals , Humans , Mice , Polymorphism, Single Nucleotide , Receptors, G-Protein-Coupled/physiology , Receptors, Metabotropic Glutamate/physiology , Sodium Glutamate , Taste/physiology , Taste Perception/physiology
2.
Br J Oral Maxillofac Surg ; 43(5): 383-91, 2005 Oct.
Article in English | MEDLINE | ID: mdl-15908073

ABSTRACT

We studied the healing process of mandibular closed fractures in osteoporotic rats using specific antibodies to bone morphogenetic protein-2 (BMP-2) and tumour necrosis factor-alpha (TNF-alpha). We confirmed the osteoporosis in rats after oophorectomy by micro-CT, and then caused unilateral closed fractures in the mandible and monitored the healing process after 7, 14, 21, and 28 days. Data were compared simultaneously with those from a group of rats that had a sham operation. During healing of the fracture in the osteoporotic group there was a prolonged phase of endochondral ossification, with an increased number of osteoclasts (p<0.01). Expressions of BMP-2 and TNFalpha were more pronounced in the osteoporotic group and there was an increase in the number of osteoblasts and TNFalpha(+) cells compared with the normal control (p<0.01). BMP-2 was related to the differentiation of osteoblasts and the higher values of TNFalpha were correlated with the up-regulation of osteoclasts during the prolonged phase of bone turnover. We conclude that the healing of fractures in osteoporotic bone is delayed about a week compared with controls. In the healing of fractures in osteoporotic bone, there were more osteoblasts and osteoclasts but there was a predominance of osteoclasts probably induced by TNFalpha. The prolonged phase of bone turnover with osteoclast predominance in the osteoporotic group is suggestive of the cause of delay in the healing of the fracture.


Subject(s)
Fracture Healing/physiology , Mandibular Fractures/metabolism , Mandibular Fractures/physiopathology , Osteoporosis/physiopathology , Animals , Bone Morphogenetic Protein 2 , Bone Morphogenetic Proteins/biosynthesis , Bony Callus/cytology , Female , Fractures, Closed/metabolism , Fractures, Closed/physiopathology , Immunohistochemistry , Mandibular Fractures/etiology , Osteoclasts/physiology , Osteoporosis/complications , Ovariectomy , Rats , Rats, Wistar , Tomography, X-Ray Computed , Transforming Growth Factor beta/biosynthesis , Tumor Necrosis Factor-alpha/biosynthesis
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