Validation of the Japanese Version of the Yale Food Addiction Scale 2.0 (J-YFAS 2.0).

The Yale Food Addiction Scale 2.0 (YFAS 2.0) is used for assessing food addiction (FA). Our study aimed at validating its Japanese version (J-YFAS 2.0). The subjects included 731 undergraduate students. Confirmatory factor analysis indicated the root-mean-square error of approximation, comparative fit index, Tucker⁻Lewis index, and standardized root-mean-square residual were 0.065, 0.904, 0.880, and 0.048, respectively, for a one-factor structure model. Kuder⁻Richardson α was 0.78. Prevalence of the J-YFAS 2.0-diagnosed mild, moderate, and severe FA was 1.1%, 1.2%, and 1.0%, respectively. High uncontrolled eating and emotional eating scores of the 18-item Three-Factor Eating Questionnaire (TFEQ R-18) (p < 0.001), a high Kessler Psychological Distress Scale score (p < 0.001), frequent desire to overeat (p = 0.007), and frequent snacking (p = 0.003) were associated with the J-YFAS 2.0-diagnosed FA presence. The scores demonstrated significant correlations with the J-YFAS 2.0-diagnosed FA symptom count (p < 0.01). The highest attained body mass index was associated with the J-YFAS 2.0-diagnosed FA symptom count (p = 0.026). The TFEQ R-18 cognitive restraint score was associated with the J-YFAS 2.0-diagnosed FA presence (p < 0.05) and symptom count (p < 0.001), but not with the J-YFAS 2.0-diagnosed FA severity. Like the YFAS 2.0 in other languages, the J-YFAS 2.0 has a one-factor structure and adequate convergent validity and reliability.

Possible involvement of thyrotropin-releasing hormone receptor 3 in the release of prolactin in the metamorphosing bullfrog larvae.

In amphibians, thyrotropin (TSH), corticotropin (ACTH) and prolactin (PRL) are regarded as the major pituitary hormones involved in metamorphosis, their releasing factors being corticotropin-releasing factor (CRF), arginine vasotocin (AVT), and thyrotropin-releasing hormone (TRH), respectively. It is also known that thyrotropes and corticotropes are equipped with CRF type-2 receptor and AVT V1b receptor, respectively. As for PRL cells, information about the type of receptor for TRH (TRHR) through which the action of TRH is mediated to induce the release of PRL is lacking. In order to fill this gap, an attempt was made to characterize the TRHR subtype existing in the PRL cells of the anterior pituitary gland of the bullfrog, Rana catesbeiana. We cloned cDNAs for three types of bullfrog TRHRs, namely TRHR1, TRHR2 and TRHR3, and confirmed that all of them are functional receptors for TRH by means of reporter gene assay. Analyses with semi-quantitative reverse transcription-PCR and in situ hybridization revealed that TRHR3 mRNA is expressed in the anterior lobe and that the signals reside mostly in the PRL cells. It was also noted that the expression levels of TRHR3 mRNA in the anterior pituitary as well as in the PRL cells of metamorphosing tadpoles elevate as metamorphosis progresses. Since the pattern of changes in TRHR3 mRNA levels in the larval pituitary is almost similar to that previously observed in the pituitary PRL mRNA and plasma PRL levels, we provide a view that TRHR3 mediates the action of TRH on the PRL cells to induce the release of PRL that is prerequisite for growth and metamorphosis in amphibians.

D2 Dopamine receptor subtype mediates the inhibitory effect of dopamine on TRH-induced prolactin release from the bullfrog pituitary.

Dopamine receptors in mammals are known to consist of two D1-like receptors (D1 and D5) and three D2-like receptors (D2, D3 and D4). The aim of this study was to determine the dopamine receptor subtype that mediates the inhibitory action of dopamine on the release of prolactin (PRL) from the amphibian pituitary. Distal lobes of the bullfrog (Rana catesbeiana) were perifused and the amount of PRL released in the effluent medium was measured by means of a homologous enzyme-immunoassay. TRH stimulated the release of PRL from perifused pituitaries. Dopamine suppressed TRH-induced elevation of PRL release. Quinpirole (a D2 receptor agonist) also suppressed the stimulatory effect of TRH on the release of PRL, whereas SKF-38393 (a D1 receptor agonist) exhibited no such an effect. The inhibitory action of dopamine on TRH-induced PRL release from the pituitary was nullified by the addition of L-741,626 (a selective D2 receptor antagonist) to the medium, but not by the addition of SCH-23390 (a selective D1 receptor antagonist). These data indicate that the inhibitory effect of dopamine on TRH-evoked PRL release from the bullfrog pituitary gland is mediated through D2 dopamine receptors.