Biomedical subjects

Rie Ohta

Publications and source records attributed to Rie Ohta.

3 recordsLinked to original sources

PubMed2003

Leptin modulates behavioral responses to sweet substances by influencing peripheral taste structures.

Leptin is a hormone that regulates body weight homeostasis mainly via the hypothalamic functional leptin receptor Ob-Rb. Recently, we proposed that the taste organ is a new peripheral target for leptin. Leptin selectively inhibits mouse taste cell responses to sweet substances and thereby may act as a sweet taste modulator. The present study further investigated leptin action on the taste system by examining expression of Ob-Rb in taste cells and behavioral responses to sweet substances in leptin-deficient ob/ob, and Ob-Rb-deficient db/db mice and their normal litter mates. RT-PCR analysis showed that Ob-Rb was expressed in taste cells in all strains tested. The db/db mice, however, had a RT-PCR product containing an abnormal db insertion that leads to an impaired shorter intracellular domain. In situ hybridization analysis showed that the hybridization signals for normal Ob-Rb mRNA were detected in taste cells in lean and ob/ob mice but not in db/db mice. Two different behavioral tests, one using sweet-bitter mixtures as taste stimuli and the other a conditioned taste aversion paradigm, demonstrated that responses to sucrose and saccharin were significantly decreased after ip injection of leptin in ob/ob and normal littermates, but not in db/db mice. These results suggest that leptin suppresses behavioral responses to sweet substances through its action on Ob-Rb in taste cells. Such taste modulation by leptin may be involved in regulation for food intake.

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PubMed2003

Conditioned taste aversion learning in leptin-receptor-deficient db/db mice.

The db/db mouse has defective leptin receptors. The defects lead to impairments of leptin regulation of food intake and body weight, and result in the expression of diabetic symptoms such as hyperinsulinemia, hyperglicemia, and extreme obesity. Recent studies have proposed that leptin may also affect memory and learning processes. To examine this possibility, we compared the ability of leptin-receptor-deficient db/db mice and their normal lean litter mates to form and extinguish a conditioned taste aversion (CTA) for saccharin. We used a short-term (10 s) lick test and a long-term (48 h) two bottle preference test for measurement of consumption of test solutions. On the first day after conditioning to avoid saccharin, the db/db mice showed preference scores for saccharin as low, and aversion thresholds for sucrose lower than that of the lean mice. During the extinction test trials beginning from the second up to the 30th day after conditioning, numbers of licks and preference scores for aversive saccharin and sucrose appeared to be larger, and recovered faster to the control levels in db/db mice. These results indicate that db/db mice with leptin-receptor-deficiency may show equal capacity to form CTAs for saccharin, greater generalization from saccharin to sucrose, and a faster rate of extinction. This suggests that disruption of leptin signalling does not inhibit acquisition of CTA learning, but impairs its extinction. This differential contribution of the leptin system on CTA processes may be due to differential distribution of leptin receptors in the CTA-related brain areas.

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PubMed2002

Leptin and sweet taste.

Leptin, the product of the obese (ob) gene, is a hormone primarily produced in adipose cells, and also at smaller amounts in some other peripheral organs. It regulates food intake, energy expenditure, and body weight. Leptin is thought to promote weight loss, at least in rodents, by suppressing appetite and stimulating metabolism. Mutant mice that lack either leptin or functional leptin receptors, such as ob/ob and db/db mice, are hyperphagic, massively obese, and diabetic. Central hypothalamic targets are mainly responsible for the effects of leptin on food intake and weight loss. However, there are also direct effects on peripheral tissues. Recently, the taste organ was found to be one of the peripheral targets for leptin. The hormone specifically inhibits sweet taste responses in lean mice and not in db/db mice. Thus leptin appears to act as a modulator of sweet taste, provided a functional leptin receptor is expressed by the taste cells. This chapter reviews the genetics and molecular biology of leptin and its receptors, the receptor mechanisms for sweet taste, the modulating action of leptin on taste receptor cells, and the consequences for the regulation of food intake.

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