• Proceedings of the Korean Society of Potoscience Conference
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• 2006.06a
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• pp.27-27
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• 2006

• Biomolecules & Therapeutics
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• v.21 no.2
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• pp.121-125
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• 2013

Hesperetin (3',5,7-trihydroxy 4'-methoxyflavanone) and its glycoside hesperidin (hesperetin 7-rhamnoglucoside) in oranges have been reported to possess pharmacological effects related to anti-obesity. However, hesperetin and hesperidin have not been studied on suppressive effects on appetite. This study examined that hesperetin and hesperidin can stimulate the release of cholecystokinin (CCK), one of appetite-regulating hormones, from the enteroendocrine STC-1 cells, and then examined the mechanisms involved in the CCK release. Hesperetin significantly and dose-dependently stimulated CCK secretion with an $EC_{50}$ of 0.050 mM and increased the intracellular $Ca^{2+}$ concentrations ($[Ca^{2+}]_i$) compared to the untreated control. The stimulatory effect by hesperetin was mediated via the entry of extracellular $Ca^{2+}$ and the activation of TRP channels including TRPA1. These results suggest that hesperetin can be a candidate biomolecule for the suppression of appetite and eventually for the therapeutics of obesity.

• Proceedings of the Korean Society of Potoscience Conference
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• 2002.06a
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• pp.54-54
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• 2002

• 한국약용작물학회:학술대회논문집
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• 2010.10a
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• pp.485-486
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• 2010

• 한국약용작물학회:학술대회논문집
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• 2008.05a
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• pp.166-167
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• 2008

• Proceedings of the Korean Society of Potoscience Conference
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• 2005.06a
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• pp.109-109
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• 2005

• 한국약용작물학회:학술대회논문집
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• 2008.11a
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• pp.281-282
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• 2008

• Proceedings of the Korean Society of Potoscience Conference
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• 2002.06a
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• pp.49-49
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• 2002

• 한국약용작물학회:학술대회논문집
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• 2008.05a
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• pp.168-169
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• 2008

• Journal of Biosystems Engineering
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• v.38 no.2
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• pp.129-137
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• 2013

Purpose: Modeling has been used for elucidating the mechanism of complex biosystems. In spite of importance and uniqueness of adolescent calcium (Ca) metabolism characterized by a threshold Ca intake, its regulatory mechanism has not been covered and even not proposed. Hence, this study aims at model-based proposing potential mechanisms regulating adolescent Ca metabolism. Methods: Two different hypothetic mechanisms were proposed. The main mechanism is conceived based on Ca-protein binding which induces renal Ca filtration, while additional mechanism assumed that active renal Ca re-absorption regulated Ca metabolism in adolescents. Mathematical models were developed to represent the proposed mechanism and simulated them whether they could produce adolescent Ca profiles in serum and urine. Results: Simulation showed that both mechanisms resulted in the unique behavior of Ca metabolism in adolescents. Based on the simulation insulin-like growth factor-1 (IGF-1) is suggested as a potential regulator because it is related to both growth, a remarkable characteristic of adolescence, and Ca metabolism including absorption and bone accretion. Then, descriptive modeling is employed to conceptualize the hypothesized mechanisms governing adolescent Ca metabolism. Conclusions: This study demonstrated that modeling is a powerful tool for elucidating an unknown mechanism by simulating potential regulatory mechanisms in adolescent Ca metabolism. It is expected that various analytic applications would be plausible in the study of biosystems, particularly with combination of experimental and modeling approaches.