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Effect of dietary nutrient composition on compensatory growth of juvenile olive flounder, Paralichthys olivaceus using different feeding regimes was determined. Six treatments were prepared in triplicate: fish were daily hand‐fed with the control (C) diet twice a day, 7 days a week, for 8 weeks (8WF‐C); fish were starved for 1 week, and then fed with the C and high protein and lipid (HPL) diets twice a day, 7 days a week, for 7 weeks, referred to as 7WF‐C and 7WF‐HPL, respectively; and fish were starved for 2 weeks, and then fed with the C, HPL and HPL with supplementation of the mixture of amino acids (HPLA) diets twice a day, 7 days a week, for 6 weeks, referred to as 6WF‐C, 6WF‐HPL and 6WF‐HPLA, respectively. Growth of fish in 7WF‐HPL treatment was greater than that of fish in any other treatments. Feed efficiency of fish in 7WF‐HPL, 6WF‐HPL and 6WF‐HPLA treatments was higher than that of fish in 8WF‐C, 7WF‐C and 6WF‐C treatments. The high protein and lipid diet effectively improved compensatory growth of fish. However, supplementation of the mixture of amino acids into the high protein and lipid diet did not improve compensatory growth of fish further.

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BACKGROUND AND PURPOSEcAMP as a second messenger stimulates expression of microphthalmia-associated transcription factor (MITF) or the tyrosinase gene in UVB-induced skin pigmentation. Diphenylmethylene hydrazinecarbothioamide (QNT 3-80) inhibits α-melanocytestimulating hormone (α-MSH)-induced melanin production in B16 murine melanoma cells but its molecular basis remains to be defined. Here, we investigated the mechanism underlying the amelioration of skin hyperpigmentation by QNT 3-80. EXPERIMENTAL APPROACHWe used melanocyte cultures with raised levels of cAMP and UVB-irradiated dorsal skin of guinea pigs for pigmentation assays. Immunoprecipitation, kemptide phosphorylation, fluorescence analysis and docking simulation were applied to elucidate a molecular mechanism of QNT 3-80. KEY RESULTSQNT 3-80 inhibited melanin production in melanocyte cultures with elevated levels of cAMP, including those from human foreskin. This compound also ameliorated hyperpigmentation in vivo in UVB-irradiated dorsal skin of guinea pigs. As a mechanism, QNT 3-80 directly antagonized cAMP binding to the regulatory subunit of PKA, nullified the dissociation and activation of inactive PKA holoenzyme in melanocytes and fitted into the cAMP-binding site on the crystal structure of human PKA under the most energetically favourable simulation. QNT 3-80 consequently inhibited cAMP-or UVB-induced phosphorylation (activation) of cAMP-responsive element-binding protein in vitro and in vivo, thus down-regulating expression of genes for MITF or tyrosinase in the melanogenic process. CONCLUSIONS AND IMPLICATIONSOur data suggested that QNT 3-80 could contribute significantly to the treatment of skin disorders with hyperpigmented patches with the cAMP-binding site of PKA as its molecular target.

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