6 research outputs found

    Total synthesis of the marine natural products lukianols A and B

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    Total synthesis of the pyrrolic marine natural products lukianols A (1) and B (2) has been achieved using N-benzenesulfonyl-3,4-dibromopyrrole (3) as a common starting material. The key synthetic strategy developed is the combined bromine-directed lithiation and palladium-catalyzed cross-coupling of 3 to produce 3,4-diarylpyrrol-2-carboxylates. Regioselective iodination of the phenolic intermediate 24 was thoroughly investigated for the synthesis of lukianol B

    The Anti-Obesity Effect of the Palatinose-Based Formula Inslow is Likely due to an Increase in the Hepatic PPAR-α and Adipocyte PPAR-γ Gene Expressions

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    Abdominal obesity is a principal risk factor in the development of metabolic syndrome. Previously, we showed that a palatinose-based liquid formula, Inslow/MHN-01, suppressed postprandial plasma glucose level and reduced visceral fat accumulation better than the standard formula (SF). To elucidate the mechanism of Inslow-mediated anti-obesity effect, expression levels of genes involved in the glucose and lipid metabolism were compared in Inslow- and SF-fed rats. Both fasting plasma insulin level and average islet sizes were reduced in the Inslow group. We also found less abdominal fat accumulation and reduced hepatic triacylglycerol content in the Inslow group. Expression of the β-oxidation enzymes and uncoupling potein-2 (UCP-2) mRNAs in the liver of the Inslow group were higher than the SF group, which was due to a concomitant higher expression of the peroxisome proliferator-activated receptor (PPAR)-α mRNA in the former. Furthermore, expression of the UCP-2 and adiponectin mRNAs in the epididymal fat were higher in the Inslow group than the SF group, and were stimulated by a concomitant increase of the PPAR-γ gene expression in the former. These results strongly suggested that the anti-obesity effect of Inslow was due to an increase in the hepatic PPAR-α and adipocyte PPAR-γ gene expressions

    Gene expression in low glycemic index diet - impact on metabolic control.

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    Correcting postprandial hyperglycemia forms an important part of the prevention and management of type 2 diabetes.Journal ArticleResearch Support, Non-U.S. Gov'tReviewinfo:eu-repo/semantics/publishe

    Effects of a palatinose-based liquid diet (Inslow) on glycemic control and the second-meal effect in healthy men.

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    Postprandial hyperglycemia induces prolonged hyperinsulinemia, which is a risk factor for type 2 diabetes mellitus. Foods with a low glycemic index blunt the rapid rise in postprandial plasma glucose and insulin levels. We herein investigated the effects of a novel, palatinose-based liquid diet (Inslow, Meiji Dairy Products, Tokyo, Japan) on postprandial plasma glucose and insulin levels and on the rate of substrate oxidation in 7 healthy men. Furthermore, to examine the effects of Inslow on the second-meal effect, we quantified our subjects' postprandial plasma glucose, insulin, and free fatty acid levels for up to 7 hours after they ingested a breakfast containing Inslow or control formula, followed by a standard lunch 5 hours later. Our results showed that peak plasma glucose and insulin levels 30 minutes after Inslow loading were lower than after control formula loading. Postprandial fat oxidation rates in the Inslow group were higher than in the control formula group (P < .05). In the second-meal effect study, plasma glucose and insulin levels after lunch in the Inslow group were lower than in the control formula group (P < .01), although the peak levels in these groups were not different. The free fatty acid concentration in the Inslow group immediately before lunch was significantly lower than in the control formula group (P < .05). In conclusion, consumption of Inslow at breakfast appears to improve patient glycemic control by reducing their postprandial plasma glucose and insulin levels after lunch (second-meal effect).Journal ArticleRandomized Controlled TrialResearch Support, Non-U.S. Gov'tinfo:eu-repo/semantics/publishe