• Nutrition · Jul 2009

    Kochujang, a Korean fermented red pepper plus soybean paste, improves glucose homeostasis in 90% pancreatectomized diabetic rats.

    • Dae Young Kwon, Sang Mee Hong, Il Sung Ahn, Young Suk Kim, Dong Wha Shin, and Sunmin Park.
    • Korean Food Research Institutes, Sungnam, Korea.
    • Nutrition. 2009 Jul 1; 25 (7-8): 790799790-9.

    ObjectivesRed pepper and soybeans have been reported to modulate energy and glucose metabolism. However, the antidiabetic effect of kochujang, the fermented product of red pepper plus soybeans, has not been studied. We examined whether kochujang affected insulin secretion from beta-cells and/or peripheral insulin resistance in 90% pancreatectomized diabetic rats fed high-fat diets.MethodsDiabetic rats consumed a high-fat diet containing two different kinds of 5% kochujang powder or the equivalent amount of nutrients for 8 wk. Two types of kochujang were made through the fermentation of two different kinds of meju (soybeans), red peppers, glutinous rice, and malts. Meju was produced by fermenting soybeans in a traditional method (TMK) or in a more modern method in which soybeans are inoculated with Bacillus subtilus and Aspergillus sojae (MMK).ResultsTMK and MMK decreased body weight, visceral fat, and serum leptin levels without modulating caloric intake in diabetic rats compared with the control. TMK and MMK also improved glucose tolerance by enhancing insulin sensitivity but did not potentiate glucose-stimulated insulin secretion. The improvement in hepatic insulin sensitivity caused by TMK and MMK was explained by the potentiated phosphorylation of signal transducer and activator of transcription-3 --> adenosine monophosphate kinase --> acetyl-coenzyme A carboxylase and decreased phosphoenolpyruvate carboxykinase expression. Kochujang diets reduced hepatic glucose output and triacylglycerol accumulation and increased glycogen storage.ConclusionThe combination of red pepper and fermented soybeans in kochujang improves glucose homeostasis by reducing insulin resistance, not by enhancing beta-cell function, in diabetic rats. The improvement is associated with decreased hepatic fat storage by the activation of adenosine monophosphate kinase.

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