Improvement of glucose metabolism via mung bean protein consumption: A clinical trial of GLUCODIATM isolated mung bean protein in Japan

Background: The main component of mung bean protein, accounting for more than 80%, is 8Sα globulin. Its structure closely resembles that of soybean β-conglycinin. Thereby, the mung bean protein is expected to have similar physiological effects to those of β-conglycinin, but there is no clinical evidence for these effects.Purpose of this study: The aim of this study was to confirm the positive effects of mung bean protein (GLUCODIATM) on glucose metabolism in clinical trials.Method: This clinical study was conducted using a double-blind placebo-controlled design with 45 prediabetes patients.Results: Many of the subjects were pre-diabetes with blood glucose levels exceeding 140 mg/dL by 2-hour plasma glucose level. However, the initial mean fasting plasma glucose level was less than 100 mg/dL. Therefore, mung bean protein did not lower fasting plasma glucose levels. The test period extended from summer to autumn, and increased fasting plasma glucose levels in the placebo group were observed due to seasonal factors. However, this increase was suppressed in the test group. Similarly, the mean insulin level increased in the placebo group, but the increase was also suppressed in the test group. Among obese subjects with a high body mass index, significant increases in fasting plasma glucose and insulin levels in the placebo group were observed. In the comparison between the test and the placebo groups with the average elevation value, there was a significant difference in fasting blood glucose level and significant tendencies in insulin level and homeostatic model assessment for insulin resistance value between the two groups.Conclusion: Mung bean protein suppresses fasting plasma glucose and insulin levels. Consequently, it may have an inhibitory effect on insulin resistance, a trigger of metabolic syndrome.Key words: mung bean protein, insulin, obesity, body mass index, randomized clinical trial, seasonal variation.

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20-HETE Induces Hyperglycemia through the cAMP/PKA-PhK-GP Pathway

Molecular Endocrinology ◽

10.1210/me.2012-1139 ◽

2012 ◽

Vol 26 (11) ◽

pp. 1907-1916 ◽

Cited By ~ 13

Author(s):

Guangrui Lai ◽

Jingjing Wu ◽

Xiaoliang Liu ◽

Yanyan Zhao

Keyword(s):

Transgenic Mice ◽

Plasma Glucose ◽

Insulin Signaling ◽

Fasting Plasma Glucose ◽

Insulin Level ◽

Glucose Levels ◽

Fasting Plasma ◽

Hepatic Microsomes

Abstract We previously generated cytochrome P450 4F2 (CYP4F2) transgenic mice and showed high 20-hydroxyeicosatetraenoic acid (20-HETE) production, which resulted in an elevation of blood pressure. However, it was unclear whether 20-HETE affected glucose metabolism. We measured fasting plasma glucose, insulin, hepatic CYP4F2 expression, and 20-HETE production by hepatic microsomes, and hepatic 20-HETE levels in transgenic mice. We also assessed glycogen phosphorylase (GP) activity and the cAMP/protein kinase A (PKA)-phosphorylase kinase (PhK)-GP pathway, as well as expressions of insulin receptor substrate 1 and glucose transporters in vivo and in vitro. The transgenic mice had overexpressed hepatic CYP4F2, high hepatic 20-HETE and fasting plasma glucose levels but normal insulin level. The GP activity was increased and the cAMP/PKA-PhK-GP pathway was activated in the transgenic mice compared with wild-type mice. Moreover, these alterations were eliminated with the addition of N-hydroxy-N′-(4-butyl-2 methylphenyl) formamidine, which is a selective 20-HETE inhibitor. The results were further validated in Bel7402 cells. In addition, the transgenic mice had functional insulin signaling, and 20-HETE had no effect on insulin signaling in Bel7402 cells, excluding that the observed hyperglycemia in CYP4F2 transgenic mice resulted from insulin dysfunction, because the target tissues were sensitive to insulin. Our study suggested that 20-HETE can induce hyperglycemia, at least in part, through the cAMP/PKA-PhK-GP pathway but not through the insulin-signaling pathway.

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