lignans and Glucose-Intolerance

Coffee consumption has been associated with improved glucose tolerance and a lower risk of type 2 diabetes in diverse populations in the U.S., Europe, and Japan. This review discusses the strength of the evidence, relevant mechanisms, possible implications, and directions for further research. The finding that higher consumption of decaffeinated coffee was associated with a lower risk of type 2 diabetes suggests that coffee constituents other than caffeine play a role. Coffee is a source of several compounds that improved glucose metabolism in animal studies, including the chlorogenic acids and lignans. Further research on phytochemicals in coffee may lead to the identification of novel mechanisms for effects of diet on the development of type 2 diabetes. In addition, knowledge on effects of coffee components may aid in the development or selection of types of coffee with improved health effects. Longer-term randomized intervention studies that test the effects of coffee consumption on glucose tolerance are warranted. Physical activity and weight management should be the mainstay of public health strategies to prevent type 2 diabetes. For individual choices regarding coffee consumption, potential effects of coffee on various health outcomes should be considered.

Topics: Adult; Aged; Aged, 80 and over; Caffeine; Chlorogenic Acid; Coffee; Diabetes Mellitus, Type 2; Female; Glucose Intolerance; Humans; Lignans; Male; Middle Aged; Risk Factors

Honokiol, a constituent of Magnolia obovata, has various pharmacological effects, including protection against cerebral ischemia. However, few studies have been conducted to evaluate the possible neuroprotective effects of honokiol against cerebral ischemia. We recently reported that cerebral ischemic neuronal damage could be triggered by glucose intolerance that develops after the onset of ischemic stress (i.e., post-ischemic glucose intolerance). In addition, suppression of post-ischemic glucose intolerance significantly ameliorated ischemic neuronal damage. Here, we investigated the effects of honokiol on the development of post-ischemic glucose intolerance and neuronal damage. Mice were subjected to middle cerebral artery occlusion (MCAO) for 2 h. The development of post-ischemic glucose intolerance on day 1 and neuronal damage on day 3 after MCAO were significantly reduced by intraperitoneal administration of honokiol (10 mg/kg) compared with the vehicle-treated group. Honokiol did not affect serum insulin or adiponectin levels. However, honokiol significantly decreased the expression of phosphoenolpyruvate carboxykinase and increased the expression of 5'-AMP-activated protein kinase (AMPK) on day 1 after MCAO, compared with the vehicle-treated MCAO group. The results of this study suggest that honokiol could prevent post-ischemic glucose intolerance in an AMPK-dependent manner, which may be involved in the neuroprotective effects of honokiol against cerebral ischemia.

Topics: Adiponectin; AMP-Activated Protein Kinases; Animals; Biphenyl Compounds; Brain Ischemia; Glucose Intolerance; Infarction, Middle Cerebral Artery; Insulin; Lignans; Male; Mice; Phosphoenolpyruvate Carboxykinase (ATP)