a1 Dietary Fibre and the Metabolic Syndrome Research Group, German Institute of Human Nutrition Potsdam-Rehbruecke, Nuthetal, Germany
a2 Medical Department-Innenstadt, University Hospital, Munich, Germany
a3 Department of Clinical Nutrition, German Institute of Human Nutrition Potsdam-Rehbruecke, Nuthetal, Germany
a4 Department of Endocrinology, Diabetes and Nutrition, Charité-University-Medicine, Campus Benjamin Franklin, Berlin, Germany
a5 Department of Preventive Medicine, University of Southern California, Los Angeles, USA
Dietary fibre consumption is associated with improved glucose homeostasis. In contrast, dietary polyphenols have been suggested to exert both beneficial and detrimental effects on glucose and insulin metabolism. Recently, we reported that a polyphenol-rich insoluble dietary fibre preparation from carob pulp (carob fibre) resulted in lower postprandial acylated ghrelin levels after a liquid meal challenge test compared with a control meal without supplementation. The effects may, however, differ when a different food matrix is used. Thus, we investigated the effects of carob fibre on glucose, insulin and ghrelin responses in healthy humans in combination with a glucose load. In a randomized single-blind cross-over study involving twenty healthy subjects (aged 22–62 years), plasma glucose, total and acylated ghrelin, and serum insulin were repeatedly assessed before and after the ingestion of 200 ml water with 50 g glucose and 0, 5, 10 or 20 g carob fibre over a period of 180 min. The intake of 5 and 10 g carob fibre increased the plasma glucose by 47 % and 64 % (P < 0·001), and serum insulin by 19·9 and 24·8 % (P < 0·001), compared with the control. Plasma acylated ghrelin concentrations did not change significantly after the consumption of carob-enriched glucose solution. Total ghrelin decreased only after 10 g carob fibre (P < 0·001) compared with control. In conclusion, we showed that polyphenol-rich carob fibre, administered within a water–glucose solution, increases postprandial glucose and insulin responses, suggesting a deterioration in glycaemic control.
(Received August 22 2006)
(Revised December 19 2006)
(Accepted January 18 2007)
† Both authors contributed equally.