maltitol and Hyperglycemia

This study investigated the effects of maltitol on intestinal glucose absorption and muscle glucose uptake using ex vivo and in vivo experimental models. The ex vivo experiment was conducted in isolated jejunum and psoas muscle from normal rats. The in vivo study investigated the effects of a single bolus dose of maltitol on gastric emptying, intestinal glucose absorption and digesta transit in normal and type 2 diabetic rats. Maltitol inhibited glucose absorption in isolated rat jejunum and increased glucose uptake in isolated rat psoas muscle in the presence of insulin but not in the absence of insulin. In contrast, maltitol did not significantly (p > 0.05) alter small intestinal glucose absorption or blood glucose levels as well as gastric emptying and digesta transit in normal or type 2 diabetic rats. The results suggest that maltitol may not be a suitable dietary supplement for anti-diabetic food and food products to improve glycemic control.

Topics: Absorption, Physiological; Animals; Diabetes Mellitus, Type 2; Dietary Supplements; Disease Models, Animal; Gastric Emptying; Gastrointestinal Agents; Gastrointestinal Transit; Glucose; Hyperglycemia; Hypoglycemic Agents; In Vitro Techniques; Insulin; Intestinal Absorption; Intestinal Mucosa; Jejunum; Male; Maltose; Muscle, Skeletal; Psoas Muscles; Random Allocation; Rats, Sprague-Dawley; Sugar Alcohols

Nonalcoholic fatty liver disease (NAFLD) progresses to nonalcoholic steatohepatitis, ultimately leading to cirrhosis and liver cancer. It is important to prevent this progression during the initial stages of hepatic fatty degeneration. Maltitol is a polyol produced by the hydrogenation of maltose. We investigated the efficacy of maltitol for treating hepatic fatty degeneration in C57BL/6 male mice using a high-fat diet model. Intake of 5.0% maltitol for 8 weeks significantly suppressed weight gain, hepatic fatty degeneration, hyperglycemia, and hypercholesterolemia. With maltitol intake, sterol regulatory element-binding protein 1c (SREBP1c) mRNA expression was significantly decreased, and farnesoid X receptor (FXR), peroxisome proliferator-activated receptor α (PPARα), and hydroxymethylglutaryl-Co reductase expressions were significantly higher in the liver. The increase in SREBP1c and suppression of FXR and PPARα expressions are correlated with NAFLD. Our results suggest that maltitol may prevent steatosis of NAFLD with a high-fat diet.

Topics: Animals; Diet, High-Fat; Dietary Supplements; Gene Expression; Hydroxymethylglutaryl CoA Reductases; Hypercholesterolemia; Hyperglycemia; Liver; Male; Maltose; Mice; Mice, Inbred C57BL; Non-alcoholic Fatty Liver Disease; PPAR alpha; Receptors, Cytoplasmic and Nuclear; RNA, Messenger; Sterol Regulatory Element Binding Protein 1; Sugar Alcohols; Weight Gain