Dietary-resistant starch improves maternal glycemic control in Goto-Kakizaki rat

Mol Nutr Food Res. 2011 Oct;55(10):1499-508. doi: 10.1002/mnfr.201000605. Epub 2011 Jun 3.


Scope: Dietary prebiotics show potential in anti-diabetes. Dietary resistant starch (RS) has a favorable impact on gut hormone profiles, including glucagon-like peptide-1 (GLP-1) consistently released, a potent anti-diabetic incretin. Also RS reduced body fat and improved glucose tolerance in rats and mice. In the current project, we hypothesize that dietary-resistant starch can improve insulin sensitivity and pancreatic β cell mass in a type 2 diabetic rat model. Altered gut fermentation and microbiota are the initial mechanisms, and enhancement in serum GLP-1 is the secondary mechanism.

Methods and results: In this study, GK rats were fed an RS diet with 30% RS and an energy control diet. After 10 wk, these rats were mated and went through pregnancy and lactation. At the end of the study, pancreatic β cell mass, insulin sensitivity, pancreatic insulin content, total GLP-1 levels, cecal short-chain fatty acid concentrations and butyrate producing bacteria in cecal contents were greatly improved by RS feeding. The offspring of RS-fed dams showed improved fasting glucose levels and normal growth curves.

Conclusion: Dietary RS is potentially of great therapeutic importance in the treatment of diabetes and improvement in outcomes of pregnancy complicated by diabetes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Animals, Newborn
  • Blood Glucose / analysis
  • Body Weight
  • Butyrates / metabolism
  • Cecum / metabolism
  • Cecum / microbiology
  • Diabetes Mellitus, Type 2 / drug therapy
  • Diabetes Mellitus, Type 2 / metabolism
  • Disease Models, Animal
  • Eating
  • Fatty Acids, Volatile / metabolism
  • Female
  • Glucagon-Like Peptide 1 / blood
  • Hydrogen-Ion Concentration
  • Hyperglycemia / drug therapy*
  • Insulin Resistance
  • Insulin-Secreting Cells / drug effects
  • Insulin-Secreting Cells / metabolism
  • Intestinal Mucosa / metabolism
  • Intestinal Mucosa / microbiology
  • Ion Channels / genetics
  • Ion Channels / metabolism
  • Mitochondrial Proteins / genetics
  • Mitochondrial Proteins / metabolism
  • Pregnancy
  • Pregnancy in Diabetics / metabolism
  • Rats
  • Starch / pharmacology*
  • Uncoupling Protein 1


  • Blood Glucose
  • Butyrates
  • Fatty Acids, Volatile
  • Ion Channels
  • Mitochondrial Proteins
  • Uncoupling Protein 1
  • Glucagon-Like Peptide 1
  • Starch