title: Dietary-resistant starch improves maternal glycemic control in Goto-Kakizaki rat.
abstract: METHODS
  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.
  
  
  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.
  
  
  CONCLUSIONS
  Dietary RS is potentially of great therapeutic importance in the treatment of diabetes and improvement in outcomes of pregnancy complicated by diabetes.
authors.affiliation: Pennington Biomedical Research Center, Baton Rouge, LA, USA. shenli750@hotmail.com
authors.forename: Li
authors.initials: L
authors.lastname: Shen
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Keenan
authors.forename: Anne
authors.initials: A
authors.lastname: Raggio
authors.forename: Cathy
authors.initials: C
authors.lastname: Williams
authors.forename: Roy J
authors.initials: RJ
authors.lastname: Martin
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001786:Blood Glucose / Q000032:analysis; D001835:Body Weight; D002087:Butyrates / Q000378:metabolism; D002432:Cecum / Q000378:metabolism / Q000382:microbiology; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy / Q000378:metabolism; D004195:Disease Models, Animal; D004435:Eating; D005232:Fatty Acids, Volatile / Q000378:metabolism; D005260:Female; D052216:Glucagon-Like Peptide 1 / Q000097:blood; D006863:Hydrogen-Ion Concentration; D006943:Hyperglycemia / Q000188:drug therapy*; D007333:Insulin Resistance; D050417:Insulin-Secreting Cells / Q000187:drug effects / Q000378:metabolism; D007413:Intestinal Mucosa / Q000378:metabolism / Q000382:microbiology; D007473:Ion Channels / Q000235:genetics / Q000378:metabolism; D024101:Mitochondrial Proteins / Q000235:genetics / Q000378:metabolism; D011247:Pregnancy; D011254:Pregnancy in Diabetics / Q000378:metabolism; D051381:Rats; D013213:Starch / Q000494:pharmacology*; D000071256:Uncoupling Protein 1
chemical_list: D001786:Blood Glucose; D002087:Butyrates; D005232:Fatty Acids, Volatile; D007473:Ion Channels; D024101:Mitochondrial Proteins; D000071256:Uncoupling Protein 1; D052216:Glucagon-Like Peptide 1; D013213:Starch