title: Resistant dextrin, as a prebiotic, improves insulin resistance and inflammation in women with type 2 diabetes: a randomised controlled clinical trial.
abstract: Improvement of insulin resistance and inflammation is a basic strategy in the management of type 2 diabetes. There is limited evidence that prebiotics improve insulin resistance and inflammation. However, the ameliorating effect of resistant dextrin, as a prebiotic, on insulin resistance and inflammation in patients with type 2 diabetes has not been investigated so far. Therefore, the present study aimed to examine the effects of resistant dextrin on insulin resistance and inflammation in type 2 diabetic patients. In a randomised controlled clinical trial, fifty-five women with type 2 diabetes were assigned to two groups: the intervention group (n 30) and the control group (n 25). The intervention group received a daily supplement of 10 g resistant dextrin and the control group received a similar amount of maltodextrin as placebo for 8 weeks. Fasting plasma glucose (FPG), HbA1c, insulin, high-sensitivity C-reactive protein (hs-CRP), IL-6, TNF-α, malondialdehyde (MDA) and serum endotoxin concentrations were measured before and after the intervention. Data were analysed using SPSS (version 13). Paired and unpaired t tests and ANCOVA were used to compare quantitative variables after the intervention. Patients supplemented with resistant dextrin exhibited a significant decrease in fasting insulin (20.1 pmol/l, 22.8%), homeostasis model assessment of insulin resistance (1.3, 24.9%), quantitative insulin sensitivity check index (0.2, 7.2%), IL-6 (1.4 pg/ml, 28.4 %), TNF-α (5.4 pg/ml, 18.8 %), MDA (1.2 nmol/ml, 25.6 %) and endotoxin (6.2 endotoxin units/ml, 17.8%) concentrations than those supplemented with maltodextrin (P< 0.05). Decreases in FPG (0.05 mmol/l, 0.6%), HbA1c (0.5%, 9.6%) and hs-CRP (2.7 ng/ml, 35.1%) concentrations in the resistant dextrin group were not significant when compared with the maltodextrin group. In conclusion, resistant dextrin supplementation can modulate inflammation and improve insulin resistance in women with type 2 diabetes.
authors.affiliation: Faculty of Medicine, Bone Research Center, Tabriz University of Medical Sciences,Tabriz,Iran.
authors.forename: Akbar
authors.initials: A
authors.lastname: Aliasgharzadeh
authors.affiliation: Faculty of Nutrition, Nutrition Research Center, Student Research Committee, Tabriz University of Medical Sciences,Tabriz,Iran.
authors.forename: Parvin
authors.initials: P
authors.lastname: Dehghan
authors.affiliation: Faculty of Nutrition, Tabriz University of Medical Sciences,Tabriz,Iran.
authors.forename: Bahram Pourghassem
authors.initials: BP
authors.lastname: Gargari
authors.affiliation: Medical Education Research Center, Faculty of Health, Tabriz University of Medical Sciences,Tabriz,Iran.
authors.forename: Mohammad
authors.initials: M
authors.lastname: Asghari-Jafarabadi
mesh_terms: D000328:Adult; D000368:Aged; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use*; D000975:Antioxidants / Q000009:adverse effects / Q000627:therapeutic use; D015415:Biomarkers / Q000097:blood; D015992:Body Mass Index; D016207:Cytokines / Q000097:blood; D003912:Dextrins / Q000009:adverse effects / Q000627:therapeutic use*; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000178:diet therapy* / Q000276:immunology / Q000378:metabolism; D004311:Double-Blind Method; D004731:Endotoxins / Q000097:blood; D002149:Energy Intake; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D007333:Insulin Resistance; D007492:Iran; D008315:Malondialdehyde / Q000097:blood; D008875:Middle Aged; D050177:Overweight / Q000150:complications; D056692:Prebiotics / Q000009:adverse effects
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D000975:Antioxidants; D015415:Biomarkers; D016207:Cytokines; D003912:Dextrins; D004731:Endotoxins; D007004:Hypoglycemic Agents; C573352:NUTRIOSE; D056692:Prebiotics; D008315:Malondialdehyde
keywords: Cytokines; Insulin resistance; Resistant dextrin; Type 2 diabetes