Pourghassem Gargari B, et al. Diabetes Metab J. 2013 Apr;37(2):140-148. https://doi.org/10.4093/dmj.2013.37.2.140

There is limited evidence on the effects of prebiotics on inflammation. Therefore, the aim of this study was to evaluate the effects of inulin supplementation on inflammatory indices and metabolic endotoxemia in patients with type 2 diabetes mellitus. The participants included diabetic females (n = 49). They were divided into an intervention group (n = 24) as well as a control group (n = 25) and received 10 g/d inulin or maltodextrin for 8 weeks, respectively. Fasting blood sugar (FBS), HbA1c, insulin, high-sensitive C-reactive protein (hs-CRP), tumor necrosis factor-alpha (TNF-α), interleukin-10 (IL-10), and plasma lipopolysaccharide (LPS) were measured pre and post intervention. Inulin-supplemented patients exhibited a significant decrease in FBS (8.5%), HbA1c (10.4%), fasting insulin (34.3%), homeostasis model assessment of insulin resistance (HOMA-IR) (39.5%), hs-CRP (35.6%), TNF-α (23.1%), and LPS (27.9%) compared with the maltodextrin group (p < 0.05). Increase in IL-10 was not significant in inulin compared with the maltodextrin group. It can be concluded that inulin supplementation seems to be able to modulate inflammation and metabolic endotoxemia in women with type 2 diabetes.

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 (n30) and the control group (n25). 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 unpairedttests 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.

Aims: This trial aims to determine the effects of resistant starch (RS) subtype 2 (RS2) on glycemic status, metabolic endotoxemia and markers of oxidative stress. Methods: A randomized, controlled, parallel-group clinical trial group of 56 females with type 2 diabetes mellitus (T2DM) was divided to 2 groups. The intervention group (n = 28) and control group (n = 28) received 10 g/day RS2 or placebo for 8 weeks, respectively. Fasting blood samples were taken to determine glycemic status, endotoxin, high sensitivity C-reactive protein (hs-CRP), malondialdehyde (MDA), total antioxidant capacity (TAC), antioxidant enzymes concentrations as well as uric acid at baseline and after the intervention. Results: After 8 weeks, RS2 caused a significant decrease in the levels of MDA (-34.10%), glycosylated hemoglobin (-9.40%), insulin (-29.36%), homeostasis model of insulin resistance (-32.85%) and endotoxin (-25.00%), a significant increase in TAC (18.10%) and glutathione peroxidase (11.60%) as compared with control. No significant changes were observed in fasting plasma glucose, quantitative insulin sensitivity check index, hs-CRP, superoxide dismutase, catalase and uric acid in the RS2 group as compared with the control group. Conclusion: Supplementation with RS2 may be improved glycemic status, endotoxemia and markers of oxidative stress in patients with T2DM.