Effect of RS4-Type Resistant Starch on Inflammatory Cytokines in C57BL/6J Mice Fed High-Fat Diet

doi:10.7506/spkx1002-6630-201323047

Abstract

Abstract:

Objective: To analyze the effects of three kinds of RS4 resistant starch on inflammatory cytokines in C57/BL6J
mice fed high-fat diet. Methods: A total of 72 C57BL/6J male mice were randomly divided into six groups with 12 mice in
each group: control group (CL), high-fat group (HF) and HF-SPS, HF-HPCL-SPS, HF-CLOSA-SPS and HF-CAAC-SPS
groups, fed a high fat diet containing 15% sweet potato starch (SPS), hydroxypropyl cross-linked sweet-potato modified
starch (HPCL-SPS), cross-linked octenyl succinic anhydride sweet-potato modified starch (CLOSA-SPS) and citric acid
acetylated sweet-potato modified starch (CAAC-SPS), respectively. After 12 weeks of feeding, the levels of serum free fatty
acid (FFA), necrosis factor-α(TNF-α), interlukin6 (IL-6) and monocyte-chemoattractant protein 1 (MCP-1) were determined.
Results: The levels of serum FFA, TNF-α, IL-6 and MCP-1 of HF group and HF-SPS group were significantly higher than
those in CL group. The size of epididymal adipocyte and the levels of serum FFA, TNF-α, IL-6 and MCP-1 were reduced
by HPCL-SPS and CAAC-SPS treatments. Conclusions: HPCL-SPS and CAAC-SPS can suppress the serum FFA and
inflammatory cytokines and affect the size of epididymal adipocyte in C57BL/6J mice fed high-fat diet, and thus, have an
improvement on obesity-related low-grade inflammatory state and metabolic diseases.

Key words: RS4-type resistant starch, obesity, inflammatory cytokines, adipocyte

CLC Number:

R589

WANG Xin, WU Ying-long*. Effect of RS4-Type Resistant Starch on Inflammatory Cytokines in C57BL/6J Mice Fed High-Fat Diet[J]. FOOD SCIENCE, 2014, 35(1): 239-243.

References

[1] Maury E, Brichard S M, Adipokine dysregulation, adipose tissue inflammation and metabolic syndrome[J]. Molecular and Cellular Endocrinology ,2010,314:1–16.
[2] Zhaoxia Wang, Tomohiro Nakayama. Inflammation, a Link between Obesity and Cardiovascular Disease[J]. Mediators of Inflammation ,2010,1-17.
[3] Antuna-Puente B, Feve Fellahi B, Bastard J P. Adipokines: The missing link between insulin resistance and obesity [J].Diabetes & Metabolism, 2008, (34):2–11.
[4] Monica Bullo, Patricia Casas-Agustench, Pilar Amigo-Correig, et al. Inflammation, obesity and comorbidities: the role of diet[J].Public Health Nutrition, 2006, 10(10A), 1164–1172.
[5] Fuentes-Zaragoza E, Riquelme-Navarrete M J, Sánchez-Zapata E, et al. Resistant starch as functional ingredient: A review [J]. Food Research International, 2010,(43):931-942.
[6] Zhou J, Martin R J, Tulley R T, et al. Dietary resistant starch upregulates total GLP-1 and PYY in a sustained day-long manner through fermentation in rodents [J]. American Journal of Physiology, 2008, (295): E1160–E1166.
[7] P W So, W S Yu, Y T Kuo, et al. Impact of resistant starch on body fat patterning and central appetite regulation[J]. PLoS ONE , 2007,( 2): e1309.
[8] Sajilata M G, Singhal R S, Kulkarni P R, Resistant starch-a review [J].Comprehensive Reviews in Food Science and Food Safety, 2006, 5:1-17.
[9] Akira Shimotoyodome, Junko Suzuki, Daisuke Fukuoka, Ichiro Tokimitsu, and Tadashi Hase, RS4-type resistant starch prevents high-fat diet-induced obesity via increased hepatic fatty acid oxidation and decreased postprandial GIP in C57BL/6J mice[J], Am J Physiol Endocrinol Metab, 2010,(298): E652–E662.
[10] Li H, Lelliott C, Hakansson P, Ploj K, Tuneld A, et al. Intestinal, adipose,and liver inflammation in diet-induced obese mice[J]. Metabolism ,2008,57: 1704-1710.
[11] Bruun,J M,Lihn,A.S.,Pedersen,S.B.,Richelsen,B., Monocyte chemoattractant protein-1 release is higher in visceral than subcutaneous human adipose tissue(AT): implication of macrophages resident in the AT[J]. Clin. Endocrinol. Metab, 2005, 90:2282–2289
[12] Tilg H, Moschen A R. Insulin resistance, inflammation, and non-alcoholic fatty liver disease[J]. Trends Endocrinol Metab ,2008, 19(37):1-9.
[13] Cancello R, Henegar C, Viguerie N, Taleb S, Poitou C, Rouault C et al. Reduction of macrophage infiltration and chemoattractant gene expression changes in white adipose tissue of morbidly obese subjects after surgery-induced weight loss[J]. Diabetes, 2005, 54: 2277–2286
[14] Ahima RS. Adipose tissue as an endocrine organ[J]. Obesity(SilverSpring), 2006, 14(Suppl 5):242S-9S.
[15] Buettner R, Scholmerich J, Bollheimer LC. High-fat diets: modeling the metabolic disorders of human obesity in rodents. Obesity (Silver Spring),2007, 15:798-808.
[16] Strissel K J, Stancheva Z, Miyoshi H, et al. Adipocyte death, adipose tissue remodeling, and obesity complications[J]. Diabetes, 2007,56:2910-2918.