Dietary supplementation of A-type procyanidins from litchi pericarp improves glucose homeostasis by modulating mTOR signaling and oxidative stress in diabetic ICR mice

被引:22
作者
Li, Xiaopeng [1 ]
Wu, Qian [2 ]
Sui, Yong [3 ]
Li, Shuyi [4 ]
Xie, Bijun [1 ]
Sun, Zhida [1 ]
机构
[1] Huazhong Agr Univ, Coll Food Sci & Technol, Wuhan 430070, Hubei, Peoples R China
[2] Hubei Univ Technol, Res Ctr Food Fermentat Engn & Technol Hubei, Hubei Collaborat Innovat Ctr Ind Fermentat, Wuhan 430068, Hubei, Peoples R China
[3] Hubei Acad Agr Sci, Inst Farm Prod Proc & Nucl Agr Technol, Wuhan 430064, Hubei, Peoples R China
[4] Wuhan Polytech Univ, Coll Food Sci & Engn, Wuhan 430023, Hubei, Peoples R China
关键词
A-type procyanidins; Oxidative stress; Glucose homeostasis; Type; 2; diabetes; mTOR; HIGH-FAT DIET; GUT MICROBIOTA; MUSCLE; RATS; HYPERGLYCEMIA; METABOLISM; P66SHC; LIVER; GLUCONEOGENESIS; BIFIDOBACTERIA;
D O I
10.1016/j.jff.2017.12.024
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
This study evaluated the protective role of litchi pericarp oligomeric procyanidins (LPOPC) and synbiotics (Bifidobacterium Bb-12 and xylo-oligosaccharide) against high fat and streptozotocin (STZ)-induced diabetes. LPOPC or synbiotics have no effect on blood glucose in normal mice. Treatments with LPOPC for 12 weeks significantly reduced blood glucose, FFA, endotoxin, GHbA1c and improved glucose homeostasis, lipid metabolism and insulin level. LPOPC also attenuated hyperglycemia-induced oxidative stress in serum, liver. In addition, administration of LPOPC remarkably reversed the increase of mTOR and p66(shc) in liver, skeletal muscle and white adipose tissue (WAT). LPOPC dramatically increased glucose uptake and glycolysis in liver, skeletal muscle and WAT, while inhibiting gluconeogenesis and lipogenesis in liver and improving heat generation in brown adipose tissue (BAT). Furthermore, synbiotics strengthened the improving effect of LPOPC. These findings demonstrated that LPOPC and synbiotics may regulate glucose disposal in peripheral target tissues through p66(shc)-mTOR signaling pathway.
引用
收藏
页码:155 / 165
页数:11
相关论文
共 43 条
[1]  
Abdul-Ghani M. A., 2010, J BIOMED BIOTECHNOL, V2010
[2]   Effects of probiotic supplementation in patients with type 2 diabetes: systematic review and meta-analysis [J].
Akbari, Vajihe ;
Hendijani, Fatemeh .
NUTRITION REVIEWS, 2016, 74 (12) :774-785
[3]  
Anhe Fernando F., 2013, PharmaNutrition, V1, P105, DOI 10.1016/j.phanu.2013.07.004
[4]   Recent advances in understanding the anti-diabetic actions of dietary flavonoids [J].
Babu, Pon Velayutham Anandh ;
Liu, Dongmin ;
Gilbert, Elizabeth R. .
JOURNAL OF NUTRITIONAL BIOCHEMISTRY, 2013, 24 (11) :1777-1789
[5]   RATES AND TISSUE SITES OF NON-INSULIN-MEDIATED AND INSULIN-MEDIATED GLUCOSE-UPTAKE IN HUMANS [J].
BARON, AD ;
BRECHTEL, G ;
WALLACE, P ;
EDELMAN, SV .
AMERICAN JOURNAL OF PHYSIOLOGY, 1988, 255 (06) :E769-E774
[6]   Combined Effects of Oligofructose and Bifidobacterium animalis on Gut Microbiota and Glycemia in Obese Rats [J].
Bomhof, Marc R. ;
Saha, Dolan C. ;
Reid, Danielle T. ;
Paul, Heather A. ;
Reimer, Raylene A. .
OBESITY, 2014, 22 (03) :763-771
[7]  
Boto-Ordóñez M, 2014, FOOD FUNCT, V5, P1932, DOI [10.1039/C4FO00029C, 10.1039/c4fo00029c]
[8]   Selective versus total insulin resistance: A pathogenic paradox [J].
Brown, Michael S. ;
Goldstein, Joseph L. .
CELL METABOLISM, 2008, 7 (02) :95-96
[9]   The FoxO code [J].
Calnan, D. R. ;
Brunet, A. .
ONCOGENE, 2008, 27 (16) :2276-2288
[10]   Genetic deletion of p66Shc adaptor protein prevents hyperglycemia-induced endothelial dysfunction and oxidative stress [J].
Camici, Giovanni G. ;
Schiavoni, Marzia ;
Francia, Pietro ;
Bachschmid, Markus ;
Martin-Padura, Ines ;
Hersberger, Martin ;
Tanner, Felix C. ;
Pelicci, PierGiuseppe ;
Volpe, Massimo ;
Anversa, Piero ;
Luescher, Thomas F. ;
Cosentino, Francesco .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2007, 104 (12) :5217-5222