Astragalus mongholicus powder, a traditional Chinese medicine formula ameliorate type 2 diabetes by regulating adipoinsular axis in diabetic mice

被引:13
作者
Xu, Siyuan [1 ]
Ye, Bixian [2 ]
Li, Jinlei [3 ]
Dou, Yonghui [3 ]
Yu, Yuying [1 ]
Feng, Yifan [1 ]
Wang, Lexun [1 ]
Wan, David Chi-Cheong [4 ]
Rong, Xianglu [1 ]
机构
[1] Guangdong Pharmaceut Univ, Inst Chinese Med, Guangdong Metab Dis Res Ctr Integrated Chinese & W, Key Lab Glucolipid Metab Disorder,Guangdong TCM Ke, Guangzhou, Peoples R China
[2] Jiaying Univ, Dept Nursing, Med Coll, Meizhou, Peoples R China
[3] Guangzhou Univ Chinese Med, Sch Chinese Meteria Med, Guangzhou, Peoples R China
[4] Chinese Univ Hong Kong, Sch Biomed Sci, Hong Kong, Peoples R China
基金
中国国家自然科学基金;
关键词
Astragalus mongholicus powder; type 2 diabetes mellitus; insulin resistance; adipoinsular axis; leptin; GENETICALLY-OBESE MICE; INSULIN-RESISTANCE; GENE-EXPRESSION; LEPTIN RESISTANCE; POMC NEURONS; PPAR-ALPHA; ADIPOSE; ACTIVATION; DIET; HYPERLEPTINEMIA;
D O I
10.3389/fphar.2022.973927
中图分类号
R9 [药学];
学科分类号
100702 [药剂学];
摘要
The global morbidity of obesity and type 2 diabetes mellitus (T2DM) has dramatically increased. Insulin resistance is the most important pathogenesis and therapeutic target of T2DM. The traditional Chinese medicine formula Astragalus mongholicus powder (APF), consists of Astragalus mongholicus Bunge [Fabaceae], Pueraria montana (Lour.) Merr. [Fabaceae], and Morus alba L. [Moraceae] has a long history to be used to treat diabetes in ancient China. This work aims to investigate the effects of APF on diabetic mice and its underlying mechanism. Diabetic mice were induced by High-fat-diet (HFD) and streptozotocin (STZ). The body weight of mice and their plasma levels of glucose, insulin, leptin and lipids were examined. Reverse transcription-polymerase chain reaction, histology, and Western blot analysis were performed to validate the effects of APF on diabetic mice and investigate the underlying mechanism. APF reduced hyperglycemia, hyperinsulinemia, and hyerleptinemia and attenuate the progression of obesity and non-alcoholic fatty liver disease (NAFLD). However, these effects disappeared in leptin deficient ob/ob diabetic mice and STZ-induced insulin deficient type 1 diabetic mice. Destruction of either these hormones would abolish the therapeutic effects of APF. In addition, APF inhibited the protein expression of PTP1B suppressing insulin-leptin sensitivity, the gluconeogenic gene PEPCK, and the adipogenic gene FAS. Therefore, insulin-leptin sensitivity was normalized, and the gluconeogenic and adipogenic genes were suppressed. In conclusion, APF attenuated obesity, NAFLD, and T2DM by regulating the balance of adipoinsular axis in STZ + HFD induced T2DM mice.
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页数:13
相关论文
共 56 条
[1]
Insulin-Stimulated Increase in Serum Leptin Levels Precedes and Correlates with Weight Gain during Insulin Therapy in Type 2 Diabetes [J].
Aas, Anne-Marie ;
Hanssen, Kristian F. ;
Berg, Jens Petter ;
Thorsby, Per M. ;
Birkeland, Kare I. .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2009, 94 (08) :2900-2906
[2]
Modulation of adipoinsular axis in prediabetic Zucker diabetic fatty rats by diazoxide [J].
Alemzadeh, R ;
Tushaus, KM .
ENDOCRINOLOGY, 2004, 145 (12) :5476-5484
[3]
Deletion of Protein Tyrosine Phosphatase 1b Improves Peripheral Insulin Resistance and Vascular Function in Obese, Leptin-Resistant Mice via Reduced Oxidant Tone [J].
Ali, M. Irfan ;
Ketsawatsomkron, Pimonrat ;
de Chantemele, Eric J. Belin ;
Mintz, James D. ;
Muta, Kenjiro ;
Salet, Christina ;
Black, Stephen M. ;
Tremblay, Michel L. ;
Fulton, David J. ;
Marrero, Mario B. ;
Stepp, David W. .
CIRCULATION RESEARCH, 2009, 105 (10) :1013-U172
[4]
New insights in leptin resistance mechanisms in mice [J].
Balland, Eglantine ;
Cowley, Michael A. .
FRONTIERS IN NEUROENDOCRINOLOGY, 2015, 39 :59-65
[5]
Leptin receptor signaling in is required for normal body POW neurons weight homeostasis [J].
Balthasar, N ;
Coppari, R ;
McMinn, J ;
Liu, SM ;
Lee, CE ;
Tang, V ;
Kenny, CD ;
McGovern, RA ;
Chua, SC ;
Elmquist, JK ;
Lowell, BB .
NEURON, 2004, 42 (06) :983-991
[6]
Direct leptin action on POMC neurons regulates glucose homeostasis and hepatic insulin sensitivity in mice [J].
Berglund, Eric D. ;
Vianna, Claudia R. ;
Donato, Jose, Jr. ;
Kim, Mi Hwa ;
Chuang, Jen-Chieh ;
Lee, Charlotte E. ;
Lauzon, Danielle A. ;
Lin, Peagan ;
Brule, Laura J. ;
Scott, Michael M. ;
Coppari, Roberto ;
Elmquist, Joel K. .
JOURNAL OF CLINICAL INVESTIGATION, 2012, 122 (03) :1000-1009
[7]
Critical role of STAT3 in leptin's metabolic actions [J].
Buettner, Christoph ;
Pocai, Alessandro ;
Muse, Evan D. ;
Etgen, Anne M. ;
Myers, Martin G., Jr. ;
Rossetti, Luciano .
CELL METABOLISM, 2006, 4 (01) :49-60
[8]
Acute intravenous leptin infusion increases glucose turnover but not skeletal muscle glucose uptake in ob/ob mice [J].
Burcelin, R ;
Kamohara, S ;
Li, J ;
Tannenbaum, GS ;
Charron, MJ ;
Friedman, JM .
DIABETES, 1999, 48 (06) :1264-1269
[9]
The Metabolic Syndrome [J].
Cornier, Marc-Andre ;
Dabelea, Dana ;
Hernandez, Teri L. ;
Lindstrom, Rachel C. ;
Steig, Amy J. ;
Stob, Nicole R. ;
Van Pelt, Rachael E. ;
Wang, Hong ;
Eckel, Robert H. .
ENDOCRINE REVIEWS, 2008, 29 (07) :777-822
[10]
The pancreatic β cell is a key site for mediating the effects of leptin on glucose homeostasis [J].
Covey, Scott D. ;
Wideman, Rhonda D. ;
McDonald, Christine ;
Unniappan, Suraj ;
Huynh, Frank ;
Asadi, Ali ;
Speck, Madeleine ;
Webber, Travis ;
Chua, Streamson C. ;
Kieffer, Timothy J. .
CELL METABOLISM, 2006, 4 (04) :291-302