PMID- 30226559
OWN - NLM
STAT- MEDLINE
DCOM- 20190121
LR  - 20190121
IS  - 1791-244X (Electronic)
IS  - 1107-3756 (Print)
IS  - 1107-3756 (Linking)
VI  - 42
IP  - 5
DP  - 2018 Nov
TI  - Treatment of type 2 diabetes mellitus via reversing insulin resistance and 
      regulating lipid homeostasis in vitro and in vivo using cajanonic acid A.
PG  - 2329-2342
LID - 10.3892/ijmm.2018.3836 [doi]
AB  - The present study investigated the effects of cajanonic acid A (CAA), extracted 
      from the leaves of Cajanus cajan (L.) Millsp with a purity of 98.22%, on the 
      regulatory mechanisms of glucose and lipid metabolism. HepG2 cells transfected 
      with a protein‑tyrosine phosphatase 1B (PTP1B) overexpression plasmid were 
      established. The cells, induced with insulin resistance by dexamethasone (Dex) 
      treatment, together with type 2 diabetes mellitus (T2DM) model rats and ob/ob 
      mice, were used in the present study. The effects of CAA treatment on the 
      differentiation of 3T3‑L1 adipocytes were determined using Oil Red O. The 
      expression levels of insulin signaling factors were detected via reverse 
      transcription‑quantitative polymerase chain reaction and western blot analyses. 
      The results revealed that the overexpression of PTP1B contributed to insulin 
      resistance, which was reversed by CAA treatment via inhibiting the activity of 
      PTP1B and by regulating the expression of associated insulin signaling factors. 
      The treatment of cell lines with Dex led to increased expression of PTP1B but 
      decreased glucose consumption, and decreased tyrosine phosphorylation of insulin 
      receptor, insulin receptor substrate 1, and phosphoinositide 3‑kinase. Treatment 
      with CAA not only reduced the fasting blood glucose levels and protected organs 
      from damage, but also reduced the serum fasting levels of total cholesterol, 
      triglycerides and low‑density lipoprotein cholesterol in the T2DM rats. CAA 
      treatment also inhibited adipocyte differentiation and decreased the mRNA levels 
      of various adipogenic genes. Furthermore, CAA treatment restored the transduction 
      of insulin signaling by regulating the expression of PTP1B and associated insulin 
      signaling factors. Treatment with CAA also reduced the problems associated with 
      hyperglycemia and hyperlipidemia. In conclusion, CAA may be used to cure T2DM via 
      restoring insulin resistance and preventing obesity.
FAU - Yang, Ruiyi
AU  - Yang R
AD  - Laboratory of Chinese Herbal Drug Discovery, Institute of Tropical Medicine, 
      Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, P.R. 
      China.
FAU - Wang, Lu
AU  - Wang L
AD  - Laboratory of Chinese Herbal Drug Discovery, Institute of Tropical Medicine, 
      Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, P.R. 
      China.
FAU - Xie, Jie
AU  - Xie J
AD  - Laboratory of Chinese Herbal Drug Discovery, Institute of Tropical Medicine, 
      Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, P.R. 
      China.
FAU - Li, Xiang
AU  - Li X
AD  - Laboratory of Chinese Herbal Drug Discovery, Institute of Tropical Medicine, 
      Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, P.R. 
      China.
FAU - Liu, Shan
AU  - Liu S
AD  - Laboratory of Chinese Herbal Drug Discovery, Institute of Tropical Medicine, 
      Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, P.R. 
      China.
FAU - Qiu, Shengxiang
AU  - Qiu S
AD  - Key Laboratory of Plant Resources Conservation and Sustainable Utilization, South 
      China Botanical Garden, Chinese Academy of Sciences, Guangzhou, Guangdong 510650, 
      P.R. China.
FAU - Hu, Yingjie
AU  - Hu Y
AD  - Laboratory of Chinese Herbal Drug Discovery, Institute of Tropical Medicine, 
      Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, P.R. 
      China.
FAU - Shen, Xiaoling
AU  - Shen X
AD  - Laboratory of Chinese Herbal Drug Discovery, Institute of Tropical Medicine, 
      Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, P.R. 
      China.
LA  - eng
PT  - Journal Article
DEP - 20180823
PL  - Greece
TA  - Int J Mol Med
JT  - International journal of molecular medicine
JID - 9810955
RN  - 0 (Hypoglycemic Agents)
RN  - 0 (Stilbenes)
RN  - EC 3.1.3.48 (PTPN1 protein, human)
RN  - EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 1)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - 3T3-L1 Cells
MH  - Animals
MH  - Cajanus/*chemistry
MH  - Diabetes Mellitus, Type 2/*drug therapy/metabolism
MH  - Glucose/metabolism
MH  - Hep G2 Cells
MH  - Humans
MH  - Hypoglycemic Agents/chemistry/*therapeutic use
MH  - *Insulin Resistance
MH  - Lipid Metabolism/*drug effects
MH  - Male
MH  - Mice
MH  - Protein Tyrosine Phosphatase, Non-Receptor Type 1/metabolism
MH  - Rats, Sprague-Dawley
MH  - Stilbenes/chemistry/*therapeutic use
PMC - PMC6192715
EDAT- 2018/09/19 06:00
MHDA- 2019/01/22 06:00
PMCR- 2018/08/23
CRDT- 2018/09/19 06:00
PHST- 2017/06/26 00:00 [received]
PHST- 2018/07/25 00:00 [accepted]
PHST- 2018/09/19 06:00 [pubmed]
PHST- 2019/01/22 06:00 [medline]
PHST- 2018/09/19 06:00 [entrez]
PHST- 2018/08/23 00:00 [pmc-release]
AID - ijmm-42-05-2329 [pii]
AID - 10.3892/ijmm.2018.3836 [doi]
PST - ppublish
SO  - Int J Mol Med. 2018 Nov;42(5):2329-2342. doi: 10.3892/ijmm.2018.3836. Epub 2018 
      Aug 23.