PMID- 23057715
OWN - NLM
STAT- MEDLINE
DCOM- 20130320
LR  - 20220408
IS  - 1475-2840 (Electronic)
IS  - 1475-2840 (Linking)
VI  - 11
DP  - 2012 Oct 11
TI  - Reduction of n-3 PUFAs, specifically DHA and EPA, and enhancement of peroxisomal 
      beta-oxidation in type 2 diabetic rat heart.
PG  - 126
LID - 10.1186/1475-2840-11-126 [doi]
AB  - BACKGROUND: There is overwhelming evidence that dietary supplementation with n-3 
      polyunsaturated fatty acids (PUFAs), mainly EPA (C20:5n-3) and DHA (C22:6n-3), 
      has cardiovascular protective effects on patients with type 2 diabetes mellitus 
      (T2DM) but not on healthy people. Because the T2DM heart increases fatty acid 
      oxidation (FAO) to compensate for the diminished utilization of glucose, we 
      hypothesize that T2DM hearts consume more n-3 PUFAs and, therefore, need more n-3 
      PUFAs. In the present study, we investigated the changes in cardiac n-3 PUFAs and 
      peroxisomal beta-oxidation, which are responsible for the degradation of PUFAs in 
      a high-fat diet (HFD) and low-dose streptozotocin- (STZ) induced type 2 diabetic 
      rat model. METHODS AND RESULTS: The capillary gas chromatography results showed 
      that all the n-3 (or omega-3) PUFAs, especially DHA (~50%) and EPA (~100%), were 
      significantly decreased, and the n-6/n-3 ratio (~115%) was significantly 
      increased in the hearts of diabetic rats. The activity of peroxisomal 
      beta-oxidation, which is crucial to very-long-chain and unsaturated FA metabolism 
      (including DHA), was significantly elevated in DM hearts. Additionally, the 
      real-time PCR results showed that the mRNA expression of most peroxisomal 
      beta-oxidation key enzymes were up-regulated in T2DM rat hearts, which might 
      contribute to the reduction of n-3 (or omega-3) PUFAs. CONCLUSION: In conclusion, 
      our results indicate that T2DM hearts consume more n-3 PUFAs, especially DHA and 
      EPA, due to exaggerated peroxisomal beta-oxidation.
FAU - Hou, Lianguo
AU  - Hou L
AD  - Department of Biochemistry and Molecular Biology, The Key Laboratory of 
      Neurobiology and Vascular Biology, China Administration of Education, Hebei 
      Medical University, No, 361 Zhongshan East Road, Shijiazhuang, 050017, China.
FAU - Lian, Kaoqi
AU  - Lian K
FAU - Yao, Min
AU  - Yao M
FAU - Shi, Yun
AU  - Shi Y
FAU - Lu, Xin
AU  - Lu X
FAU - Fang, Lijia
AU  - Fang L
FAU - He, Tianbo
AU  - He T
FAU - Jiang, Lingling
AU  - Jiang L
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20121011
PL  - England
TA  - Cardiovasc Diabetol
JT  - Cardiovascular diabetology
JID - 101147637
RN  - 0 (RNA, Messenger)
RN  - 25167-62-8 (Docosahexaenoic Acids)
RN  - AAN7QOV9EA (Eicosapentaenoic Acid)
RN  - EC 1.3.3.6 (Acox3 protein, rat)
RN  - EC 1.3.3.6 (Acyl-CoA Oxidase)
SB  - IM
MH  - Acyl-CoA Oxidase/genetics/metabolism
MH  - Animals
MH  - Chromatography, Gas
MH  - Diabetes Mellitus, Experimental/blood/enzymology/genetics/*metabolism
MH  - Diabetes Mellitus, Type 2/blood/enzymology/genetics/*metabolism
MH  - Docosahexaenoic Acids/blood/*metabolism
MH  - Eicosapentaenoic Acid/blood/*metabolism
MH  - Energy Metabolism
MH  - Gene Expression Regulation, Enzymologic
MH  - Male
MH  - Mitochondria, Heart/enzymology/metabolism
MH  - Myocardium/*metabolism
MH  - Oxidation-Reduction
MH  - Peroxisomes/*metabolism
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Real-Time Polymerase Chain Reaction
PMC - PMC3490815
EDAT- 2012/10/13 06:00
MHDA- 2013/03/21 06:00
PMCR- 2012/10/11
CRDT- 2012/10/13 06:00
PHST- 2012/06/18 00:00 [received]
PHST- 2012/10/09 00:00 [accepted]
PHST- 2012/10/13 06:00 [entrez]
PHST- 2012/10/13 06:00 [pubmed]
PHST- 2013/03/21 06:00 [medline]
PHST- 2012/10/11 00:00 [pmc-release]
AID - 1475-2840-11-126 [pii]
AID - 10.1186/1475-2840-11-126 [doi]
PST - epublish
SO  - Cardiovasc Diabetol. 2012 Oct 11;11:126. doi: 10.1186/1475-2840-11-126.