PMID- 25877002
OWN - NLM
STAT- MEDLINE
DCOM- 20160325
LR  - 20150630
IS  - 1502-7708 (Electronic)
IS  - 0036-5521 (Linking)
VI  - 50
IP  - 9
DP  - 2015
TI  - The aggravation of mitochondrial dysfunction in nonalcoholic fatty liver disease 
      accompanied with type 2 diabetes mellitus.
PG  - 1152-9
LID - 10.3109/00365521.2015.1030687 [doi]
AB  - OBJECTIVE: Nonalcoholic fatty liver disease (NAFLD) is a mitochondrial disease 
      associated with the metabolic syndrome, but few data are available on the 
      mitochondrial dysfunction of NAFLD after the development of type 2 diabetes 
      mellitus (T2DM). We aimed to identify the changes of mitochondrial function in 
      rat livers when T2DM develops after NAFLD. MATERIAL AND METHODS: Rat models of 
      nonalcoholic fatty liver (NAFL) and T2DM were established using high-fat diet and 
      streptozocin. Mitochondria were isolated from the livers. The levels of reactive 
      oxygen species (ROS) and mRNA and protein levels of mitochondrial complex IV (COX 
      IV) and carnitine palmitoyltransferase-1 (CPT-1) were assessed in rat livers. The 
      mitochondrial membrane potential (MP), and the enzyme activities of COX IV and 
      CPT-1 were measured in isolated mitochondria. RESULTS: There were increased ROS, 
      decreased mitochondrial MP, and reduced COX IV and CPT-1 activity in the NAFL and 
      T2DM groups compared with controls (p < 0.05). Compared with NAFL, the T2DM group 
      had higher ROS levels and lower enzyme activity (p < 0.05), but showed no 
      difference in mitochondrial MP. Although COX IV and CPT-1 expression levels in 
      liver decreased in NAFL and T2DM, there was no significant difference between two 
      groups. CONCLUSION: This study first identified progressively impaired 
      mitochondrial respiratory chain and beta-oxidation in NAFLD when T2DM develops, 
      inducing overproduction of ROS, and finally triggering a vicious circle that 
      leads to the aggravation of mitochondrial dysfunction in NAFLD after development 
      of T2DM.
FAU - Liu, Xiaolin
AU  - Liu X
AD  - Division of Gastroenterology and Hepatology, Renji Hospital, School of Medicine, 
      Shanghai Jiao Tong University, Shanghai Institute of Digestive Disease , Shanghai 
      200000 , China.
FAU - Zhang, Jingyi
AU  - Zhang J
FAU - Ming, Yanan
AU  - Ming Y
FAU - Chen, Xiaoyu
AU  - Chen X
FAU - Zeng, Minde
AU  - Zeng M
FAU - Mao, Yimin
AU  - Mao Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150415
PL  - England
TA  - Scand J Gastroenterol
JT  - Scandinavian journal of gastroenterology
JID - 0060105
RN  - 0 (Blood Glucose)
RN  - EC 2.3.1.21 (Carnitine O-Palmitoyltransferase)
SB  - IM
MH  - Animals
MH  - Blood Glucose
MH  - Carnitine O-Palmitoyltransferase/*genetics
MH  - Diabetes Mellitus, Type 2/*complications
MH  - Disease Models, Animal
MH  - Liver/*pathology
MH  - Male
MH  - Mitochondria, Liver/*metabolism
MH  - Non-alcoholic Fatty Liver Disease/*complications
MH  - Rats
MH  - Rats, Sprague-Dawley
OTO - NOTNLM
OT  - carnitine palmitoyltransferase
OT  - diabetes mellitus
OT  - mitochondrial complex IV
OT  - mitochondrial disease
OT  - non-alcoholic fatty liver disease
EDAT- 2015/04/17 06:00
MHDA- 2016/03/26 06:00
CRDT- 2015/04/17 06:00
PHST- 2015/04/17 06:00 [entrez]
PHST- 2015/04/17 06:00 [pubmed]
PHST- 2016/03/26 06:00 [medline]
AID - 10.3109/00365521.2015.1030687 [doi]
PST - ppublish
SO  - Scand J Gastroenterol. 2015;50(9):1152-9. doi: 10.3109/00365521.2015.1030687. 
      Epub 2015 Apr 15.