PMID- 27942464
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200929
IS  - 2214-7624 (Print)
IS  - 2214-7624 (Electronic)
IS  - 2214-7624 (Linking)
VI  - 13
DP  - 2016 Dec
TI  - Short-term caloric restriction in db/db mice improves myocardial function and 
      increases high molecular weight (HMW) adiponectin.
PG  - 28-34
AB  - BACKGROUND: Obesity and metabolic syndrome lead to the development of metabolic 
      heart disease (MHD) that is characterized by left ventricular hypertrophy (LVH), 
      diastolic dysfunction, and increased mitochondrial ROS. Caloric restriction (CR) 
      is a nutritional intervention that protects against obesity, diabetes, and 
      cardiovascular disease. Healthy adipose tissue is cardioprotective via releasing 
      adipokines such as adiponectin. We tested the hypothesis that CR can ameliorate 
      MHD and it is associated with improved adipose tissue function as reflected by 
      increased circulating levels of high molecular weight (HMW) adiponectin and 
      AMP-activated protein kinase (AMPK) in db/db mice. METHODS: Genetically obese 
      db/db and lean db/+ male mice were fed either ad libitum or subjected to 30% CR 
      for 5 weeks. At the end of the study period, echocardiography was carried out to 
      assess diastolic function. Blood, heart, and epididymal fat pads were harvested 
      for mitochondrial study, ELISA, and Western blot analyses. RESULTS: CR reversed 
      the development of LVH, prevented diastolic dysfunction, and decreased cardiac 
      mitochondrial H(2)O(2) in db/db (vs. ad lib) mice. These beneficial effects on 
      the heart were associated with increased circulating level of HMW adiponectin. 
      Furthermore, CR increased AMPK and eNOS activation in white adipose tissue of 
      db/db mice, but not in the heart. CONCLUSIONS: These findings indicate that even 
      short-term CR protects the heart from MHD. Whether the beneficial effects of CR 
      on the heart could be related to the improved adipose tissue function warrants 
      future investigation.
FAU - Xu, X Julia
AU  - Xu XJ
AD  - Diabetes and Metabolism Unit, Section of Endocrinology, Department of Medicine, 
      Boston University Medical Center, Boston, Massachusetts.
FAU - Babo, Erma
AU  - Babo E
AD  - Diabetes and Metabolism Unit, Section of Endocrinology, Department of Medicine, 
      Boston University Medical Center, Boston, Massachusetts.
FAU - Qin, Fuzhong
AU  - Qin F
AD  - Cardiovascular Medicine Section, Department of Medicine, Boston University 
      Medical Center, Boston, Massachusetts.
FAU - Croteau, Dominique
AU  - Croteau D
AD  - Cardiovascular Medicine Section, Department of Medicine, Boston University 
      Medical Center, Boston, Massachusetts.
FAU - Colucci, Wilson S
AU  - Colucci WS
AD  - Cardiovascular Medicine Section, Department of Medicine, Boston University 
      Medical Center, Boston, Massachusetts.
LA  - eng
GR  - KL2 TR001411/TR/NCATS NIH HHS/United States
GR  - R01 HL064750/HL/NHLBI NIH HHS/United States
PT  - Journal Article
DEP - 20161020
PL  - Ireland
TA  - IJC Metab Endocr
JT  - IJC metabolic & endocrine
JID - 101643909
PMC - PMC5142532
MID - NIHMS827931
OTO - NOTNLM
OT  - AMPK
OT  - adipose tissue
OT  - caloric restriction
OT  - metabolic heart disease
EDAT- 2016/12/13 06:00
MHDA- 2016/12/13 06:01
PMCR- 2017/12/01
CRDT- 2016/12/13 06:00
PHST- 2016/12/13 06:00 [entrez]
PHST- 2016/12/13 06:00 [pubmed]
PHST- 2016/12/13 06:01 [medline]
PHST- 2017/12/01 00:00 [pmc-release]
AID - 10.1016/j.ijcme.2016.10.002 [doi]
PST - ppublish
SO  - IJC Metab Endocr. 2016 Dec;13:28-34. doi: 10.1016/j.ijcme.2016.10.002. Epub 2016 
      Oct 20.