PMID- 23448493
OWN - NLM
STAT- MEDLINE
DCOM- 20140319
LR  - 20190728
IS  - 1873-4286 (Electronic)
IS  - 1381-6128 (Linking)
VI  - 19
IP  - 32
DP  - 2013
TI  - Endothelial dysfunction in morbid obesity.
PG  - 5718-29
AB  - Morbid obesity is a chronic multifunctional disease characterized by an 
      accumulation of fat. Epidemiological studies have shown that obesity is 
      associated with cardiovascular and metabolic disorders. Endothelial dysfunction, 
      as defined by an imbalance between relaxing and contractile endothelial factors, 
      plays a central role in the pathogenesis of these cardiometabolic diseases. 
      Diminished bioavailability of nitric oxide (NO) contributes to endothelial 
      dysfunction and impairs endothelium- dependent vasodilatation. But this is not 
      the only mechanism that drives to endothelial dysfunction. Obesity has been 
      associated with a chronic inflammatory process, atherosclerosis, and oxidative 
      stress. Moreover levels of asymmetrical dimethyl-L-arginine (ADMA), an endogenous 
      inhibitor of endothelial nitric oxide synthase (eNOS), are elevated in obesity. 
      On the other hand, increasing prostanoid-dependent vasoconstriction and 
      decreasing vasodilator prostanoids also lead to endothelial dysfunction in 
      obesity. Other mechanisms related to endothelin-1 (ET-1) or endothelium derived 
      hyperpolarizing factor (EDHF) have been proposed. Bariatric surgery (BS) is a 
      safe and effective means to achieve significant weight loss, but its use is 
      limited only to patients with severe obesity including morbid obesity. BS also 
      proved efficient in endothelial dysfunction reduction improving cardiovascular 
      and metabolic comorbidities associated with morbid obesity such as diabetes, 
      coronary artery disease, nonalcoholic fatty liver disease and cancer. This review 
      will provide a brief overview of the mechanisms that link obesity with 
      endothelial dysfunction, and how weight loss is a cornerstone treatment for 
      cardiovascular comorbidities obesity-related. A better understanding of the 
      mechanisms of obesity-induced endothelial dysfunction may help develop new 
      therapeutic strategies to reduce cardiovascular morbidity and mortality.
FAU - Mauricio, Maria Dolores
AU  - Mauricio MD
AD  - Departamento de Fisiologia, Universidad de Valencia, Av. Blasco Ibanez 15, 46010 
      Valencia, Spain.
FAU - Aldasoro, Martin
AU  - Aldasoro M
FAU - Ortega, Joaquin
AU  - Ortega J
FAU - Vila, Jose Maria
AU  - Vila JM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United Arab Emirates
TA  - Curr Pharm Des
JT  - Current pharmaceutical design
JID - 9602487
RN  - 31C4KY9ESH (Nitric Oxide)
SB  - IM
MH  - Animals
MH  - Atherosclerosis/etiology/physiopathology
MH  - Cardiovascular Diseases/*etiology/physiopathology/prevention & control
MH  - Endothelium, Vascular/*physiopathology
MH  - Humans
MH  - Inflammation/etiology/physiopathology
MH  - Nitric Oxide/metabolism
MH  - Obesity, Morbid/complications/*physiopathology
MH  - Oxidative Stress
MH  - Vasodilation
MH  - Weight Loss
EDAT- 2013/03/02 06:00
MHDA- 2014/03/22 06:00
CRDT- 2013/03/02 06:00
PHST- 2013/01/16 00:00 [received]
PHST- 2013/02/18 00:00 [accepted]
PHST- 2013/03/02 06:00 [entrez]
PHST- 2013/03/02 06:00 [pubmed]
PHST- 2014/03/22 06:00 [medline]
AID - CPD-EPUB-20130220-16 [pii]
AID - 10.2174/1381612811319320007 [doi]
PST - ppublish
SO  - Curr Pharm Des. 2013;19(32):5718-29. doi: 10.2174/1381612811319320007.