PMID- 24957699
OWN - NLM
STAT- MEDLINE
DCOM- 20150330
LR  - 20220408
IS  - 1475-2840 (Electronic)
IS  - 1475-2840 (Linking)
VI  - 13
DP  - 2014 Jun 23
TI  - Adiponectin: a manifold therapeutic target for metabolic syndrome, diabetes, and 
      coronary disease?
PG  - 103
LID - 10.1186/1475-2840-13-103 [doi]
AB  - Adiponectin is the most abundant peptide secreted by adipocytes, being a key 
      component in the interrelationship between adiposity, insulin resistance and 
      inflammation. Central obesity accompanied by insulin resistance is a key factor 
      in the development of metabolic syndrome (MS) and future macrovascular 
      complications. Moreover, the remarkable correlation between coronary artery 
      disease (CAD) and alterations in glucose metabolism has raised the likelihood 
      that atherosclerosis and type 2 diabetes mellitus (T2DM) may share a common 
      biological background. We summarize here the current knowledge about the 
      influence of adiponectin on insulin sensitivity and endothelial function, 
      discussing its forthcoming prospects and potential role as a therapeutic target 
      for MS, T2DM, and cardiovascular disease. Adiponectin is present in the 
      circulation as a dimer, trimer or protein complex of high molecular weight 
      hexamers, >400 kDa. AdipoR1 and AdipoR2 are its major receptors in vivo mediating 
      the metabolic actions. Adiponectin stimulates phosphorylation and AMP (adenosin 
      mono phosphate) kinase activation, exerting direct effects on vascular 
      endothelium, diminishing the inflammatory response to mechanical injury and 
      enhancing endothelium protection in cases of apolipoprotein E deficiency. 
      Hypoadiponectinemia is consistently associated with obesity, MS, atherosclerosis, 
      CAD, T2DM. Lifestyle correction helps to favorably modify plasma adiponectin 
      levels. Low adiponectinemia in obese patients is raised via continued weight loss 
      programs in both diabetic and nondiabetic individuals and is also accompanied by 
      reductions in pro-inflammatory factors. Diet modifications, like intake of fish, 
      omega-3 supplementation, adherence to a Mediterranean dietary pattern and coffee 
      consumption also increase adiponectin levels. Antidiabetic and cardiovascular 
      pharmacological agents, like glitazones, glimepiride, angiotensin converting 
      enzyme inhibitors and angiotensin receptor blockers are also able to improve 
      adiponectin concentration. Fibric acid derivatives, like bezafibrate and 
      fenofibrate, have been reported to enhance adiponectin levels as well. 
      T-cadherin, a membrane-associated adiponectin-binding protein lacking 
      intracellular domain seems to be a main mediator of the antiatherogenic 
      adiponectin actions. The finding of novel pharmacologic agents proficient to 
      improve adiponectin plasma levels should be target of exhaustive research. 
      Interesting future approaches could be the development of adiponectin-targeted 
      drugs chemically designed to induce the activaton of its receptors and/or 
      postreceptor signaling pathways, or the development of specific adiponectin 
      agonists.
FAU - Fisman, Enrique Z
AU  - Fisman EZ
AD  - Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv 69978, Israel. 
      zfisman@post.tau.ac.il.
FAU - Tenenbaum, Alexander
AU  - Tenenbaum A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20140623
PL  - England
TA  - Cardiovasc Diabetol
JT  - Cardiovascular diabetology
JID - 101147637
RN  - 0 (Adiponectin)
RN  - 0 (Biomarkers)
RN  - 0 (Cardiovascular Agents)
RN  - 0 (Hypoglycemic Agents)
SB  - IM
MH  - Adiponectin/*blood
MH  - Animals
MH  - Biomarkers/blood
MH  - Cardiovascular Agents/administration & dosage
MH  - Coronary Disease/*blood/drug therapy
MH  - Diabetes Mellitus, Type 2/*blood/drug therapy
MH  - Drug Delivery Systems/*trends
MH  - Humans
MH  - Hypoglycemic Agents/administration & dosage
MH  - Metabolic Syndrome/*blood/drug therapy
MH  - Obesity/blood/drug therapy
MH  - Signal Transduction/drug effects/physiology
PMC - PMC4230016
EDAT- 2014/06/25 06:00
MHDA- 2015/03/31 06:00
PMCR- 2014/06/23
CRDT- 2014/06/25 06:00
PHST- 2014/05/23 00:00 [received]
PHST- 2014/05/26 00:00 [accepted]
PHST- 2014/06/25 06:00 [entrez]
PHST- 2014/06/25 06:00 [pubmed]
PHST- 2015/03/31 06:00 [medline]
PHST- 2014/06/23 00:00 [pmc-release]
AID - 1475-2840-13-103 [pii]
AID - 10.1186/1475-2840-13-103 [doi]
PST - epublish
SO  - Cardiovasc Diabetol. 2014 Jun 23;13:103. doi: 10.1186/1475-2840-13-103.