TY - JOUR
T1 - Hypoadiponectinemia as a marker of adipocyte dysfunction -- Part I
T2 - the biology of adiponectin.
AU - Stern, Naftali
AU - Osher, Etty
AU - Greenman, Yona
PY - 2007
Y1 - 2007
N2 - Adiponectin is the most abundantly secreted adipocyte-derived peptide hormone, possessing an array of antidiabetogenic and cardiovascular protective effects. Acting through 2 distinct membrane receptors, adiponectin receptors 1 and 2 (which utilize 5'-adenosine monophosphate-activated protein kinase phosphorylation, p38 mitogen-activated protein kinase, and peroxisome proliferator-activated receptor alpha as key cell signaling elements), adiponectin increases hepatic and skeletal muscle sensitivity to insulin, enhances fatty acid oxidation, suppresses monocyte-endothelial interaction, supports endothelial cell growth, lowers blood pressure, and moderates adipose tissue growth. The secretion of adiponectin can be suppressed by adipose factors, which are turned on once fat cell mass increases, such as cytokines, adipose renin-angiotensin system, and increased oxidative stress. Inhibition of adiponectin secretion results in the loss of an array of mechanisms, which under normal conditions of fat cell homeostasis provide protection from insulin resistance, diabetes, and atherosclerosis.
AB - Adiponectin is the most abundantly secreted adipocyte-derived peptide hormone, possessing an array of antidiabetogenic and cardiovascular protective effects. Acting through 2 distinct membrane receptors, adiponectin receptors 1 and 2 (which utilize 5'-adenosine monophosphate-activated protein kinase phosphorylation, p38 mitogen-activated protein kinase, and peroxisome proliferator-activated receptor alpha as key cell signaling elements), adiponectin increases hepatic and skeletal muscle sensitivity to insulin, enhances fatty acid oxidation, suppresses monocyte-endothelial interaction, supports endothelial cell growth, lowers blood pressure, and moderates adipose tissue growth. The secretion of adiponectin can be suppressed by adipose factors, which are turned on once fat cell mass increases, such as cytokines, adipose renin-angiotensin system, and increased oxidative stress. Inhibition of adiponectin secretion results in the loss of an array of mechanisms, which under normal conditions of fat cell homeostasis provide protection from insulin resistance, diabetes, and atherosclerosis.
UR - http://www.scopus.com/inward/record.url?scp=38449089805&partnerID=8YFLogxK
U2 - 10.1111/j.1559-4564.2007.06597.x
DO - 10.1111/j.1559-4564.2007.06597.x
M3 - ???researchoutput.researchoutputtypes.contributiontojournal.systematicreview???
C2 - 17786081
AN - SCOPUS:38449089805
SN - 1559-4564
VL - 2
SP - 174
EP - 182
JO - Journal of the CardioMetabolic Syndrome
JF - Journal of the CardioMetabolic Syndrome
IS - 3
ER -