[Metabolic syndrome].
Angiotensin II suppresses the insulin sensitivity via enhancement of serine phosphorylation of insulin receptor and suppression of tyrosine phosphorylation of IRS-1. Adiponectin increases insulin sensitivity, and TNF-alpha decreases insulin sensitivity. From our studies, the suppressed adiponectin and increased TNF-alpha may play an important role of the insulin resistance mechanisms. Angiotensin II suppresses the differentiation of adipocyte. Large sized adipocytes increase TNF-alpha and decrease adiponectin. Angiotensin II also has the direct stimulating action on TNF-alpha synthesis. ARB increases adiponectin a nddecreases TNF-alpha. Improvements of these adipocytokines dysfunction by ARB may concern tothe improvement of insulin resistance. The significance of various adipocytokines in insulin resistance and metabolic syndrome is also introduced.
Shimamoto
Kazuaki
K
Second Department of Internal Medicine, Sapporo Medical University School of Medicine.
Miura
Tetsuji
T
D057911:Angiotensin Receptor Antagonists; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology; D024821:Metabolic Syndrome / Q000188:drug therapy* / Q000503:physiopathology; D012084:Renin-Angiotensin System / Q000502:physiology
D057911:Angiotensin Receptor Antagonists