[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.
Second Department of Internal Medicine, Sapporo Medical University School of Medicine.
Kazuaki
K
Shimamoto
Tetsuji
T
Miura
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