[Insulin resistance syndrome].
Insulin resistance and hyperinsulinemia have been observed in essential hypertension. The selective impairment of glucose metabolism in skeletal muscle may accompanied hyperinsulinemia and raise blood pressure through sympathetic nervous system and/or renin-angiotensin system activation, renal sodium retention, proliferation of vascular smooth muscle and leptin. Recently, molecular techniques have applied for investigating the mechanisms of insulin resistance. The mutation of insulin receptor gene, changes of muscle fiber composition and muscle blood flow, abnormalities of insulin signal transduction, and TNF-alpha are considered as involvement of insulin resistance in the skeletal muscle. While further study will be necessary to clarify the mechanisms of insulin resistance and hypertension.
Murakami
H
H
Second Department of Internal Medicine, Sapporo Medical University School of Medicine.
Shimamoto
K
K
D000818:Animals; D002455:Cell Division; D005947:Glucose / Q000378:metabolism; D006801:Humans; D006946:Hyperinsulinism / Q000209:etiology; D006973:Hypertension / Q000209:etiology; D007333:Insulin Resistance / Q000235:genetics; D020738:Leptin / Q000502:physiology; D018482:Muscle, Skeletal / Q000098:blood supply / Q000378:metabolism; D009131:Muscle, Smooth, Vascular / Q000166:cytology; D017526:Receptor, IGF Type 1 / Q000378:metabolism; D011972:Receptor, Insulin / Q000502:physiology; D012084:Renin-Angiotensin System / Q000502:physiology; D015398:Signal Transduction; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D013564:Sympathetic Nervous System / Q000502:physiology; D013577:Syndrome; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
D020738:Leptin; D014409:Tumor Necrosis Factor-alpha; D017526:Receptor, IGF Type 1; D011972:Receptor, Insulin; D000254:Sodium-Potassium-Exchanging ATPase; D005947:Glucose