No abstract

We described here a 12-year-old male patient with the syndrome of insulin resistance and acanthosis nigricans type A. Insulin levels at fasting state and after glucose loading were 149 + 63 ,uU/ml (mean± S.D.) and over 1,000 pU/ml respectively, while the fasting level of blood glucose was 77.7+8.9 mg/ml (mean+s.D.). A marked resistance to exogenous insulin was observed. Circulating levels of insulin antagonists such as growth hormone, cortisol and glucagon were within the normal range. Proinsulin was less than 5% of the radioimmunoassayable insulin. No insulin antibody or antireceptor antibody was detected. Insulin binding to mononuclear cells was decreased to about 50% of the controls. Analysis of membrane receptors demonstrated the normal average affinity, dissociation kinetics and negative cooperativity with a decreased number of receptors. After two days fasting, plasma IRI levels decreased to 27,aU/ml, while insulin binding kinetics were not affected ; which suggests that the receptor decrease was not secondary to hyperinsulinemia. These findings indicate that the decreased number of receptors was one of the causes for insulin resistance in this patient. insulin resistance ; acanthosis nigricans ; type A ; teen-age boy

We described a 12 7/12-year-old boy presenting the syndrome of insulin resistance and acanthosis nigricans Type A. Insulin levels at fasting state and after glucose loading were 149 +/- 63 microunits/ml (mean +/- SD) and over 1000 microunits/ml, respectively, while fasting levels of blood glucose were 77.7 +/- 8.9 mg/dl (mean +/- SD). A marked resistance to exogenous insulin was observed. Circulating levels of insulin antagonists such as growth hormone, cortisol and glucagon, were within the normal range. Proinsulin was less than 5% of the total radioimmunoassayable insulin. Insulin antibody and anti-receptor antibody were not detected. Insulin binding to mononuclear cells were decreased to about 50% of controls. Analysis of membrane receptors demonstrated the normal average affinity, dissociation kinetics and negative cooperativity with a decreased number of receptors. After two days fasting, plasma IRI levels decreased to 27 microunits/ml, however insulin binding kinetics were not affected. This might suggesting that the receptor decrease was not secondary to hyperinsulinemia. These findings indicate that a decreased number of receptors was one of the causes for insulin resistance in the patient.

No abstract