Elsevier

Metabolism

Volume 31, Issue 3, March 1982, Pages 209-212
Metabolism

Sex difference in the influence of obesity on the 24 hr mean plasma concentration of cortisol

https://doi.org/10.1016/0026-0495(82)90054-3Get rights and content

Abstract

The 24 hr mean plasma cortisol concentration was measured in 65 healthy women ranging from 21% below to 218% above desirable weight and in 47 healthy men ranging from 5% below to 330% above desirable weight. In the women, there was a clear-cut inverse linear correlation between the plasma cortisol concentration and the percent deviation from desirable weight (y = 7.5 − 0.3 x; r = −0.49; p < 0.001); the relation of free to total cortisol concentration was weight-invariant; the MCR of cortisol in the most obese women was much higher than that of nonobese women (340 ± 76 versus 211 ± 31 liters/gm urinary creatinine; p < 0.01). In the men, the plasma cortisol level and MCR were weight-invariant. To account for the finding in women of a linear correlation of the decrement in plasma cortisol level with the percent deviation from desirable weight (which in turn is nearly perfectly correlated with the total body fat content), we postulate that a given weight of adipose tissue in women takes up a constant amount of cortisol; this in turn suggests that their adipose tissue contains a saturable binding system such as corticosteroid receptor. By the same logic, the weight-invariance of plasma cortisol and MCR in men suggests the absence of significant amounts of corticosteroid receptor in their adipose tissue. The finding that the increased cortisol MCR of obese women results in decreased plasma cortisol levels rather than an increase in cortisol production (the latter, corrected for muscle mass, is normal in obesity: Strain et al, Metabolism 29:980, 1980) suggests a defect in their cortisol ACTH feedback system. Such a defect, presumably hypothalamic, is not unexpected in the light of reports of defective hypothalamic control of prolactin and growth hormone secretion in obesity.

References (30)

  • S.H. Schachner et al.

    Alterations in adrenal cortical function in fasting obese subjects

    Metabolism

    (1965)
  • G.W. Strain et al.

    Cortisol production in obesity

    Metabolism

    (1980)
  • E.C. Arendt et al.

    Studies on obesity. I. The insulin glucose tolerance curve

    J. Clin Endocrinol Metab

    (1956)
  • E.C. Arendt et al.

    Studies on obesity. III. Effect of ascorbic acid on the insulin-glucose tolerance curve

    J Clin Endocrinol Metab

    (1956)
  • H Cohen

    17-Ketogenic steroid excretion in obese children before and after weight reduction

    Br Med J

    (1958)
  • P Szenos et al.

    Studies of adrenocortical function in obesity

    J Clin Endocrinol Metab

    (1959)
  • P Mlynaryk et al.

    Cortisol production rates in obesity

    J Clin Endocrinol Metab

    (1962)
  • A.N. Gogate et al.

    Adrenal cortical function in “obesity with pink striae” in the young adult

    J Clin Endocrinol

    (1963)
  • D.E. Schteingart et al.

    A comparison of the characteristics of increased adrenocortical function in obesity and in Cushing's syndrome

    Metabolism

    (1963)
  • C.J. Migeon et al.

    Study of adrenocortical function in obesity

    Metabolism

    (1963)
  • J.A. Prezio et al.

    Influence of body composition on adrenal function in obesity

    J Clin Endocrinol Metab

    (1964)
  • D.H.P. Streeten et al.

    The diagnosis of hypercortisolism. Biochemical criteria differentiating patients from lean and obese normal subjects and from females on oral contraceptives

    J Clin Endocrinol Metab

    (1969)
  • S.S. Dunkelmann et al.

    Cortisol metabolism in obesity

    J Clin Endocrinol Metab

    (1964)
  • D.E. Schteingart et al.

    Characteristics of the increased adrenocortical function observed in many obese patients

    Ann NY Acad Sci

    (1964)
  • G Sabeh et al.

    Adrenocortical indices during fasting in obesity

    J Clin Endocrinol Metab

    (1969)
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