Influence of Body Composition on Adrenal Function in Obesity

Prezio, J. A.; Carreon, G G; Clerkin, Elise M.; Meloni, Carlo; Kyle, Laurence H.; Canary, John J.

doi:10.1210/jcem-24-6-481

Cited by 38 publications

(14 citation statements)

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“…Correction for differences in lean body mass by calculating the ratio of daily glucocorticoid excretion rates to urine creatinine, an established surrogate parameter of muscle mass, resulted in similar cortisol production rates in obese and non-obese adult subjects [9,15]. In agreement with these data, we have recently shown that the differences in absolute daily glucocorticoid secretion and the potentially bioactive-freeglucocorticoids between severely obese subjects and lean controls were no longer detectable after correction for body surface area [16].…”

Section: Influence Of Lean Body Mass On Glucocorticoid Excretionsupporting

confidence: 74%

Brief review: Glucocorticoid excretion in obesity

Müssig

Maser-Gluth

2010

The Journal of Steroid Biochemistry and Molecular Biology

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Section: Influence Of Lean Body Mass On Glucocorticoid Excretionsupporting

confidence: 74%

Brief review: Glucocorticoid excretion in obesity

Müssig

Maser-Gluth

2010

The Journal of Steroid Biochemistry and Molecular Biology

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“…In the presence of glycosuria, 250 mg sodium bisulphite should be added before incubation with /?-glucuronidase to avoid the development of a colored compound which otherwise spuriously increases the color developed with phenylhydrazine (7). Urinary 17-OHCS excretion rates, like cortisol secretion rates, have been found to be dependent on body size (3), and should be expressed in mg/g creatinine or mg/M=\ The elevation in daily urinary 17-OHCS excretion which has been described in obesity (8)(9)(10)(11)(12) correlated well with lean body mass (13), and body surface area (8), and the difference in 17-OHCS excretion in obese subjects disappeared when the urinary excretion of 17-OHCS or specific cortisol metabolites in patients was related to concomitant creatinine excretion (3,14). The normal range of 17-OHCS excretion, 2.0-6.5 mg/g creatinine • day, is exceeded in individuals who have lost muscle mass such as amputees, paraplegics, patients with muscle-wasting disorders, is spuriously increased by certain drugs (15) and thyrotoxicosis, and is reduced by estrogen administration (3).…”

Section: Measurements Of Urinary Excretion Of Cortisol and Its Metabomentioning

confidence: 99%

Normal and Abnormal Function of the Hypothalamic Pituitary-Adrenocortical System in Man*

et al. 1984

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The first half of this manuscript is devoted to a review of the methods used and the results obtained in the published measurements of the normal responses to tests of the three main types of hypothalamic-pituitary-adrenocortical (HPA) activity in man. These are, I, basal, unstressed activity leading to appropriate levels of total daily production of cortisol in the characteristic circadian pattern; II, responses to feedback stimulation of HPA activity by metyrapone administration; and III, responses to tests of the effects of stress on the HPA system including the effects of hypoglycemia, induced fever, vasopressin administration, and ACTH injections and infusions. The advantages and shortcomings of each type of procedure are discussed. The second half of this paper describes the authors' attempts to establish the limits of normality of standard and modified methods of evaluating the HPA system. The defined limits of normality have been used to assess the HPA function in 158 patients with known or suspected disorders of the HPA system. In normal controls, halfhourly plasma cortisol determinations established the normality of circadian and postprandial fluctuations and of mean plasma cortisol concentration, 6.2 +/- 0.3 (SEM) micrograms/dl, which were closely approximated by determinations every 6 h. Metyrapone, given in a dose of 500 mg every 2 h for 24 h increased urinary 17-OHCS excretion to 10.5-32.6 mg/day or to 1.7-7.8 times basal excretion rate. Increasing rates of insulin infusion disclosed significant relationships between resulting plasma glucose and cortisol concentrations. The slopes of the delta cortisol/delta glucose responses were similar after insulin infusions (0.46 +/- 0.05) and after insulin injections, 0.15 U/kg (0.43 +/- 0.09), and were always greater than 0.20 micrograms/mg. This index provides a useful objective measure of the normality of responses to hypoglycemic stress, 0.20-0.87 micrograms/mg. Adrenocortical responses to iv infusions of ACTH (cosyntropin 0.25 mg) may be equivocal at 2 h but are clear cut at 4, 6 and 8 h. Of 158 patients in whom hypopituitarism was known or suspected because of the presence of a pituitary tumor, acromegaly, hyperprolactinemia, or clinical features, HPA function was found to be entirely normal in 88 patients and partially or severely abnormal in the remaining 70 patients.(ABSTRACT TRUNCATED AT 400 WORDS)

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“…These primarily adrenal androgens, dehydroepiandrosterone sulphate and dehydroepiandrosterone, are the principal contributors to urinary 17-ketosteroids [11], and renal excretion of 17-ketosteroids has frequently been found to be elevated or at the upper limits of the normal laboratory values in obese subjects [8,12,13]. Even a positive correlation between body weight and urinary 17-ketosteroids could be demonstrated in a group of patients with menstrual disorders [14].…”

Section: Obesitymentioning

confidence: 99%

Concept of the Importance of Nutritional Status in the Regulation of Adrenal Androgen Secretion

Pietrzik¹

1987

J. Clin. Biochem. Nutr.

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It is well known that in anorexia nervosa and during fasting the urinary excretion of adrenal androgens is decreased [1]. On the other hand obese persons frequently show increased urinary excretion, plasma levels, or production of adrenal androgens [2][3][4]. The cause of this relationship between nutritional status and adrenal androgen secretion is not yet fully understood [1, 2].One main reason for this obscurity is to be seen in the fact that the mechanism of control of adrenal androgen secretion itself is also still a subject of investigation and controversial hypotheses abound. Adrenocorticotropic hormone (ACTH) is not always accepted as the only important modulator of adrenal androgen secretion [1, 2]. Pintor et al. [5] for instance argued an involvement of a yet unknown but frequently postulated cortico-adrenal-stimulating hormone in the increased adrenal androgen secretion seen in obese children. According to Adams[2] nutritional status may also play a direct role in the control of adrenal androgens, for example, by decreasing the synthesis of certain adrenal enzymes of androgen formation during severe food deprivation.Studies in rabbits and rats clearly reveal that the capacity for adrenal androgen secretion is preferentially enhanced when ithe ACTH-dependent basal activity of the adrenal gland is increased due to chronical stress [6,7]. And since increases in the ACTH-controlled adrenocortical function occur in obesity or disappear during fasting [8] an alternative explanation (summarizing hypothesis) is presented here, one which considers additional endocrine and metabolic events related to the nutritional status. OBESITYIn human obesity elevated production rates of dehydroepiandrosterone (DHEA) [4] and dehydroepiandrosterone sulphate (DHEA-S) [4,9], as well as increased blood levels of dehydroepiandrosterone [3, 5,10] and its sulphate ester [9], have been demon-

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Influence of Body Composition on Adrenal Function in Obesity

Cited by 38 publications

References 0 publications

Brief review: Glucocorticoid excretion in obesity

Brief review: Glucocorticoid excretion in obesity

Normal and Abnormal Function of the Hypothalamic Pituitary-Adrenocortical System in Man*

Concept of the Importance of Nutritional Status in the Regulation of Adrenal Androgen Secretion

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