HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 291/5/E995    most recent 00654.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (9) Citing Articles via Google Scholar Google Scholar Articles by Darmon, P. Articles by Dutour, A. Search for Related Content PubMed PubMed Citation Articles by Darmon, P. Articles by Dutour, A.

Insulin resistance induced by hydrocortisone is increased in patients with abdominal obesity

¹Endocrinology and Nutrition Department, Hôpital Nord, Marseille; ²Laboratory of Hematology, Institut National de la Santé et de la Recherche Médicale (INSERM) Unité Mixte de Recherche 626, Faculté de Médecine, Université de la Méditerranée, Marseille; and ³Centre of Clinical Investigations, Hôpital Nord, Marseille, France

Submitted 29 December 2005 ; accepted in final form 7 June 2006

Glucocorticoids hypersensitivity may be involved in the development of abdominal obesity and insulin resistance. Eight normal weight and eight obese women received on two occasions a 3-h intravenous infusion of saline or hydrocortisone (HC) (1.5 µg·kg^–1·min^–1). Plasma cortisol, insulin, and glucose levels were measured every 30 min from time_–30 (min) (time_–30) to time₂₄₀. Free fatty acids, adiponectin, and plasminogen activator inhibitor-1 (PAI-1) levels were measured at time_–30, time₁₈₀, and time₂₄₀. At time₂₄₀, subjects underwent an insulin tolerance test to obtain an index of insulin sensitivity (K_ITT). Mean_30–240 cortisol level was similar in control and obese women after saline (74 ± 16 vs. 75 ± 20 µg/l) and HC (235 ± 17 vs. 245 ± 47 µg/l). The effect of HC on mean_180–240 insulin, mean_180–240 insulin resistance obtained by homeostasis model assessment (HOMA-IR), and K_ITT was significant in obese (11.4 ± 2.0 vs. 8.2 ± 1.3 mU/l, P < 0.05; 2.37 ± 0.5 vs. 1.64 ± 0.3, P < 0.05; 2.81 ± 0.9 vs. 3.32 ± 1.02%/min, P < 0.05) but not in control women (3.9 ± 0.6 vs. 2.8 ± 0.5 mU/l; 0.78 ± 0.1 vs. 0.49 ± 0.1; 4.36 ± 1.1 vs. 4.37 ± 1.2%/min). In the whole population, the quantity of visceral fat, estimated by computerized tomography scan, was correlated with the increment of plasma insulin and HOMA-IR during HC infusion [mean_30–240 insulin (r = 0.61, P < 0.05), mean_30–240 HOMA-IR (r = 0.66, P < 0.01)]. The increase of PAI-1 between time₁₈₀ and time₂₄₀ after HC was higher in obese women (+25%) than in controls (+12%) (P < 0.05), whereas no differential effect between groups was observed for free fatty acids or adiponectin. A moderate hypercortisolism, equivalent to that induced by a mild stress, has more pronounced consequences on insulin sensitivity in abdominally obese women than in controls. These deleterious effects are correlated with the amount of visceral fat.

glucocorticoid hypersensitivity; visceral obesity; metabolic effects of hydrocortisone

This article has been cited by other articles:

				S. Boullu-Ciocca, V. Achard, V. Tassistro, A. Dutour, and M. Grino Postnatal Programming of Glucocorticoid Metabolism in Rats Modulates High-Fat Diet-Induced Regulation of Visceral Adipose Tissue Glucocorticoid Exposure and Sensitivity and Adiponectin and Proinflammatory Adipokines Gene Expression in Adulthood Diabetes, March 1, 2008; 57(3): 669 - 677. [Abstract] [Full Text] [PDF]