J Uddén1, P Björntorp, P Arner, B Barkeling, L Meurling, S Rössner. 1. Centre for Metabolism and Endocrinology, Obesity Unit M73, Karolinska Institute at Huddinge University Hospital, 141 86 Stockholm, Sweden. joanna.udden@medhs.ki.se
Abstract
OBJECTIVE: Long-term treatment with glucocorticoids induces weight gain and increased risk to develop obesity-related metabolic complications. The underlying mechanisms are not fully understood. Glucocorticoid therapy has previously been associated with increased levels of circulating leptin. In this study the eating behaviour was therefore studied in relation to leptin levels before and after short-term prednisolone treatment. DESIGN: Within-subject design. SUBJECTS: Twelve healthy postmenopausal women with a mean body mass index (BMI) of 28.9 kg m-2 (+/-0.8 SEM) volunteered after recruitment by an advertisement in the local paper. INTERVENTIONS: The subjects received 25 mg prednisolone daily for 7 days. MAIN OUTCOME MEASUREMENTS: Fasting serum samples were obtained before, during and after treatment for determination of leptin and insulin, glucose and fractionated lipoproteins in plasma. The microstructure of the eating behaviour was registered with a universal eating monitor, VIKTOR. Appetite was estimated by visual analogue rating scales and food intake by a 48-h recall. RESULTS: Serum leptin increased after 2 and 7 days of glucocorticoid administration (P < 0.01), and the food intake measured by VIKTOR after 7 days of treatment (P < 0.05). No statistically significant changes were however, found in the 48-h food- recall or in the subjective appetite registrations. Insulin levels were borderline elevated (P = 0.062) after treatment, but no significant changes of fasting glucose were seen. High density lipoprotein cholesterol (HDL) increased (P < 0.05), whilst low density lipoprotein cholesterol (LDL) decreased (P < 0.05). CONCLUSION: Food intake was elevated after glucocorticoid administration as observed with an objective, quantitative method, in spite of increased levels of circulating leptin.
OBJECTIVE: Long-term treatment with glucocorticoids induces weight gain and increased risk to develop obesity-related metabolic complications. The underlying mechanisms are not fully understood. Glucocorticoid therapy has previously been associated with increased levels of circulating leptin. In this study the eating behaviour was therefore studied in relation to leptin levels before and after short-term prednisolone treatment. DESIGN: Within-subject design. SUBJECTS: Twelve healthy postmenopausal women with a mean body mass index (BMI) of 28.9 kg m-2 (+/-0.8 SEM) volunteered after recruitment by an advertisement in the local paper. INTERVENTIONS: The subjects received 25 mg prednisolone daily for 7 days. MAIN OUTCOME MEASUREMENTS: Fasting serum samples were obtained before, during and after treatment for determination of leptin and insulin, glucose and fractionated lipoproteins in plasma. The microstructure of the eating behaviour was registered with a universal eating monitor, VIKTOR. Appetite was estimated by visual analogue rating scales and food intake by a 48-h recall. RESULTS: Serum leptin increased after 2 and 7 days of glucocorticoid administration (P < 0.01), and the food intake measured by VIKTOR after 7 days of treatment (P < 0.05). No statistically significant changes were however, found in the 48-h food- recall or in the subjective appetite registrations. Insulin levels were borderline elevated (P = 0.062) after treatment, but no significant changes of fasting glucose were seen. High density lipoprotein cholesterol (HDL) increased (P < 0.05), whilst low density lipoprotein cholesterol (LDL) decreased (P < 0.05). CONCLUSION: Food intake was elevated after glucocorticoid administration as observed with an objective, quantitative method, in spite of increased levels of circulating leptin.
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