Reduced Energy Expenditure and Impaired Feeding-Related Signals But Not High Energy Intake Reinforces Hypothalamic Obesity in Adults with Childhood Onset Craniopharyngioma

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Holmer, HeleneKristianstad University,Skåne University Hospital,Central Hospital, Kristianstad, Sweden (author)

Reduced Energy Expenditure and Impaired Feeding-Related Signals But Not High Energy Intake Reinforces Hypothalamic Obesity in Adults with Childhood Onset Craniopharyngioma

Article/chapterEnglish2010

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Endocrine Society,2010
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LIBRIS-ID:oai:DiVA.org:liu-63945
https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-63945URI
https://doi.org/10.1210/jc.2010-0993DOI
https://lup.lub.lu.se/record/1688368URI

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Language:English
Summary in:English

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Subject category:art swepub-publicationtype

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Context: Obesity is a frequent manifestation of hypothalamic damage from a craniopharyngioma (CP). It is not yet clarified whether the obesity is due to alterations in energy expenditure, i.e. basal metabolic rate (BMR) and physical activity, or to increased energy intake (EI). Objective: The aim was to investigate whether energy expenditure and EI differed between childhood onset CP patients and matched population controls and whether these measures were related to hypothalamic damage, as tumor growth into the third ventricle (TGTV). Design and Methods: Forty-two CP patients (20 women) aged 28 yr (range, 17-57 yr) operated between 1958 and 2000 in the South Medical Region of Sweden (population, 2.5 million) were studied. Body composition, satiety hormones, BMR (indirect calorimetry), physical activity, EI, and attitudes toward eating were assessed. Comparisons were made with matched controls and between patients with (n = 25) and without (n = 17) TGTV. Results: After adjustment, patients had lower BMR compared to controls (-90 kcal/24 h; P = 0.02) and also had lower EI (1778 vs. 2094 kcal/24h; P = 0.008), and the EI/BMR ratio was significantly lower in TGTV patients. Similar dietary macronutrient composition was found, and only significantly higher scales in restricting food intake were recorded in patients. Ghrelin levels were significantly lower in patients, whereas serum insulin and leptin levels were higher (P less than 0.001), and both ghrelin and insulin correlated significantly to tumor growth. Lower levels of physical activity (P less than 0.01) were recorded in patients. Conclusions: The major mechanisms that reinforced obesity were hypothalamic damage causing disrupted or impaired sensitivity to feeding-related signals for leptin, insulin, and ghrelin, and reductions in both BMR and physical activity.

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MEDICIN OCH HÄLSOVETENSKAP Klinisk medicin Endokrinologi och diabetes hsv//swe
MEDICAL AND HEALTH SCIENCES Clinical Medicine Endocrinology and Diabetes hsv//eng
MEDICINE
MEDICIN

Added entries (persons, corporate bodies, meetings, titles ...)

Pozarek, GabriellaLund-Malmö University Hospital, Lund, Sweden,Skåne University Hospital(Swepub:lu)vard-gpr (author)
Wirfält, ElisabetLund University,Lunds universitet,Nutritionsepidemiologi,Forskargrupper vid Lunds universitet,Nutrition Epidemiology,Lund University Research Groups,Lund University, Sweden(Swepub:lu)medf-ewi (author)
Popovic, VeraUniversity Clinical Center, Belgrade, Serbia (author)
Ekman, BertilLinköping University,Östergötlands Läns Landsting,Linköpings universitet,Internmedicin,Hälsouniversitetet,Endokrin- och magtarmmedicinska kliniken US(Swepub:liu)berek83 (author)
Björk, JonasLund University,Lunds universitet,Avdelningen för arbets- och miljömedicin,Institutionen för laboratoriemedicin,Medicinska fakulteten,Division of Occupational and Environmental Medicine, Lund University,Department of Laboratory Medicine,Faculty of Medicine,Lund University Hospital, Sweden(Swepub:lu)ymed-jbj (author)
Erfurth, Eva MarieLund University,Lunds universitet,Medicin, Lund,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Medicine, Lund,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine,Lund-Malmö University Hospital, Lund, Sweden(Swepub:lu)med-ee0 (author)
Kristianstad UniversitySkåne University Hospital (creator_code:org_t)

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In:Journal of Clinical Endocrinology and Metabolism: Endocrine Society95:12, s. 5395-54020021-972X1945-7197

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