Increased meal-induced neurotensin response predicts successful maintenance of weight loss – Data from a randomized controlled trial

The gut derived anorexigenic hormone neurotensin (NT) is upregulated after bariatric surgery which may contribute to the sustained weight loss. In contrast, diet-induced weight loss is most often followed by weight regain. We therefore investigated whether diet-induced weight loss impacts levels of...

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Veröffentlicht in:Metabolism, clinical and experimental clinical and experimental, 2023-06, Vol.143, p.155534-155534, Article 155534
Hauptverfasser: Brethvad, Annemette Overgaard, Zakariassen, Hannah Louise, Holt, Joachim, Lundgren, Julie Rehné, Jakobsen, Alexander, Hartmann, Bolette, Lehmann, Eva Winning, Kissow, Hannelouise, Holst, Jens Juul, Madsbad, Sten, Torekov, Signe Sørensen, Holst, Birgitte
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Sprache:eng
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Zusammenfassung:The gut derived anorexigenic hormone neurotensin (NT) is upregulated after bariatric surgery which may contribute to the sustained weight loss. In contrast, diet-induced weight loss is most often followed by weight regain. We therefore investigated whether diet-induced weight loss impacts levels of circulating NT in mice and humans and whether NT levels predicts body weight change after weight loss in humans. In vivo mice study: Obese mice were fed ad-libitum or a restricted diet (40–60 % of average food intake) for 9 days to obtain similar weight loss as observed in the human study. At termination, intestinal segments, the hypothalamus and plasma were collected for histological, real time PCR, and radioimmunoassay (RIA) analysis. Clinical trial: Plasma samples from 42 participants with obesity, completing an 8-week low-calorie diet in a randomized controlled trial, were analyzed. Plasma NT was measured by RIA at fasting and during a meal test before and after diet-induced weight loss and after one year of intended weight maintenance. In obese mice, food restriction-induced body weight loss of 14 % was associated with a 64 % reduction in fasting plasma NT (p 
ISSN:0026-0495
1532-8600
DOI:10.1016/j.metabol.2023.155534