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Obesity alters adipose tissue response to fasting and refeeding in women: A study on lipolytic and endocrine dynamics and acute insulin resistance

L. Rossmeislová, E. Krauzová, M. Koc, M. Wilhelm, V. Šebo, Z. Varaliová, V. Šrámková, M. Schouten, P. Šedivý, P. Tůma, J. Kovář, D. Langin, J. Gojda, M. Šiklová

. 2024 ; 10 (18) : e37875. [pub] 20240914

Status not-indexed Language English Country England, Great Britain

Document type Journal Article

Persistent link   https://www.medvik.cz/link/bmc24017749

Fasting induces significant shifts in substrate utilization with signs of acute insulin resistance (IR), while obesity is associated with chronic IR. Nonetheless, both states substantially influence adipose tissue (AT) function. Therefore, in this interventional study (NCT04260542), we investigated if excessive adiposity in premenopausal women alters insulin sensitivity and AT metabolic and endocrine activity in response to a 60-h fast and a subsequent 48-h refeeding period. Using physiological methods, lipidomics, and AT explants, we showed that obesity partially modified AT endocrine activity and blunted the dynamics of AT insulin resistance in response to the fasting/refeeding challenge compared to that observed in lean women. AT adapted to its own excess by reducing lipolytic activity/free fatty acids (FFA) flux per mass. This adaptation persisted even after a 60-h fast, resulting in lower ketosis in women with obesity. This could be a protective mechanism that limits the lipotoxic effects of FFA; however, it may ultimately impede desirable weight loss induced by caloric restriction in women with obesity.

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$a Fasting induces significant shifts in substrate utilization with signs of acute insulin resistance (IR), while obesity is associated with chronic IR. Nonetheless, both states substantially influence adipose tissue (AT) function. Therefore, in this interventional study (NCT04260542), we investigated if excessive adiposity in premenopausal women alters insulin sensitivity and AT metabolic and endocrine activity in response to a 60-h fast and a subsequent 48-h refeeding period. Using physiological methods, lipidomics, and AT explants, we showed that obesity partially modified AT endocrine activity and blunted the dynamics of AT insulin resistance in response to the fasting/refeeding challenge compared to that observed in lean women. AT adapted to its own excess by reducing lipolytic activity/free fatty acids (FFA) flux per mass. This adaptation persisted even after a 60-h fast, resulting in lower ketosis in women with obesity. This could be a protective mechanism that limits the lipotoxic effects of FFA; however, it may ultimately impede desirable weight loss induced by caloric restriction in women with obesity.
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$a Koc, Michal $u Department of Pathophysiology, Centre for Research on Nutrition, Metabolism and Diabetes, Third Faculty of Medicine, Charles University, Prague, Czech Republic
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$a Wilhelm, Marek $u Department of Pathophysiology, Centre for Research on Nutrition, Metabolism and Diabetes, Third Faculty of Medicine, Charles University, Prague, Czech Republic
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$a Šebo, Viktor $u Department of Pathophysiology, Centre for Research on Nutrition, Metabolism and Diabetes, Third Faculty of Medicine, Charles University, Prague, Czech Republic $u Department of Internal Medicine, Third Faculty of Medicine, Charles University and Královské Vinohrady University Hospital, Prague, Czech Republic $7 xx0335505
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$a Varaliová, Zuzana $u Department of Pathophysiology, Centre for Research on Nutrition, Metabolism and Diabetes, Third Faculty of Medicine, Charles University, Prague, Czech Republic
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