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Liver fat response to two days fasting and two days isocaloric high-carbohydrate refeeding in lean and obese women

P. Šedivý, T. Dusilová, B. Šetinová, D. Pajuelo, M. Hájek, L. Rossmeislová, M. Šiklová, V. Šrámková, E. Krauzová, J. Gojda, M. Koc, M. Dezortová, J. Kovář

. 2024 ; 34 (12) : 2690-2695. [pub] 20241001

Jazyk angličtina Země Nizozemsko

Typ dokumentu časopisecké články, srovnávací studie

Perzistentní odkaz   https://www.medvik.cz/link/bmc25003201

BACKGROUND AND AIMS: Prolonged fasting, which leads to the mobilization of fat from adipose tissue, can result in the development of hepatosteatosis. However, it is not yet known whether the accumulation of fat in the liver after fasting can be affected by concurrent obesity. Therefore, this study aimed to assess how excessive adiposity influences changes in liver fat content induced by fasting and subsequent refeeding. METHODS AND RESULTS: Ten lean women and eleven women with obesity (age: 36.4 ± 7.9 and 34.5 ± 7.9 years, BMI: 21.4 ± 1.7 and 34.5 ± 4.8 kg/m2) underwent a 60-h fasting period followed by 2 days of isocaloric high-carbohydrate refeeding. Magnetic resonance spectroscopy (MRS) examinations of liver were conducted at baseline, after 48 h of fasting, and at the end of refeeding period. Hepatic fat content (HFC) increased in lean women after fasting, whereas no statistically significant change in HFC was observed in women with obesity. Additionally, fasting led to significant reductions in liver volume in both groups, likely attributable to glycogen depletion, with subsequent restoration upon refeeding. Notably, changes in hepatic fat volume (HFV) rather than HFC inversely correlated with baseline liver fat content and HOMA-IR. CONCLUSION: We demonstrated that prolonged fasting results in accumulation of fat in the liver in lean subjects only and that this accumulation is inversely related to baseline fat content and insulin resistance. Moreover, the study underscored the importance of evaluating hepatic fat volume rather than hepatic fat content in studies that involve considerable changes in hepatic lean volume.

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$a BACKGROUND AND AIMS: Prolonged fasting, which leads to the mobilization of fat from adipose tissue, can result in the development of hepatosteatosis. However, it is not yet known whether the accumulation of fat in the liver after fasting can be affected by concurrent obesity. Therefore, this study aimed to assess how excessive adiposity influences changes in liver fat content induced by fasting and subsequent refeeding. METHODS AND RESULTS: Ten lean women and eleven women with obesity (age: 36.4 ± 7.9 and 34.5 ± 7.9 years, BMI: 21.4 ± 1.7 and 34.5 ± 4.8 kg/m2) underwent a 60-h fasting period followed by 2 days of isocaloric high-carbohydrate refeeding. Magnetic resonance spectroscopy (MRS) examinations of liver were conducted at baseline, after 48 h of fasting, and at the end of refeeding period. Hepatic fat content (HFC) increased in lean women after fasting, whereas no statistically significant change in HFC was observed in women with obesity. Additionally, fasting led to significant reductions in liver volume in both groups, likely attributable to glycogen depletion, with subsequent restoration upon refeeding. Notably, changes in hepatic fat volume (HFV) rather than HFC inversely correlated with baseline liver fat content and HOMA-IR. CONCLUSION: We demonstrated that prolonged fasting results in accumulation of fat in the liver in lean subjects only and that this accumulation is inversely related to baseline fat content and insulin resistance. Moreover, the study underscored the importance of evaluating hepatic fat volume rather than hepatic fat content in studies that involve considerable changes in hepatic lean volume.
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$a Dusilová, Tereza $u MR Unit, Department of Diagnostic and Interventional Radiology, Institute for Clinical and Experimental Medicine, Prague, Czech Republic
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$a Rossmeislová, Lenka $u Department of Pathophysiology, Centre for Research on Nutrition, Metabolism and Diabetes, Third Faculty of Medicine, Charles University, Prague, Czech Republic
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$a Šiklová, Michaela $u Department of Pathophysiology, Centre for Research on Nutrition, Metabolism and Diabetes, Third Faculty of Medicine, Charles University, Prague, Czech Republic
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$a Šrámková, Veronika $u Department of Pathophysiology, Centre for Research on Nutrition, Metabolism and Diabetes, Third Faculty of Medicine, Charles University, Prague, Czech Republic
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$a Krauzová, Eva $u Department of Pathophysiology, Centre for Research on Nutrition, Metabolism and Diabetes, Third Faculty of Medicine, Charles University, Prague, Czech Republic; Department of Internal Medicine, Third Faculty of Medicine, Charles University and Kralovske Vinohrady University Hospital, Prague, Czech Republic
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$a Gojda, Jan $u Department of Pathophysiology, Centre for Research on Nutrition, Metabolism and Diabetes, Third Faculty of Medicine, Charles University, Prague, Czech Republic; Department of Internal Medicine, Third Faculty of Medicine, Charles University and Kralovske Vinohrady University Hospital, Prague, Czech Republic
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$a Dezortová, Monika $u MR Unit, Department of Diagnostic and Interventional Radiology, Institute for Clinical and Experimental Medicine, Prague, Czech Republic. Electronic address: monika.dezortova@ikem.cz
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