Background. Fatty liver is believed to be sustained by a higher than normal adipose-derived NEFA flux to the liver. Also, hepatic energy metabolism may be a rate-limiting step of intrahepatic fat (IHF) accumulation. Aims. To assess whole-body energy metabolism and hepatic high-energy phosphates (HEPs) in individuals with fatty liver. Methods. We studied 22 individuals with fatty liver and 22 control individuals matched for anthropometric features by means of (1) hepatic 1H-magnetic resonance spectroscopy (MRS) to measure the IHF content, (2) hepatic 31P-MRS to assess the relative content of HEPs (phosphomonoesters, phosphodiesters, inorganic phosphorus, and ATP), and (3) indirect calorimetry to assess whole-body resting energy expenditure and substrate oxidation. Results. Patients with newly diagnosed fatty liver and controls were not different for anthropometric parameters. Based on HOMA2%-S, individuals with fatty liver were more insulin resistant than controls. Resting energy expenditure and the pattern of substrate oxidation were not different between groups. Relative content of HEPs was not different between groups; in particular, the Pi/γ-ATP ratio, the most important signals in terms of monitoring energy homeostasis, was not different even if it was associated with indirect calorimetry-derived parameters of oxidative substrate disposal. Conclusions. These data demonstrate that fasting whole-body energy metabolism and the relative content of HEPs in nondiabetic patients with fatty liver are not different than those in controls when they are matched for anthropometric features.

Lattuada, G., Radaelli, M., De Cobelli, F., Esposito, A., Manzoni, G., Perra, S., et al. (2019). Fasting whole-body energy homeostasis and hepatic energy metabolism in nondiabetic humans with fatty liver. OXIDATIVE MEDICINE AND CELLULAR LONGEVITY, 2019, 1-7 [10.1155/2019/9796175].

Fasting whole-body energy homeostasis and hepatic energy metabolism in nondiabetic humans with fatty liver

Castoldi, Giovanna
Penultimo
;
Perseghin, Gianluca
Ultimo
2019

Abstract

Background. Fatty liver is believed to be sustained by a higher than normal adipose-derived NEFA flux to the liver. Also, hepatic energy metabolism may be a rate-limiting step of intrahepatic fat (IHF) accumulation. Aims. To assess whole-body energy metabolism and hepatic high-energy phosphates (HEPs) in individuals with fatty liver. Methods. We studied 22 individuals with fatty liver and 22 control individuals matched for anthropometric features by means of (1) hepatic 1H-magnetic resonance spectroscopy (MRS) to measure the IHF content, (2) hepatic 31P-MRS to assess the relative content of HEPs (phosphomonoesters, phosphodiesters, inorganic phosphorus, and ATP), and (3) indirect calorimetry to assess whole-body resting energy expenditure and substrate oxidation. Results. Patients with newly diagnosed fatty liver and controls were not different for anthropometric parameters. Based on HOMA2%-S, individuals with fatty liver were more insulin resistant than controls. Resting energy expenditure and the pattern of substrate oxidation were not different between groups. Relative content of HEPs was not different between groups; in particular, the Pi/γ-ATP ratio, the most important signals in terms of monitoring energy homeostasis, was not different even if it was associated with indirect calorimetry-derived parameters of oxidative substrate disposal. Conclusions. These data demonstrate that fasting whole-body energy metabolism and the relative content of HEPs in nondiabetic patients with fatty liver are not different than those in controls when they are matched for anthropometric features.
Articolo in rivista - Articolo scientifico
31P Magnetic Resonance Spectroscopy, intra-hepatic fat, hepatic high energy phosphates
English
11-apr-2019
2019
2019
1
7
9796175
reserved
Lattuada, G., Radaelli, M., De Cobelli, F., Esposito, A., Manzoni, G., Perra, S., et al. (2019). Fasting whole-body energy homeostasis and hepatic energy metabolism in nondiabetic humans with fatty liver. OXIDATIVE MEDICINE AND CELLULAR LONGEVITY, 2019, 1-7 [10.1155/2019/9796175].
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10281/227041
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