Liver fat and lipid oxidation in humans.
BACKGROUND: Studies in animals show that changes in hepatic fatty acid oxidation alter liver fat content. Human data regarding whole-body and hepatic lipid oxidation are controversial and based on studies of only a few subjects. AIMS: We examined whether whole-body and hepatic lipid oxidation are a...
| Main Authors: | , , , , , , |
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| Format: | Journal article |
| Language: | English |
| Published: |
2009
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| _version_ | 1826268187917811712 |
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| author | Kotronen, A Seppälä-Lindroos, A Vehkavaara, S Bergholm, R Frayn, K Fielding, B Yki-Järvinen, H |
| author_facet | Kotronen, A Seppälä-Lindroos, A Vehkavaara, S Bergholm, R Frayn, K Fielding, B Yki-Järvinen, H |
| author_sort | Kotronen, A |
| collection | OXFORD |
| description | BACKGROUND: Studies in animals show that changes in hepatic fatty acid oxidation alter liver fat content. Human data regarding whole-body and hepatic lipid oxidation are controversial and based on studies of only a few subjects. AIMS: We examined whether whole-body and hepatic lipid oxidation are altered in subjects with non-alcoholic fatty liver disease (NAFLD) compared with controls. METHODS: In vivo measurements of rates of substrate oxidation and insulin sensitivity (using the euglycaemic hyperinsulinaemic clamp technique in combination with indirect calorimetry and infusion of [3-(3)H]glucose) were performed in subjects with NAFLD [mean liver fat 14.0% (interquartile range 7.5-20.5%), n=29] and in control subjects [1.6% (1.0-3.0%), n=29]. Liver fat was measured using proton magnetic resonance spectroscopy. Plasma concentrations of 3-hydroxybutyrate (3-OHB) were measured as markers of hepatic lipid oxidation. RESULTS: In the basal state, substrate oxidation rates and serum 3-OHB concentrations were comparable in subjects with and without NAFLD. Plasma 3-OHB concentrations were similarly suppressed by insulin in both the groups. During the insulin infusion, whole-body lipid oxidation was inversely correlated with insulin-stimulated glucose disposal (r=-0.48, P<0.0001), which was lower in subjects with NAFLD [3.7+/-0.2 mg/(kg fat-free mass min)] than in the control subjects [5.0+/-0.3 mg/(kg fat-free mass min), P=0.0008]. CONCLUSIONS: Hepatic lipid oxidation is unchanged in NAFLD. Whole-body lipid oxidation is increased because of peripheral insulin resistance. These data imply that alterations in hepatic fatty acid oxidation do not contribute to liver fat content in humans. |
| first_indexed | 2024-03-06T21:05:48Z |
| format | Journal article |
| id | oxford-uuid:3c67969d-af11-48c7-a626-f8add0f5ed64 |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-06T21:05:48Z |
| publishDate | 2009 |
| record_format | dspace |
| spelling | oxford-uuid:3c67969d-af11-48c7-a626-f8add0f5ed642022-03-26T14:13:29ZLiver fat and lipid oxidation in humans.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:3c67969d-af11-48c7-a626-f8add0f5ed64EnglishSymplectic Elements at Oxford2009Kotronen, ASeppälä-Lindroos, AVehkavaara, SBergholm, RFrayn, KFielding, BYki-Järvinen, H BACKGROUND: Studies in animals show that changes in hepatic fatty acid oxidation alter liver fat content. Human data regarding whole-body and hepatic lipid oxidation are controversial and based on studies of only a few subjects. AIMS: We examined whether whole-body and hepatic lipid oxidation are altered in subjects with non-alcoholic fatty liver disease (NAFLD) compared with controls. METHODS: In vivo measurements of rates of substrate oxidation and insulin sensitivity (using the euglycaemic hyperinsulinaemic clamp technique in combination with indirect calorimetry and infusion of [3-(3)H]glucose) were performed in subjects with NAFLD [mean liver fat 14.0% (interquartile range 7.5-20.5%), n=29] and in control subjects [1.6% (1.0-3.0%), n=29]. Liver fat was measured using proton magnetic resonance spectroscopy. Plasma concentrations of 3-hydroxybutyrate (3-OHB) were measured as markers of hepatic lipid oxidation. RESULTS: In the basal state, substrate oxidation rates and serum 3-OHB concentrations were comparable in subjects with and without NAFLD. Plasma 3-OHB concentrations were similarly suppressed by insulin in both the groups. During the insulin infusion, whole-body lipid oxidation was inversely correlated with insulin-stimulated glucose disposal (r=-0.48, P<0.0001), which was lower in subjects with NAFLD [3.7+/-0.2 mg/(kg fat-free mass min)] than in the control subjects [5.0+/-0.3 mg/(kg fat-free mass min), P=0.0008]. CONCLUSIONS: Hepatic lipid oxidation is unchanged in NAFLD. Whole-body lipid oxidation is increased because of peripheral insulin resistance. These data imply that alterations in hepatic fatty acid oxidation do not contribute to liver fat content in humans. |
| spellingShingle | Kotronen, A Seppälä-Lindroos, A Vehkavaara, S Bergholm, R Frayn, K Fielding, B Yki-Järvinen, H Liver fat and lipid oxidation in humans. |
| title | Liver fat and lipid oxidation in humans. |
| title_full | Liver fat and lipid oxidation in humans. |
| title_fullStr | Liver fat and lipid oxidation in humans. |
| title_full_unstemmed | Liver fat and lipid oxidation in humans. |
| title_short | Liver fat and lipid oxidation in humans. |
| title_sort | liver fat and lipid oxidation in humans |
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