Limits...
Greater dietary fat oxidation in obese compared with lean men: an adaptive mechanism to prevent liver fat accumulation?

Hodson L, McQuaid SE, Humphreys SM, Milne R, Fielding BA, Frayn KN, Karpe F - Am. J. Physiol. Endocrinol. Metab. (2010)

Bottom Line: We found a similar contribution of dietary fatty acids to VLDL-TG in the two groups over 24 h.Ketogenesis occurred to a significantly greater extent in abdominally obese compared with lean males, largely due to lessened downregulation of postprandial ketogenesis (P < 0.001).These alterations may represent further pathways for redirection of fatty acids into export from the liver or oxidation to prevent liver fat accumulation.

View Article: PubMed Central - PubMed

Affiliation: Oxford Centre for Diabetes, Endocrinology and Metabolism, Nuffield Department of Clinical Medicine, University of Oxford, United Kingdom. leanne.hodson@oxlip.ox.ac.uk

ABSTRACT
Liver fat represents a balance between input, secretion, and oxidation of fatty acids. As humans spend the majority of a 24-h period in a postprandial state, dietary fatty acids make an important contribution to liver fat metabolism. We compared hepatic fatty acid partitioning in healthy lean (n = 9) and abdominally obese (n = 10) males over 24 h. Volunteers received three mixed meals adjusted for basal metabolic rate. U-13C-labeled fatty acids were incorporated into the meals, and [2H2]palmitate was infused intravenously to distinguish between sources of fatty acids incorporated into VLDL-TG. Immunoaffinity chromatography was used to isolate VLDL-TG of hepatic origin. Liver and whole body fatty acid oxidation was assessed by isotopic enrichment of 3-hydoxybutyrate and breath CO2. We found a similar contribution of dietary fatty acids to VLDL-TG in the two groups over 24 h. The contribution of fatty acids from splanchnic sources was higher (P < 0.05) in the abdominally obese group. Ketogenesis occurred to a significantly greater extent in abdominally obese compared with lean males, largely due to lessened downregulation of postprandial ketogenesis (P < 0.001). The appearance of 13C in breath CO2 was also greater (P < 0.001) in abdominally obese compared with lean men. Hepatic elongation and desaturation of palmitic acid were higher (P < 0.05) in abdominally obese than in lean males. Oxidation of dietary fatty acids and hepatic desaturation and elongation of palmitic acid occurred to a greater extent in abdominally obese men. These alterations may represent further pathways for redirection of fatty acids into export from the liver or oxidation to prevent liver fat accumulation.

Show MeSH

Related in: MedlinePlus

Plasma 3-OHB concentrations (A, P = 0.007) and enrichment of plasma 3-OHB (B, P = 0.035) and breath CO2 (C, P < 0.001) with 13C from dietary fatty acids in lean (●) and abdominally obese (○) males (n = 9 and 10, respectively). Data are presented as means ± SE.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC2957864&req=5

Figure 5: Plasma 3-OHB concentrations (A, P = 0.007) and enrichment of plasma 3-OHB (B, P = 0.035) and breath CO2 (C, P < 0.001) with 13C from dietary fatty acids in lean (●) and abdominally obese (○) males (n = 9 and 10, respectively). Data are presented as means ± SE.

Mentions: The systemic concentration of blood 3-OHB over the 24-h period was greater in abdominally obese than in the lean males (P = 0.007; Fig. 5A). We then measured the incorporation of 13C (from dietary fatty acids) into blood 3-OHB over the 24-h period. Greater blood [13C]3-OHB concentrations were detected in the abdominally obese compared with the lean males over the 24-h period (AUC 0.06 ± 0.02 vs. 0.02 ± 0.01 μmol/l, respectively, P = 0.035; Fig. 5B).


Greater dietary fat oxidation in obese compared with lean men: an adaptive mechanism to prevent liver fat accumulation?

Hodson L, McQuaid SE, Humphreys SM, Milne R, Fielding BA, Frayn KN, Karpe F - Am. J. Physiol. Endocrinol. Metab. (2010)

Plasma 3-OHB concentrations (A, P = 0.007) and enrichment of plasma 3-OHB (B, P = 0.035) and breath CO2 (C, P < 0.001) with 13C from dietary fatty acids in lean (●) and abdominally obese (○) males (n = 9 and 10, respectively). Data are presented as means ± SE.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2957864&req=5

Figure 5: Plasma 3-OHB concentrations (A, P = 0.007) and enrichment of plasma 3-OHB (B, P = 0.035) and breath CO2 (C, P < 0.001) with 13C from dietary fatty acids in lean (●) and abdominally obese (○) males (n = 9 and 10, respectively). Data are presented as means ± SE.
Mentions: The systemic concentration of blood 3-OHB over the 24-h period was greater in abdominally obese than in the lean males (P = 0.007; Fig. 5A). We then measured the incorporation of 13C (from dietary fatty acids) into blood 3-OHB over the 24-h period. Greater blood [13C]3-OHB concentrations were detected in the abdominally obese compared with the lean males over the 24-h period (AUC 0.06 ± 0.02 vs. 0.02 ± 0.01 μmol/l, respectively, P = 0.035; Fig. 5B).

Bottom Line: We found a similar contribution of dietary fatty acids to VLDL-TG in the two groups over 24 h.Ketogenesis occurred to a significantly greater extent in abdominally obese compared with lean males, largely due to lessened downregulation of postprandial ketogenesis (P < 0.001).These alterations may represent further pathways for redirection of fatty acids into export from the liver or oxidation to prevent liver fat accumulation.

View Article: PubMed Central - PubMed

Affiliation: Oxford Centre for Diabetes, Endocrinology and Metabolism, Nuffield Department of Clinical Medicine, University of Oxford, United Kingdom. leanne.hodson@oxlip.ox.ac.uk

ABSTRACT
Liver fat represents a balance between input, secretion, and oxidation of fatty acids. As humans spend the majority of a 24-h period in a postprandial state, dietary fatty acids make an important contribution to liver fat metabolism. We compared hepatic fatty acid partitioning in healthy lean (n = 9) and abdominally obese (n = 10) males over 24 h. Volunteers received three mixed meals adjusted for basal metabolic rate. U-13C-labeled fatty acids were incorporated into the meals, and [2H2]palmitate was infused intravenously to distinguish between sources of fatty acids incorporated into VLDL-TG. Immunoaffinity chromatography was used to isolate VLDL-TG of hepatic origin. Liver and whole body fatty acid oxidation was assessed by isotopic enrichment of 3-hydoxybutyrate and breath CO2. We found a similar contribution of dietary fatty acids to VLDL-TG in the two groups over 24 h. The contribution of fatty acids from splanchnic sources was higher (P < 0.05) in the abdominally obese group. Ketogenesis occurred to a significantly greater extent in abdominally obese compared with lean males, largely due to lessened downregulation of postprandial ketogenesis (P < 0.001). The appearance of 13C in breath CO2 was also greater (P < 0.001) in abdominally obese compared with lean men. Hepatic elongation and desaturation of palmitic acid were higher (P < 0.05) in abdominally obese than in lean males. Oxidation of dietary fatty acids and hepatic desaturation and elongation of palmitic acid occurred to a greater extent in abdominally obese men. These alterations may represent further pathways for redirection of fatty acids into export from the liver or oxidation to prevent liver fat accumulation.

Show MeSH
Related in: MedlinePlus