What question did this study set out to answer?

To directly quantify the biological sources of hepatic and circulating lipoprotein triacylglycerols in patients diagnosed with nonalcoholic fatty liver disease.

May 2, 2005Journal of Clinical InvestigationOpen Access

Sources of fatty acids stored in liver and secreted via lipoproteins in patients with nonalcoholic fatty liver disease

View Full Paper

Ask AI

Bookmark

Authors

KDKerry L. DonnellyUniversity of Minnesota CSColeman I. SmithGeorgetown University SSSarah Jane SchwarzenbergUniversity of Minnesota

Discussion

Member takes

Implication

Stable isotope tracer study uncovers primary sources of hepatic triacylglycerol in nonalcoholic fatty liver disease, highlighting peripheral lipolysis and de novo lipogenesis as major drivers.

Key Points

To directly quantify the biological sources of hepatic and circulating lipoprotein triacylglycerols in patients diagnosed with nonalcoholic fatty liver disease.
Infused and fed stable isotopes over 4 days in patients (N=9; 5 male, 4 female; mean age 44 ± 10 years) scheduled for medically indicated liver biopsies.
Tracked fatty acids originating from serum nonesterified fatty acids (NEFAs), diet, and the de novo lipogenesis (DNL) pathway in liver tissue and plasma lipoprotein triacylglycerols using gas chromatography/mass spectrometry.
Liver triacylglycerols derived primarily from serum NEFAs (59.0% ± 9.9%), followed by DNL (26.1% ± 6.7%) and dietary sources (14.9% ± 7.0%).
Very low-density lipoprotein (VLDL) triacylglycerol showed labeling patterns similar to liver tissue, with reciprocal utilization of adipose and dietary fatty acids over 4 days.
DNL was markedly elevated in the fasting state and exhibited no normal diurnal variation.

Cite This Study

Donnelly et al. (2005) studied this question.

synapsesocial.com/papers/69dc378e1fd473d97f9f5564 https://doi.org/10.1172/jci23621

View Full Paper

Ask AI

Bookmark

May 2, 2005Journal of Clinical InvestigationOpen Access

Sources of fatty acids stored in liver and secreted via lipoproteins in patients with nonalcoholic fatty liver disease

View Full Paper

Ask AI

Bookmark

Authors

KDKerry L. DonnellyUniversity of Minnesota CSColeman I. SmithGeorgetown University SSSarah Jane SchwarzenbergUniversity of Minnesota

Discussion

Member takes

Implication

Stable isotope tracer study uncovers primary sources of hepatic triacylglycerol in nonalcoholic fatty liver disease, highlighting peripheral lipolysis and de novo lipogenesis as major drivers.

Key Points

To directly quantify the biological sources of hepatic and circulating lipoprotein triacylglycerols in patients diagnosed with nonalcoholic fatty liver disease.
Infused and fed stable isotopes over 4 days in patients (N=9; 5 male, 4 female; mean age 44 ± 10 years) scheduled for medically indicated liver biopsies.
Tracked fatty acids originating from serum nonesterified fatty acids (NEFAs), diet, and the de novo lipogenesis (DNL) pathway in liver tissue and plasma lipoprotein triacylglycerols using gas chromatography/mass spectrometry.
Liver triacylglycerols derived primarily from serum NEFAs (59.0% ± 9.9%), followed by DNL (26.1% ± 6.7%) and dietary sources (14.9% ± 7.0%).
Very low-density lipoprotein (VLDL) triacylglycerol showed labeling patterns similar to liver tissue, with reciprocal utilization of adipose and dietary fatty acids over 4 days.
DNL was markedly elevated in the fasting state and exhibited no normal diurnal variation.

Cite This Study

Donnelly et al. (2005) studied this question.

synapsesocial.com/papers/69dc378e1fd473d97f9f5564 https://doi.org/10.1172/jci23621

Also Consider

Synapse has enriched 3 closely related papers on similar clinical questions. Consider them for comparative context:

View Full Paper

Ask AI

Bookmark