Alterations in adipose tissue and hepatic lipid kinetics in obese men and women with nonalcoholic fatty liver disease
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Alterations in adipose tissue and hepatic lipid kinetics in obese men and women with nonalcoholic fatty liver disease. / Fabbrini, Elisa; Mohammed, B Selma; Magkos, Faidon; Korenblat, Kevin M; Patterson, Bruce W; Klein, Samuel.
I: Gastroenterology, Bind 134, Nr. 2, 2008, s. 424-431.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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TY - JOUR
T1 - Alterations in adipose tissue and hepatic lipid kinetics in obese men and women with nonalcoholic fatty liver disease
AU - Fabbrini, Elisa
AU - Mohammed, B Selma
AU - Magkos, Faidon
AU - Korenblat, Kevin M
AU - Patterson, Bruce W
AU - Klein, Samuel
N1 - (Ekstern)
PY - 2008
Y1 - 2008
N2 - Background & aims: Steatosis in patients with nonalcoholic fatty liver disease (NAFLD) is due to an imbalance between intrahepatic triglyceride (IHTG) production and export. The purpose of this study was to evaluate TG metabolism in adipose tissue and liver in NAFLD.Methods: Fatty acid, VLDL-TG, and VLDL-apolipoprotein B-100 (apoB100) kinetics were assessed by using stable isotope tracers in 14 nondiabetic obese subjects with NAFLD (IHTG, 22.7% +/- 2.0%) and 14 nondiabetic obese subjects with normal IHTG content (IHTG, 3.4% +/- 0.4%), matched on age, sex, body mass index, and percent body fat.Results: Compared with the normal IHTG group, the NAFLD group had greater rates of palmitate release from adipose tissue into plasma (85.4 +/- 6.6 and 114.1 +/- 8.1 micromol/min, respectively; P = .01) and VLDL-TG secretion (11.4 +/- 1.1 and 24.3 +/- 3.1 micromol/min, respectively; P = .001); VLDL-apoB100 secretion rates were not different between groups. The increase in VLDL-TG secretion was primarily due to an increased contribution from "nonsystemic" fatty acids, presumably derived from lipolysis of intrahepatic and intra-abdominal fat and de novo lipogenesis. VLDL-TG secretion rate increased linearly with increasing IHTG content in subjects with normal IHTG but reached a plateau when IHTG content was >/=10% (r = 0.618, P < .001).Conclusions: Obese persons with NAFLD have marked alterations in both adipose tissue (increased lipolytic rates) and hepatic (increased VLDL-TG secretion) TG metabolism. Fatty acids derived from nonsystemic sources are responsible for the increase in VLDL-TG secretion. However, the increase in hepatic TG export is not adequate to normalize IHTG content.
AB - Background & aims: Steatosis in patients with nonalcoholic fatty liver disease (NAFLD) is due to an imbalance between intrahepatic triglyceride (IHTG) production and export. The purpose of this study was to evaluate TG metabolism in adipose tissue and liver in NAFLD.Methods: Fatty acid, VLDL-TG, and VLDL-apolipoprotein B-100 (apoB100) kinetics were assessed by using stable isotope tracers in 14 nondiabetic obese subjects with NAFLD (IHTG, 22.7% +/- 2.0%) and 14 nondiabetic obese subjects with normal IHTG content (IHTG, 3.4% +/- 0.4%), matched on age, sex, body mass index, and percent body fat.Results: Compared with the normal IHTG group, the NAFLD group had greater rates of palmitate release from adipose tissue into plasma (85.4 +/- 6.6 and 114.1 +/- 8.1 micromol/min, respectively; P = .01) and VLDL-TG secretion (11.4 +/- 1.1 and 24.3 +/- 3.1 micromol/min, respectively; P = .001); VLDL-apoB100 secretion rates were not different between groups. The increase in VLDL-TG secretion was primarily due to an increased contribution from "nonsystemic" fatty acids, presumably derived from lipolysis of intrahepatic and intra-abdominal fat and de novo lipogenesis. VLDL-TG secretion rate increased linearly with increasing IHTG content in subjects with normal IHTG but reached a plateau when IHTG content was >/=10% (r = 0.618, P < .001).Conclusions: Obese persons with NAFLD have marked alterations in both adipose tissue (increased lipolytic rates) and hepatic (increased VLDL-TG secretion) TG metabolism. Fatty acids derived from nonsystemic sources are responsible for the increase in VLDL-TG secretion. However, the increase in hepatic TG export is not adequate to normalize IHTG content.
KW - Adipose Tissue/metabolism
KW - Adult
KW - Apolipoprotein B-100/metabolism
KW - Body Composition/physiology
KW - Case-Control Studies
KW - Fatty Acids/metabolism
KW - Fatty Liver/complications
KW - Female
KW - Humans
KW - Lipid Metabolism/physiology
KW - Lipoproteins/metabolism
KW - Lipoproteins, VLDL/metabolism
KW - Liver/metabolism
KW - Male
KW - Middle Aged
KW - Obesity/complications
KW - Triglycerides/metabolism
U2 - 10.1053/j.gastro.2007.11.038
DO - 10.1053/j.gastro.2007.11.038
M3 - Journal article
C2 - 18242210
VL - 134
SP - 424
EP - 431
JO - Gastroenterology
JF - Gastroenterology
SN - 0016-5085
IS - 2
ER -
ID: 290676569