Obesity in db and ob animals leads to impaired hepatic very low density lipoprotein secretion and differential secretion of apolipoprotein B-48 and B-100

Dyslipidemia secondary to obesity is commonly observed in both animals and humans. As it has been hypothesized that obesity can result in overproduction of VLDL, leading to the subsequent dyslipidemia, we have examined the triglyceride and apoB secretion rates in vivo in obese C57BI/ KsJ db/db and C...

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Main Authors: X Li, S M Grundy, S B Patel
Format: Article
Language:English
Published: Elsevier 1997-07-01
Series:Journal of Lipid Research
Online Access:http://www.sciencedirect.com/science/article/pii/S0022227520374125
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author X Li
S M Grundy
S B Patel
author_facet X Li
S M Grundy
S B Patel
author_sort X Li
collection DOAJ
description Dyslipidemia secondary to obesity is commonly observed in both animals and humans. As it has been hypothesized that obesity can result in overproduction of VLDL, leading to the subsequent dyslipidemia, we have examined the triglyceride and apoB secretion rates in vivo in obese C57BI/ KsJ db/db and C57BI/6J ob/ob mice and their lean littermates. In ob/ob animals, obesity resulted in significantly lower, not higher, triglyceride secretion rates in both males (3.94 +/- 0.49 mg/h per g liver vs. 5.45 +/- 0.29 mg/h per g liver in lean littermates, P < 0.001) and females (4.29 +/- 0.81 mg/h per g liver vs. 5.25 +/- 0.59 mg/h/g liver, P < 0.001). For db/db, the obese females did not show a statistically significant triglyceride secretion rate compared to their lean littermates. Only the male db/db animals showed a significantly higher triglyceride secretion rate compared with lean littermates (5.50 +/- 1.1 mg/h per g liver vs. 3.37 +/- 0.36 mg/h/g liver, P < 0.001). Examination of the apolipoprotein B (apoB) secretion rates showed that for ob/ob animals and db/db obese females, apoB48 secretion was significantly decreased compared to that of normal littermates, with a small increase in apoB-100 secretion. Total apoB secreted, however, was not increased. Our data further suggest that the predominant cause of the dyslipidemia under these conditions is a defect in removal of VLDL from the circulation.
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spelling doaj.art-aec616ef21244684b787dfdc0953f86e2022-12-21T19:41:17ZengElsevierJournal of Lipid Research0022-22751997-07-0138712771288Obesity in db and ob animals leads to impaired hepatic very low density lipoprotein secretion and differential secretion of apolipoprotein B-48 and B-100X Li0S M Grundy1S B Patel2Center for Human Nutrition, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235-9052, USA.Center for Human Nutrition, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235-9052, USA.Center for Human Nutrition, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235-9052, USA.Dyslipidemia secondary to obesity is commonly observed in both animals and humans. As it has been hypothesized that obesity can result in overproduction of VLDL, leading to the subsequent dyslipidemia, we have examined the triglyceride and apoB secretion rates in vivo in obese C57BI/ KsJ db/db and C57BI/6J ob/ob mice and their lean littermates. In ob/ob animals, obesity resulted in significantly lower, not higher, triglyceride secretion rates in both males (3.94 +/- 0.49 mg/h per g liver vs. 5.45 +/- 0.29 mg/h per g liver in lean littermates, P < 0.001) and females (4.29 +/- 0.81 mg/h per g liver vs. 5.25 +/- 0.59 mg/h/g liver, P < 0.001). For db/db, the obese females did not show a statistically significant triglyceride secretion rate compared to their lean littermates. Only the male db/db animals showed a significantly higher triglyceride secretion rate compared with lean littermates (5.50 +/- 1.1 mg/h per g liver vs. 3.37 +/- 0.36 mg/h/g liver, P < 0.001). Examination of the apolipoprotein B (apoB) secretion rates showed that for ob/ob animals and db/db obese females, apoB48 secretion was significantly decreased compared to that of normal littermates, with a small increase in apoB-100 secretion. Total apoB secreted, however, was not increased. Our data further suggest that the predominant cause of the dyslipidemia under these conditions is a defect in removal of VLDL from the circulation.http://www.sciencedirect.com/science/article/pii/S0022227520374125
spellingShingle X Li
S M Grundy
S B Patel
Obesity in db and ob animals leads to impaired hepatic very low density lipoprotein secretion and differential secretion of apolipoprotein B-48 and B-100
Journal of Lipid Research
title Obesity in db and ob animals leads to impaired hepatic very low density lipoprotein secretion and differential secretion of apolipoprotein B-48 and B-100
title_full Obesity in db and ob animals leads to impaired hepatic very low density lipoprotein secretion and differential secretion of apolipoprotein B-48 and B-100
title_fullStr Obesity in db and ob animals leads to impaired hepatic very low density lipoprotein secretion and differential secretion of apolipoprotein B-48 and B-100
title_full_unstemmed Obesity in db and ob animals leads to impaired hepatic very low density lipoprotein secretion and differential secretion of apolipoprotein B-48 and B-100
title_short Obesity in db and ob animals leads to impaired hepatic very low density lipoprotein secretion and differential secretion of apolipoprotein B-48 and B-100
title_sort obesity in db and ob animals leads to impaired hepatic very low density lipoprotein secretion and differential secretion of apolipoprotein b 48 and b 100
url http://www.sciencedirect.com/science/article/pii/S0022227520374125
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AT smgrundy obesityindbandobanimalsleadstoimpairedhepaticverylowdensitylipoproteinsecretionanddifferentialsecretionofapolipoproteinb48andb100
AT sbpatel obesityindbandobanimalsleadstoimpairedhepaticverylowdensitylipoproteinsecretionanddifferentialsecretionofapolipoproteinb48andb100