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John R. Burnett - One of the best experts on this subject based on the ideXlab platform.

  • Lipoprotein Metabolism in APOB L343V Familial HypobetaLipoproteinemia
    The Journal of Clinical Endocrinology & Metabolism, 2015
    Co-Authors: Amanda J. Hooper, K. Robertson, P. Hugh R. Barrett, Klaus G. Parhofer, Frank M. Van Bockxmeer, Liesl V. Heeks, Danie Champain, Jianmin Hua, Swithin Song, John R. Burnett
    Abstract:

    Context: Familial hypobetaLipoproteinemia (FHBL) is a codominant disorder of Lipoprotein Metabolism characterized by decreased plasma concentrations of low-density Lipoprotein (LDL)-cholesterol and apoLipoprotein B (apoB). Objective: The objective was to examine the effect of heterozygous APOB L343V FHBL on postprandial triglyceride-rich Lipoprotein (TRL) and fasting Lipoprotein Metabolism. Methods: Plasma incremental area under the curve apoB-48 and apoB-48 kinetics were determined after ingestion of a standardized oral fat load using compartmental modeling. Very low-density Lipoprotein (VLDL)-, intermediate-density Lipoprotein (IDL)-, and LDL-apoB kinetics were determined in the fasting state using stable isotope methods and compartmental modeling. Results: The postprandial incremental area under the curve (0–10 h) in FHBL subjects (n = 3) was lower for large TRL-triglyceride (−77%; P < .0001), small TRL-cholesterol (−83%; P < .001), small TRL-triglyceride (−88%; P < .001), and for plasma triglyceride (...

  • Abstract 236: Lipoprotein Metabolism in APOB L343V Familial HypobetaLipoproteinemia
    Arteriosclerosis Thrombosis and Vascular Biology, 2014
    Co-Authors: Amanda J. Hooper, K. Robertson, P. Hugh R. Barrett, Klaus G. Parhofer, Frank M. Van Bockxmeer, Liesl V. Heeks, Danie Champain, John R. Burnett
    Abstract:

    Familial hypobetaLipoproteinemia (FHBL) is a codominant disorder of Lipoprotein Metabolism characterized by decreased plasma concentrations of LDL-cholesterol and apoLipoprotein (apo) B. We examined the effect of heterozygous APOB L343V FHBL on fasting and postprandial Lipoprotein Metabolism. VLDL, IDL-, and LDL-apoB kinetics were determined in the fasting state using stable isotope methods and compartmental modeling. VLDL-apoB concentrations in FHBL subjects (n=2) were reduced by more than 75% compared to healthy, normolipidemic control subjects (P

  • abstract 236 Lipoprotein Metabolism in apob l343v familial hypobetaLipoproteinemia
    Arteriosclerosis Thrombosis and Vascular Biology, 2014
    Co-Authors: Amanda J. Hooper, K. Robertson, Klaus G. Parhofer, Frank M. Van Bockxmeer, Liesl V. Heeks, Danie Champain, Hugh P R Barrett, John R. Burnett
    Abstract:

    Familial hypobetaLipoproteinemia (FHBL) is a codominant disorder of Lipoprotein Metabolism characterized by decreased plasma concentrations of LDL-cholesterol and apoLipoprotein (apo) B. We examined the effect of heterozygous APOB L343V FHBL on fasting and postprandial Lipoprotein Metabolism. VLDL, IDL-, and LDL-apoB kinetics were determined in the fasting state using stable isotope methods and compartmental modeling. VLDL-apoB concentrations in FHBL subjects (n=2) were reduced by more than 75% compared to healthy, normolipidemic control subjects (P<0.01). VLDL-apoB fractional catabolic rate (FCR) was more than 5-fold higher in the FHBL subjects (P=0.07). ApoB production rates and IDL- and LDL-apoB FCRs were not different between FHBL subjects and controls. To assess postprandial Lipoprotein Metabolism, a standardized oral fat load was given after a 12 h fast to heterozygous APOB L343V FHBL subjects (n=3) and normolipidemic controls. The postprandial incremental area under the curve (0-10 h) in FHBL subje...

  • Postprandial Lipoprotein Metabolism in familial hypobetaLipoproteinemia.
    The Journal of Clinical Endocrinology & Metabolism, 2007
    Co-Authors: Amanda J. Hooper, K. Robertson, P. Hugh R. Barrett, Klaus G. Parhofer, Frank M. Van Bockxmeer, John R. Burnett
    Abstract:

    Objective: Familial hypobetaLipoproteinemia (FHBL) is an autosomal codominantly inherited disorder of Lipoprotein Metabolism characterized by decreased plasma concentrations of low-density Lipoprotein-cholesterol and apoLipoprotein (apo) B. We examined the effect of truncated apoB variants (

  • postprandial Lipoprotein Metabolism in familial hypobetaLipoproteinemia
    The Journal of Clinical Endocrinology and Metabolism, 2007
    Co-Authors: Amanda J. Hooper, K. Robertson, Klaus G. Parhofer, Frank M. Van Bockxmeer, John R. Burnett, Hugh P R Barrett
    Abstract:

    Objective: Familial hypobetaLipoproteinemia (FHBL) is an autosomal codominantly inherited disorder of Lipoprotein Metabolism characterized by decreased plasma concentrations of low-density Lipoprotein-cholesterol and apoLipoprotein (apo) B. We examined the effect of truncated apoB variants (triglyceride-rich Lipoprotein (TRL) Metabolism. Methods and Results: A standardized oral fat load was given after a 12-h fast to six heterozygous [apoB-6.9 (n = 3), apoB-25.8 (n = 1), apoB-40.3 (n = 2)] FHBL subjects and 10 normolipidemic controls. Plasma was obtained every 2 h for 10 h. Large TRLs [containing chylomicrons (CM)] and small TRLs (containing CM remnants) were isolated by ultracentrifugation. Compared with controls, FHBL subjects had significantly decreased fasting plasma cholesterol (2.3 ± 0.5 vs. 4.8 ± 0.5 mmol/liter), triglyceride (0.4 ± 0.3 vs. 1.5 ± 0.5 mmol/liter), low-density Lipoprotein-cholesterol (0.6 ± 0.4 vs. 3.0 ± 0.5 mmol/liter), and apoB (0.22 ± 0.05 vs...

P. Hugh R. Barrett - One of the best experts on this subject based on the ideXlab platform.

  • Lipoprotein Metabolism in APOB L343V Familial HypobetaLipoproteinemia
    The Journal of Clinical Endocrinology & Metabolism, 2015
    Co-Authors: Amanda J. Hooper, K. Robertson, P. Hugh R. Barrett, Klaus G. Parhofer, Frank M. Van Bockxmeer, Liesl V. Heeks, Danie Champain, Jianmin Hua, Swithin Song, John R. Burnett
    Abstract:

    Context: Familial hypobetaLipoproteinemia (FHBL) is a codominant disorder of Lipoprotein Metabolism characterized by decreased plasma concentrations of low-density Lipoprotein (LDL)-cholesterol and apoLipoprotein B (apoB). Objective: The objective was to examine the effect of heterozygous APOB L343V FHBL on postprandial triglyceride-rich Lipoprotein (TRL) and fasting Lipoprotein Metabolism. Methods: Plasma incremental area under the curve apoB-48 and apoB-48 kinetics were determined after ingestion of a standardized oral fat load using compartmental modeling. Very low-density Lipoprotein (VLDL)-, intermediate-density Lipoprotein (IDL)-, and LDL-apoB kinetics were determined in the fasting state using stable isotope methods and compartmental modeling. Results: The postprandial incremental area under the curve (0–10 h) in FHBL subjects (n = 3) was lower for large TRL-triglyceride (−77%; P < .0001), small TRL-cholesterol (−83%; P < .001), small TRL-triglyceride (−88%; P < .001), and for plasma triglyceride (...

  • Effect of Dietary Fatty Acids on Human Lipoprotein Metabolism: A Comprehensive Update
    Nutrients, 2015
    Co-Authors: Esther M. M. Ooi, Gerald F. Watts, P. Hugh R. Barrett
    Abstract:

    Dyslipidemia is a major risk factor for cardiovascular disease (CVD). Dietary fatty-acid composition regulates lipids and Lipoprotein Metabolism and may confer CVD benefit. This review updates understanding of the effect of dietary fatty-acids on human Lipoprotein Metabolism. In elderly participants with hyperlipidemia, high n-3 polyunsaturated fatty-acids (PUFA) consumption diminished hepatic triglyceride-rich Lipoprotein (TRL) secretion and enhanced TRL to low-density Lipoprotein (LDL) conversion. n-3 PUFA also decreased TRL-apoB-48 concentration by decreasing TRL-apoB-48 secretion. High n-6 PUFA intake decreased very low-density Lipoprotein (VLDL) cholesterol and triglyceride concentrations by up-regulating VLDL lipolysis and uptake. In a study of healthy subjects, the intake of saturated fatty-acids with increased palmitic acid at the sn-2 position was associated with decreased postprandial lipemia. Low medium-chain triglyceride may not appreciably alter TRL Metabolism. Replacing carbohydrate with monounsaturated fatty-acids increased TRL catabolism. Trans-fatty-acid decreased LDL and enhanced high-density Lipoprotein catabolism. Interactions between APOE genotype and n-3 PUFA in regulating lipid responses were also described. The major advances in understanding the effect of dietary fatty-acids on Lipoprotein Metabolism has centered on n-3 PUFA. This knowledge emphasizes the importance of regulating Lipoprotein Metabolism as a mode to improve plasma lipids and potentially CVD risk. Additional studies are required to better characterize the cardiometabolic effects of other dietary fatty-acids.

  • Abstract 236: Lipoprotein Metabolism in APOB L343V Familial HypobetaLipoproteinemia
    Arteriosclerosis Thrombosis and Vascular Biology, 2014
    Co-Authors: Amanda J. Hooper, K. Robertson, P. Hugh R. Barrett, Klaus G. Parhofer, Frank M. Van Bockxmeer, Liesl V. Heeks, Danie Champain, John R. Burnett
    Abstract:

    Familial hypobetaLipoproteinemia (FHBL) is a codominant disorder of Lipoprotein Metabolism characterized by decreased plasma concentrations of LDL-cholesterol and apoLipoprotein (apo) B. We examined the effect of heterozygous APOB L343V FHBL on fasting and postprandial Lipoprotein Metabolism. VLDL, IDL-, and LDL-apoB kinetics were determined in the fasting state using stable isotope methods and compartmental modeling. VLDL-apoB concentrations in FHBL subjects (n=2) were reduced by more than 75% compared to healthy, normolipidemic control subjects (P

  • Dietary fatty acids and Lipoprotein Metabolism: new insights and updates.
    Current opinion in lipidology, 2013
    Co-Authors: Esther M. M. Ooi, Gerald F. Watts, P. Hugh R. Barrett
    Abstract:

    Purpose of reviewDyslipidemia is a powerful risk factor for cardiovascular disease (CVD). Dietary fatty acid composition regulates lipids and Lipoprotein Metabolism and may confer CVD benefit. This review updates understanding of the effect of dietary fatty acids on Lipoprotein Metabolism in humans.

  • Postprandial Lipoprotein Metabolism in familial hypobetaLipoproteinemia.
    The Journal of Clinical Endocrinology & Metabolism, 2007
    Co-Authors: Amanda J. Hooper, K. Robertson, P. Hugh R. Barrett, Klaus G. Parhofer, Frank M. Van Bockxmeer, John R. Burnett
    Abstract:

    Objective: Familial hypobetaLipoproteinemia (FHBL) is an autosomal codominantly inherited disorder of Lipoprotein Metabolism characterized by decreased plasma concentrations of low-density Lipoprotein-cholesterol and apoLipoprotein (apo) B. We examined the effect of truncated apoB variants (

Amanda J. Hooper - One of the best experts on this subject based on the ideXlab platform.

  • Lipoprotein Metabolism in APOB L343V Familial HypobetaLipoproteinemia
    The Journal of Clinical Endocrinology & Metabolism, 2015
    Co-Authors: Amanda J. Hooper, K. Robertson, P. Hugh R. Barrett, Klaus G. Parhofer, Frank M. Van Bockxmeer, Liesl V. Heeks, Danie Champain, Jianmin Hua, Swithin Song, John R. Burnett
    Abstract:

    Context: Familial hypobetaLipoproteinemia (FHBL) is a codominant disorder of Lipoprotein Metabolism characterized by decreased plasma concentrations of low-density Lipoprotein (LDL)-cholesterol and apoLipoprotein B (apoB). Objective: The objective was to examine the effect of heterozygous APOB L343V FHBL on postprandial triglyceride-rich Lipoprotein (TRL) and fasting Lipoprotein Metabolism. Methods: Plasma incremental area under the curve apoB-48 and apoB-48 kinetics were determined after ingestion of a standardized oral fat load using compartmental modeling. Very low-density Lipoprotein (VLDL)-, intermediate-density Lipoprotein (IDL)-, and LDL-apoB kinetics were determined in the fasting state using stable isotope methods and compartmental modeling. Results: The postprandial incremental area under the curve (0–10 h) in FHBL subjects (n = 3) was lower for large TRL-triglyceride (−77%; P < .0001), small TRL-cholesterol (−83%; P < .001), small TRL-triglyceride (−88%; P < .001), and for plasma triglyceride (...

  • Abstract 236: Lipoprotein Metabolism in APOB L343V Familial HypobetaLipoproteinemia
    Arteriosclerosis Thrombosis and Vascular Biology, 2014
    Co-Authors: Amanda J. Hooper, K. Robertson, P. Hugh R. Barrett, Klaus G. Parhofer, Frank M. Van Bockxmeer, Liesl V. Heeks, Danie Champain, John R. Burnett
    Abstract:

    Familial hypobetaLipoproteinemia (FHBL) is a codominant disorder of Lipoprotein Metabolism characterized by decreased plasma concentrations of LDL-cholesterol and apoLipoprotein (apo) B. We examined the effect of heterozygous APOB L343V FHBL on fasting and postprandial Lipoprotein Metabolism. VLDL, IDL-, and LDL-apoB kinetics were determined in the fasting state using stable isotope methods and compartmental modeling. VLDL-apoB concentrations in FHBL subjects (n=2) were reduced by more than 75% compared to healthy, normolipidemic control subjects (P

  • abstract 236 Lipoprotein Metabolism in apob l343v familial hypobetaLipoproteinemia
    Arteriosclerosis Thrombosis and Vascular Biology, 2014
    Co-Authors: Amanda J. Hooper, K. Robertson, Klaus G. Parhofer, Frank M. Van Bockxmeer, Liesl V. Heeks, Danie Champain, Hugh P R Barrett, John R. Burnett
    Abstract:

    Familial hypobetaLipoproteinemia (FHBL) is a codominant disorder of Lipoprotein Metabolism characterized by decreased plasma concentrations of LDL-cholesterol and apoLipoprotein (apo) B. We examined the effect of heterozygous APOB L343V FHBL on fasting and postprandial Lipoprotein Metabolism. VLDL, IDL-, and LDL-apoB kinetics were determined in the fasting state using stable isotope methods and compartmental modeling. VLDL-apoB concentrations in FHBL subjects (n=2) were reduced by more than 75% compared to healthy, normolipidemic control subjects (P<0.01). VLDL-apoB fractional catabolic rate (FCR) was more than 5-fold higher in the FHBL subjects (P=0.07). ApoB production rates and IDL- and LDL-apoB FCRs were not different between FHBL subjects and controls. To assess postprandial Lipoprotein Metabolism, a standardized oral fat load was given after a 12 h fast to heterozygous APOB L343V FHBL subjects (n=3) and normolipidemic controls. The postprandial incremental area under the curve (0-10 h) in FHBL subje...

  • Postprandial Lipoprotein Metabolism in familial hypobetaLipoproteinemia.
    The Journal of Clinical Endocrinology & Metabolism, 2007
    Co-Authors: Amanda J. Hooper, K. Robertson, P. Hugh R. Barrett, Klaus G. Parhofer, Frank M. Van Bockxmeer, John R. Burnett
    Abstract:

    Objective: Familial hypobetaLipoproteinemia (FHBL) is an autosomal codominantly inherited disorder of Lipoprotein Metabolism characterized by decreased plasma concentrations of low-density Lipoprotein-cholesterol and apoLipoprotein (apo) B. We examined the effect of truncated apoB variants (

  • postprandial Lipoprotein Metabolism in familial hypobetaLipoproteinemia
    The Journal of Clinical Endocrinology and Metabolism, 2007
    Co-Authors: Amanda J. Hooper, K. Robertson, Klaus G. Parhofer, Frank M. Van Bockxmeer, John R. Burnett, Hugh P R Barrett
    Abstract:

    Objective: Familial hypobetaLipoproteinemia (FHBL) is an autosomal codominantly inherited disorder of Lipoprotein Metabolism characterized by decreased plasma concentrations of low-density Lipoprotein-cholesterol and apoLipoprotein (apo) B. We examined the effect of truncated apoB variants (triglyceride-rich Lipoprotein (TRL) Metabolism. Methods and Results: A standardized oral fat load was given after a 12-h fast to six heterozygous [apoB-6.9 (n = 3), apoB-25.8 (n = 1), apoB-40.3 (n = 2)] FHBL subjects and 10 normolipidemic controls. Plasma was obtained every 2 h for 10 h. Large TRLs [containing chylomicrons (CM)] and small TRLs (containing CM remnants) were isolated by ultracentrifugation. Compared with controls, FHBL subjects had significantly decreased fasting plasma cholesterol (2.3 ± 0.5 vs. 4.8 ± 0.5 mmol/liter), triglyceride (0.4 ± 0.3 vs. 1.5 ± 0.5 mmol/liter), low-density Lipoprotein-cholesterol (0.6 ± 0.4 vs. 3.0 ± 0.5 mmol/liter), and apoB (0.22 ± 0.05 vs...

Klaus G. Parhofer - One of the best experts on this subject based on the ideXlab platform.

  • Lipoprotein Metabolism in APOB L343V Familial HypobetaLipoproteinemia
    The Journal of Clinical Endocrinology & Metabolism, 2015
    Co-Authors: Amanda J. Hooper, K. Robertson, P. Hugh R. Barrett, Klaus G. Parhofer, Frank M. Van Bockxmeer, Liesl V. Heeks, Danie Champain, Jianmin Hua, Swithin Song, John R. Burnett
    Abstract:

    Context: Familial hypobetaLipoproteinemia (FHBL) is a codominant disorder of Lipoprotein Metabolism characterized by decreased plasma concentrations of low-density Lipoprotein (LDL)-cholesterol and apoLipoprotein B (apoB). Objective: The objective was to examine the effect of heterozygous APOB L343V FHBL on postprandial triglyceride-rich Lipoprotein (TRL) and fasting Lipoprotein Metabolism. Methods: Plasma incremental area under the curve apoB-48 and apoB-48 kinetics were determined after ingestion of a standardized oral fat load using compartmental modeling. Very low-density Lipoprotein (VLDL)-, intermediate-density Lipoprotein (IDL)-, and LDL-apoB kinetics were determined in the fasting state using stable isotope methods and compartmental modeling. Results: The postprandial incremental area under the curve (0–10 h) in FHBL subjects (n = 3) was lower for large TRL-triglyceride (−77%; P < .0001), small TRL-cholesterol (−83%; P < .001), small TRL-triglyceride (−88%; P < .001), and for plasma triglyceride (...

  • Abstract 236: Lipoprotein Metabolism in APOB L343V Familial HypobetaLipoproteinemia
    Arteriosclerosis Thrombosis and Vascular Biology, 2014
    Co-Authors: Amanda J. Hooper, K. Robertson, P. Hugh R. Barrett, Klaus G. Parhofer, Frank M. Van Bockxmeer, Liesl V. Heeks, Danie Champain, John R. Burnett
    Abstract:

    Familial hypobetaLipoproteinemia (FHBL) is a codominant disorder of Lipoprotein Metabolism characterized by decreased plasma concentrations of LDL-cholesterol and apoLipoprotein (apo) B. We examined the effect of heterozygous APOB L343V FHBL on fasting and postprandial Lipoprotein Metabolism. VLDL, IDL-, and LDL-apoB kinetics were determined in the fasting state using stable isotope methods and compartmental modeling. VLDL-apoB concentrations in FHBL subjects (n=2) were reduced by more than 75% compared to healthy, normolipidemic control subjects (P

  • abstract 236 Lipoprotein Metabolism in apob l343v familial hypobetaLipoproteinemia
    Arteriosclerosis Thrombosis and Vascular Biology, 2014
    Co-Authors: Amanda J. Hooper, K. Robertson, Klaus G. Parhofer, Frank M. Van Bockxmeer, Liesl V. Heeks, Danie Champain, Hugh P R Barrett, John R. Burnett
    Abstract:

    Familial hypobetaLipoproteinemia (FHBL) is a codominant disorder of Lipoprotein Metabolism characterized by decreased plasma concentrations of LDL-cholesterol and apoLipoprotein (apo) B. We examined the effect of heterozygous APOB L343V FHBL on fasting and postprandial Lipoprotein Metabolism. VLDL, IDL-, and LDL-apoB kinetics were determined in the fasting state using stable isotope methods and compartmental modeling. VLDL-apoB concentrations in FHBL subjects (n=2) were reduced by more than 75% compared to healthy, normolipidemic control subjects (P<0.01). VLDL-apoB fractional catabolic rate (FCR) was more than 5-fold higher in the FHBL subjects (P=0.07). ApoB production rates and IDL- and LDL-apoB FCRs were not different between FHBL subjects and controls. To assess postprandial Lipoprotein Metabolism, a standardized oral fat load was given after a 12 h fast to heterozygous APOB L343V FHBL subjects (n=3) and normolipidemic controls. The postprandial incremental area under the curve (0-10 h) in FHBL subje...

  • Postprandial Lipoprotein Metabolism in familial hypobetaLipoproteinemia.
    The Journal of Clinical Endocrinology & Metabolism, 2007
    Co-Authors: Amanda J. Hooper, K. Robertson, P. Hugh R. Barrett, Klaus G. Parhofer, Frank M. Van Bockxmeer, John R. Burnett
    Abstract:

    Objective: Familial hypobetaLipoproteinemia (FHBL) is an autosomal codominantly inherited disorder of Lipoprotein Metabolism characterized by decreased plasma concentrations of low-density Lipoprotein-cholesterol and apoLipoprotein (apo) B. We examined the effect of truncated apoB variants (

  • postprandial Lipoprotein Metabolism in familial hypobetaLipoproteinemia
    The Journal of Clinical Endocrinology and Metabolism, 2007
    Co-Authors: Amanda J. Hooper, K. Robertson, Klaus G. Parhofer, Frank M. Van Bockxmeer, John R. Burnett, Hugh P R Barrett
    Abstract:

    Objective: Familial hypobetaLipoproteinemia (FHBL) is an autosomal codominantly inherited disorder of Lipoprotein Metabolism characterized by decreased plasma concentrations of low-density Lipoprotein-cholesterol and apoLipoprotein (apo) B. We examined the effect of truncated apoB variants (triglyceride-rich Lipoprotein (TRL) Metabolism. Methods and Results: A standardized oral fat load was given after a 12-h fast to six heterozygous [apoB-6.9 (n = 3), apoB-25.8 (n = 1), apoB-40.3 (n = 2)] FHBL subjects and 10 normolipidemic controls. Plasma was obtained every 2 h for 10 h. Large TRLs [containing chylomicrons (CM)] and small TRLs (containing CM remnants) were isolated by ultracentrifugation. Compared with controls, FHBL subjects had significantly decreased fasting plasma cholesterol (2.3 ± 0.5 vs. 4.8 ± 0.5 mmol/liter), triglyceride (0.4 ± 0.3 vs. 1.5 ± 0.5 mmol/liter), low-density Lipoprotein-cholesterol (0.6 ± 0.4 vs. 3.0 ± 0.5 mmol/liter), and apoB (0.22 ± 0.05 vs...

Gary F. Lewis - One of the best experts on this subject based on the ideXlab platform.

  • Gut-liver interaction in triglyceride-rich Lipoprotein Metabolism
    American journal of physiology. Endocrinology and metabolism, 2011
    Co-Authors: Changting Xiao, Joanne Hsieh, Khosrow Adeli, Gary F. Lewis
    Abstract:

    The liver and intestine have complementary and coordinated roles in Lipoprotein Metabolism. Despite their highly specialized functions, assembly and secretion of triglyceride-rich Lipoproteins (TRL; apoB-100-containing VLDL in the liver and apoB-48-containing chylomicrons in the intestine) are regulated by many of the same hormonal, inflammatory, nutritional, and metabolic factors. Furthermore, Lipoprotein Metabolism in these two organs may be affected in a similar fashion by certain disorders. In insulin resistance, for example, overproduction of TRL by both liver and intestine is a prominent component of and underlies other features of a complex dyslipidemia and increased risk of atherosclerosis. The intestine is gaining increasing recognition for its importance in affecting whole body lipid homeostasis, in part through its interaction with the liver. This review aims to integrate recent advances in our understanding of these processes and attempts to provide insight into the factors that coordinate lipid homeostasis in these two organs in health and disease.

  • Triglyceride-Rich Lipoprotein Metabolism and Diabetes
    Cardiovascular Disease 2, 1995
    Co-Authors: George Steiner, Gary F. Lewis
    Abstract:

    The most frequent form of hyperlipidemia in diabetes is hypertriglyceridemial. Therefore, this paper will focus on triglyceride-rich Lipoprotein Metabolism. The major metabolic effects of diabetes stem from abnormalities in insulin. Hence, the chapter will deal with the effect of insulin on triglyceride-rich Lipoprotein Metabolism.