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Apolipoprotein B-48

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Gerald F. Watts – One of the best experts on this subject based on the ideXlab platform.

  • Effect of niacin on triglyceride-rich lipoprotein Apolipoprotein B-48 kinetics in statin-treated patients with type 2 diabetes.
    Diabetes obesity & metabolism, 2016
    Co-Authors: Jing Pang, Gerald F. Watts, Dick C. Chan, Vijay S. Tenneti, Sandra J. Hamilton, P.h.r. Barrett

    Abstract:

    Aim
    To investigate the effects of extended-release (ER) niacin on Apolipoprotein B-48 (apoB-48) kinetics in statin-treated patients with type 2 diabetes (T2DM).

    Methods
    A total of 12 men with T2DM were randomized to rosuvastatin or rosuvastatin plus ER niacin for 12 weeks and then crossed to the alternate therapy. Postprandial metabolic studies were performed at the end of each treatment period. D3-leucine tracer was administered as subjects consumed a high-fat liquid meal. ApoB-48 kinetics were determined using stable isotope tracer kinetics with fractional catabolic rates (FCRs) and secretion rates derived using a non-steady-state compartmental model. Area-under-the-curve (AUC) and incremental AUC (iAUC) for plasma triglyceride and apoB-48 were also calculated over the 10-h period after ingestion of the fat meal.

    Results
    In statin-treated patients with T2DM, apoB-48 concentration was lower with ER niacin (8.24 ± 1.98 vs 5.48 ± 1.14 mg/l, p = 0.03) compared with statin alone. Postprandial triglyceride and apoB-48 AUC were also significantly lower on ER niacin treatment (-15 and -26%, respectively; p < 0.05), without any change to triglyceride and apoB-48 iAUC. ApoB-48 secretion rate in the basal state (3.21 ± 0.34 vs 2.50 ± 0.31 mg/kg/day; p = 0.04) and number of apoB-48-containing particles secreted in response to the fat load (1.35 ± 0.19 vs 0.84 ± 0.12 mg/kg; p = 0.02) were lower on ER niacin. ApoB-48 FCR was not altered with ER niacin (8.78 ± 1.04 vs 9.17 ± 1.26 pools/day; p = 0.79).

    Conclusions
    ER niacin reduces apoB-48 concentration by lowering fasting and postprandial apoB-48 secretion rate. This effect may be beneficial for lowering atherogenic postprandial lipoproteins and may provide cardiovascular disease risk benefit in patients with T2DM.

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  • Abstract 10: Improving Postprandial Lipoprotein Apolipoprotein B-48 Metabolism in Statin-Treated Patients With Diabetes
    Arteriosclerosis Thrombosis and Vascular Biology, 2014
    Co-Authors: Jing Pang, Gerald F. Watts, Dick C. Chan, Sandy Hamilton, Vijay S. Tenneti, Hugh Barrett

    Abstract:

    Background: Type 2 diabetics often have elevated plasma TG and Apolipoprotein B-48 (apoB-48) concentrations, particularly during the postprandial (PP) period. Evidence suggests that apoB-48 plays a central role in the development of atherosclerosis. Statins are frontline therapy to reduce CVD risk, however, residual risk still remains, suggesting that additional interventions are required to further reduce CVD risk.

    Aim: To compare PP apoB-48 kinetics in optimally statin-treated diabetic men with a group of normolipidemic healthy controls, and to investigate the effect of niacin on apoB-48 kinetics in these diabetic men.

    Methods: Twelve type 2 diabetic men and fourteen age-matched non-diabetic controls were recruited. Diabetics required a statin-treated LDL-C < 2.5 mmol/L to enter the trial: they were randomized to rosuvastatin or rosuvastatin plus niacin (titrated from 1 to 2 g daily) for 12 weeks and then crossed to the alternate therapy (3 week washout). PP metabolic studies were performed at the end of each treatment period, and on a single occasion in control subjects. D3-leucine tracer was administered as subjects consumed a high-fat liquid meal. Blood samples were collected over 24 h. ApoB-48 tracer/tracee ratios were measured using GCMS. Kinetic parameters, including fractional catabolic rate (FCR) and production rate (PR), were derived using a compartmental model.

    Results: Fasting plasma TG (+112%, p

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  • abstract p270 niacin lowers triglyceride rich lipoprotein Apolipoprotein b 48 secretion in statin treated type 2 diabetics
    Circulation, 2014
    Co-Authors: Jing Pang, Gerald F. Watts, Dick C. Chan, Sandy Hamilton, Vijay S. Tenneti, Hugh Barrett

    Abstract:

    Background: Type 2 diabetic subjects often have hypertriglyceridemia and an increased concentration of Apolipoprotein B-48 (apoB-48) in circulation, particularly during the postprandial period. There is an accumulating body of evidence to suggest that apoB-48 plays a central role in the development of atherosclerosis. Statins are the frontline therapy to reduce cardiovascular risk, however, a large residual risk still remains. This residual risk suggests that additional therapeutic interventions may be required to further reduce CVD risk. Aim: To investigate the effect of niacin on the metabolism of triglyceride-rich lipoprotein (TRL) apoB-48 in men with type 2 diabetes on background statin therapy. Methods: Twelve type 2 diabetic men were recruited for this randomized, cross-over design study. Patients required a statin-treated low density lipoprotein (LDL) cholesterol of less than 2.5 mmol/L to enter the trial. Patients were then randomized to rosuvastatin alone or rosuvastatin plus niacin (titrated up from 1 to 2 g daily) for a period of 12 weeks and then were crossed over to the alternate therapy with a 3 week washout period in between. Metabolic studies were performed at the end of each treatment period. A bolus intravenous infusion of D3-leucine was administered as subjects consumed a standardised high-fat liquid meal. Blood samples were collected over 24 hours and TRL apoB-48 tracer/tracee ratios were measured using gas chromatography-mass spectrometry. Kinetic parameters, including fractional catabolic rate (FCR) and production rate (PR), were derived using a multicompartmental model. Results: Niacin significantly reduced triglyceride, plasma cholesterol, LDL cholesterol and apoB (all p Conclusion: Niacin reduces TRL apoB-48 concentration by lowering basal and postprandial apoB-48 PR. This effect on apoB-48 metabolism may be beneficial for reducing atherogenic postprandial TRL particles and may provide CVD risk benefit to patients with type 2 diabetes.

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Dick C. Chan – One of the best experts on this subject based on the ideXlab platform.

  • Effect of niacin on triglyceride-rich lipoprotein Apolipoprotein B-48 kinetics in statin-treated patients with type 2 diabetes.
    Diabetes obesity & metabolism, 2016
    Co-Authors: Jing Pang, Gerald F. Watts, Dick C. Chan, Vijay S. Tenneti, Sandra J. Hamilton, P.h.r. Barrett

    Abstract:

    Aim
    To investigate the effects of extended-release (ER) niacin on Apolipoprotein B-48 (apoB-48) kinetics in statin-treated patients with type 2 diabetes (T2DM).

    Methods
    A total of 12 men with T2DM were randomized to rosuvastatin or rosuvastatin plus ER niacin for 12 weeks and then crossed to the alternate therapy. Postprandial metabolic studies were performed at the end of each treatment period. D3-leucine tracer was administered as subjects consumed a high-fat liquid meal. ApoB-48 kinetics were determined using stable isotope tracer kinetics with fractional catabolic rates (FCRs) and secretion rates derived using a non-steady-state compartmental model. Area-under-the-curve (AUC) and incremental AUC (iAUC) for plasma triglyceride and apoB-48 were also calculated over the 10-h period after ingestion of the fat meal.

    Results
    In statin-treated patients with T2DM, apoB-48 concentration was lower with ER niacin (8.24 ± 1.98 vs 5.48 ± 1.14 mg/l, p = 0.03) compared with statin alone. Postprandial triglyceride and apoB-48 AUC were also significantly lower on ER niacin treatment (-15 and -26%, respectively; p < 0.05), without any change to triglyceride and apoB-48 iAUC. ApoB-48 secretion rate in the basal state (3.21 ± 0.34 vs 2.50 ± 0.31 mg/kg/day; p = 0.04) and number of apoB-48-containing particles secreted in response to the fat load (1.35 ± 0.19 vs 0.84 ± 0.12 mg/kg; p = 0.02) were lower on ER niacin. ApoB-48 FCR was not altered with ER niacin (8.78 ± 1.04 vs 9.17 ± 1.26 pools/day; p = 0.79).

    Conclusions
    ER niacin reduces apoB-48 concentration by lowering fasting and postprandial apoB-48 secretion rate. This effect may be beneficial for lowering atherogenic postprandial lipoproteins and may provide cardiovascular disease risk benefit in patients with T2DM.

    Free Register to Access Article

  • Abstract 10: Improving Postprandial Lipoprotein Apolipoprotein B-48 Metabolism in Statin-Treated Patients With Diabetes
    Arteriosclerosis Thrombosis and Vascular Biology, 2014
    Co-Authors: Jing Pang, Gerald F. Watts, Dick C. Chan, Sandy Hamilton, Vijay S. Tenneti, Hugh Barrett

    Abstract:

    Background: Type 2 diabetics often have elevated plasma TG and Apolipoprotein B-48 (apoB-48) concentrations, particularly during the postprandial (PP) period. Evidence suggests that apoB-48 plays a central role in the development of atherosclerosis. Statins are frontline therapy to reduce CVD risk, however, residual risk still remains, suggesting that additional interventions are required to further reduce CVD risk.

    Aim: To compare PP apoB-48 kinetics in optimally statin-treated diabetic men with a group of normolipidemic healthy controls, and to investigate the effect of niacin on apoB-48 kinetics in these diabetic men.

    Methods: Twelve type 2 diabetic men and fourteen age-matched non-diabetic controls were recruited. Diabetics required a statin-treated LDL-C < 2.5 mmol/L to enter the trial: they were randomized to rosuvastatin or rosuvastatin plus niacin (titrated from 1 to 2 g daily) for 12 weeks and then crossed to the alternate therapy (3 week washout). PP metabolic studies were performed at the end of each treatment period, and on a single occasion in control subjects. D3-leucine tracer was administered as subjects consumed a high-fat liquid meal. Blood samples were collected over 24 h. ApoB-48 tracer/tracee ratios were measured using GCMS. Kinetic parameters, including fractional catabolic rate (FCR) and production rate (PR), were derived using a compartmental model.

    Results: Fasting plasma TG (+112%, p

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  • abstract p270 niacin lowers triglyceride rich lipoprotein Apolipoprotein b 48 secretion in statin treated type 2 diabetics
    Circulation, 2014
    Co-Authors: Jing Pang, Gerald F. Watts, Dick C. Chan, Sandy Hamilton, Vijay S. Tenneti, Hugh Barrett

    Abstract:

    Background: Type 2 diabetic subjects often have hypertriglyceridemia and an increased concentration of Apolipoprotein B-48 (apoB-48) in circulation, particularly during the postprandial period. There is an accumulating body of evidence to suggest that apoB-48 plays a central role in the development of atherosclerosis. Statins are the frontline therapy to reduce cardiovascular risk, however, a large residual risk still remains. This residual risk suggests that additional therapeutic interventions may be required to further reduce CVD risk. Aim: To investigate the effect of niacin on the metabolism of triglyceride-rich lipoprotein (TRL) apoB-48 in men with type 2 diabetes on background statin therapy. Methods: Twelve type 2 diabetic men were recruited for this randomized, cross-over design study. Patients required a statin-treated low density lipoprotein (LDL) cholesterol of less than 2.5 mmol/L to enter the trial. Patients were then randomized to rosuvastatin alone or rosuvastatin plus niacin (titrated up from 1 to 2 g daily) for a period of 12 weeks and then were crossed over to the alternate therapy with a 3 week washout period in between. Metabolic studies were performed at the end of each treatment period. A bolus intravenous infusion of D3-leucine was administered as subjects consumed a standardised high-fat liquid meal. Blood samples were collected over 24 hours and TRL apoB-48 tracer/tracee ratios were measured using gas chromatography-mass spectrometry. Kinetic parameters, including fractional catabolic rate (FCR) and production rate (PR), were derived using a multicompartmental model. Results: Niacin significantly reduced triglyceride, plasma cholesterol, LDL cholesterol and apoB (all p Conclusion: Niacin reduces TRL apoB-48 concentration by lowering basal and postprandial apoB-48 PR. This effect on apoB-48 metabolism may be beneficial for reducing atherogenic postprandial TRL particles and may provide CVD risk benefit to patients with type 2 diabetes.

    Free Register to Access Article

Daisaku Masuda – One of the best experts on this subject based on the ideXlab platform.

  • Abstract 13452: Serum Apolipoprotein B-48 levels Are Significantly Correlated with Plaque Score of Carotid Arteries
    Circulation, 2014
    Co-Authors: Daisaku Masuda, Manabu Okubo, Hiroyuki Hanada, Yoh Hidaka, Yasushi Sakata, Masahiro Matsui, Shizuya Yamashita

    Abstract:

    Introduction: Fasting hypertriglyceridemia is a “residual risk” factor for atherosclerotic cardiovascular diseases and related to postprandial hypertriglyceridemia (PHTG). Intestine-derived lipoproteins such as chylomicrons and chylomicron remnants (CM-Rs), which contain one Apolipoprotein(apo) B-48 molecule per one particle, are accumulated in patients with PHTG. Basic studies showed that CM-R had an atherogenic nature and apoB-48 molecule was observed in atherosclerotic plaque twice as many as apoB-100 molecule histologically. We established a CLEIA for measuring serum apoB-48 concentrations and reported that high apoB-48 concentrations correlated with the prevalence of dyslipidemia, diabetes mellitus, metabolic syndrome, chronic kidney disease and coronary heart disease. Hypothesis: We investigated whether serum apoB-48 concentration correlated with subclinical carotid atherosclerosis. Methods: A total of 163 subjects who received ultrasonography of carotid arteries in Osaka University were enrolled. B…

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  • abstract 14993 proteomic analysis of chylomicron remnants isolated by Apolipoprotein b 48 immunoprecipitation
    Circulation, 2014
    Co-Authors: Daisaku Masuda, Manabu Okubo, Tohru Ohama, Hajime Nakaoka, Ryota Kawase, Kazuhiro Nakatani, Takuya Kobayashi, Takeshi Okada, Masahiro Koseki, Hiroyuki Hanada

    Abstract:

    Introduction: Postprandial hypertriglyceridemia is caused by overproduction or impaired clearance of Apolipoprotein (apo)B-48-containing lipoproteins, chylomicrons (CMs) and CM remnants (CM-Rs). In vitro studies have suggested that CM-Rs may lead to the formation of atherosclerotic plaques. By our ELISA and CLEIA for measuring human serum apoB-48 concentrations, we reported fasting apoB-48 concentrations are significantly higher in patients with dyslipidemia, diabetes mellitus, metabolic syndrome and chronic kidney disease than in normal subjects, and correlated with the IMT of carotid arteries and the prevalence of coronary heart disease. However, it has been technically very difficult to isolate CM-Rs and to evaluate the atherogenicity of pure CM-Rs.

    Hypothesis: We tried to selectively isolate CM-Rs and analyze their lipoprotein and proteomics profiles and assessed their atherogenicity.

    Methods: Fractions containing CM-Rs and VLDL (d<1.01 mg/dL) were isolated from the postprandial sera of healthy volunteers by two-step ultracentrifugation. CM-Rs were selectively eluted and isolated by immunoprecipitation using anti-human apoB-48 monoclonal antibodies conjugated with magnetic beads. Mouse peritoneal macrophages were incubated with isolated CM-Rs and stained with Oil-red O. Lipoprotein profiles of isolated human CM-Rs and mouse CMs collected from the intestinal lymph were examined by high performance liquid chromatography and proteomic analyses were performed by mass spectrometry using Synapt G2 HDMS PRO.

    Results: Compared with the lipoprotein profile of postprandial serum, particle size of isolated lipoproteins varied in size from small chylomicrons to large LDL, which suggested CM-Rs. When incubated with isolated CM-Rs, foam cell formation of mouse peritoneal macrophages was observed. By proteomic analysis, isolated human CM-Rs and mouse CMs contained a variety of complements (C3, C4 and more), Apolipoproteins (apoB, apoA2, apoD and apoH), paraoxonase 1 (PON-1) and many serine protease inhibitors.

    Conclusions: The current study has demonstrated for the first time that human CM-Rs and CMs have an atherogenic nature and contain many types of complements, Apolipoproteins, PON-1 and serine protease inhibitors.

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  • Abstract 14993: Proteomic Analysis of Chylomicron Remnants Isolated by Apolipoprotein B-48 Immunoprecipitation
    Circulation, 2014
    Co-Authors: Daisaku Masuda, Manabu Okubo, Tohru Ohama, Hajime Nakaoka, Ryota Kawase, Kazuhiro Nakatani, Takuya Kobayashi, Takeshi Okada, Masahiro Koseki, Hiroyuki Hanada

    Abstract:

    Introduction: Postprandial hypertriglyceridemia is caused by overproduction or impaired clearance of Apolipoprotein (apo)B-48-containing lipoproteins, chylomicrons (CMs) and CM remnants (CM-Rs). In vitro studies have suggested that CM-Rs may lead to the formation of atherosclerotic plaques. By our ELISA and CLEIA for measuring human serum apoB-48 concentrations, we reported fasting apoB-48 concentrations are significantly higher in patients with dyslipidemia, diabetes mellitus, metabolic syndrome and chronic kidney disease than in normal subjects, and correlated with the IMT of carotid arteries and the prevalence of coronary heart disease. However, it has been technically very difficult to isolate CM-Rs and to evaluate the atherogenicity of pure CM-Rs.

    Hypothesis: We tried to selectively isolate CM-Rs and analyze their lipoprotein and proteomics profiles and assessed their atherogenicity.

    Methods: Fractions containing CM-Rs and VLDL (d

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