scholarly journals Plasma Markers of Cholesterol Homeostasis and Apolipoprotein B-100 Kinetics in the Metabolic Syndrome

2003 ◽  
Vol 11 (4) ◽  
pp. 591-596 ◽  
Author(s):  
Dick C. Chan ◽  
Gerald F. Watts ◽  
P. Hugh R. Barrett ◽  
Frans H. O'Neill ◽  
Gilbert R. Thompson
Keyword(s):  
Metabolic Syndrome ◽  
Apolipoprotein B ◽  
Cholesterol Homeostasis ◽  
The Metabolic Syndrome ◽  
Plasma Markers

The Apolipoprotein B/Apolipoprotein AI Ratio in the Metabolic Syndrome—Should We Start Using It?

2008 ◽  
Vol 3 (1) ◽  
pp. 53-54 ◽  
Author(s):  
Justo Sierra-Johnson ◽  
Abel Romero-Corral ◽  
Virend K. Somers ◽  
Francisco Lopez-Jimenez
Keyword(s):  
Metabolic Syndrome ◽  
Apolipoprotein B ◽  
Apolipoprotein Ai ◽  
The Metabolic Syndrome

Plasma markers of cholesterol homeostasis in metabolic syndrome subjects with or without type-2 diabetes

2009 ◽  
Vol 85 (3) ◽  
pp. 310-316 ◽  
Author(s):  
Esther M.M. Ooi ◽  
Theodore W.K. Ng ◽  
Dick C. Chan ◽  
Gerald F. Watts
Keyword(s):  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Cholesterol Homeostasis ◽  
Plasma Markers

Autoantibodies against modified apolipoprotein B-100 in relation to low-density lipoprotein size and the metabolic syndrome in otherwise healthy men

Metabolism ◽  
2008 ◽  
Vol 57 (3) ◽  
pp. 362-366 ◽  
Author(s):  
Per Sjögren ◽  
Gunilla N. Fredrikson ◽  
Magdalena Rosell ◽  
Ulf de Faire ◽  
Anders Hamsten ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Apolipoprotein B ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Healthy Men ◽  
The Metabolic Syndrome ◽  
Lipoprotein Size

Generation and characterization of two novel mouse models exhibiting the phenotypes of the metabolic syndrome: Apob48−/−Lepob/ob mice devoid of ApoE or Ldlr

2008 ◽  
Vol 294 (3) ◽  
pp. E496-E505 ◽  
Author(s):  
David J. Lloyd ◽  
Jocelyn McCormick ◽  
Joan Helmering ◽  
Ki Won Kim ◽  
Minghan Wang ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Food Intake ◽  
Apolipoprotein B ◽  
Plasma Cholesterol ◽  
Density Lipoprotein ◽  
Suppressive Effect ◽  
Human Condition ◽  
Atherogenic Dyslipidemia ◽  
Direct Role ◽  
The Metabolic Syndrome

The metabolic syndrome is a group of disorders including obesity, insulin resistance, atherogenic dyslipidemia, hyperglycemia, and hypertension. To date, few animal models have been described to recapitulate the phenotypes of the syndrome. In this study, we generated and characterized two lines of triple-knockout mice that are deficient in either apolipoprotein E (Apoe−/−) or low-density lipoprotein receptor (Ldlr−/−) and express no leptin (Lepob/ob) or apolipoprotein B-48 but exclusively apolipoprotein B-100 (Apob100/100). These two lines are referred to as Apoe triple-knockout-Apoe 3KO (Apoe−/−Apob100/100Lepob/ob) and Ldlr triple-knockout-Ldlr 3KO (Ldlr−/−Apob100/100Lepob/ob) mice. Both lines develop obesity, hyperinsulinemia, hyperlipidemia, hypertension, and atherosclerosis. However, only Apoe 3KO mice are hyperglycemic and glucose intolerant and are more obese than Ldlr 3KO mice. To evaluate the utility of these lines as pharmacological models, we treated both with leptin and found that leptin therapy ameliorated most metabolic derangements. Leptin was more effective in improving glucose tolerance in Ldlr 3KO than Apoe 3KO animals. The reduction of plasma cholesterol by leptin in Ldlr 3KO mice can be accounted for by its suppressive effect on food intake. However, in Apoe 3KO mice, leptin further reduced plasma cholesterol independently of its effect on food intake, and this improvement correlated with a smaller plaque lesion area. These effects suggest a direct role of leptin in modulating VLDL levels and, likewise, the lesion areas in VLDL-enriched animals. These two lines of mice represent new models with features of the metabolic syndrome and will be useful in testing therapies targeted for combating the human condition.

Comparison of Apolipoprotein-B/Apolipoprotein-AI in Subjects With Versus Without the Metabolic Syndrome

2006 ◽  
Vol 98 (10) ◽  
pp. 1369-1373 ◽  
Author(s):  
Justo Sierra-Johnson ◽  
Virend Kristen Somers ◽  
Fatima Helena Sert Kuniyoshi ◽  
Carolina Ana Garza ◽  
William Luther Isley ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Apolipoprotein B ◽  
Apolipoprotein Ai ◽  
The Metabolic Syndrome

Relationships between cholesterol homoeostasis and triacylglycerol-rich lipoprotein remnant metabolism in the metabolic syndrome

2003 ◽  
Vol 104 (4) ◽  
pp. 383-388 ◽  
Author(s):  
Dick C. CHAN ◽  
Gerald F. WATTS ◽  
P. Hugh R. BARRETT ◽  
Frans H. O'NEILL ◽  
Trevor G. REDGRAVE ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Cholesterol Metabolism ◽  
Visceral Obesity ◽  
Cholesterol Absorption ◽  
Dietary Energy ◽  
Lower Plasma ◽  
Apo B ◽  
The Metabolic Syndrome ◽  
Catabolic Rate ◽  
Plasma Markers

The dysmetabolic syndrome of insulin resistance and visceral obesity is characterized by elevated plasma concentration of triacylglycerol-rich lipoprotein (TRL) remnants that may be related to increased cardiovascular risk. Perturbed hepato-intestinal cholesterol metabolism may play a contributory role in this abnormality. We therefore investigated the association between plasma markers of cholesterol absorption and synthesis with TRL remnant metabolism in 35 men with the metabolic syndrome (MS). Plasma campesterol:cholesterol and lathosterol:cholesterol ratios were measured as estimates of cholesterol absorption and synthesis respectively. Remnant metabolism was assessed by measuring remnant-like particle-cholesterol (RLP-C), apolipoprotein (apo)B-48 and the fractional catabolic rate (FCR) of a labelled remnant-like emulsion. Compared with controls, subjects with the MS had significantly lower plasma campesterol:cholesterol ratio, but higher lathosterol:cholesterol ratio (P<0.05). Plasma RLP-C and apoB-48 concentrations were also higher (P<0.01) and the remnant-like emulsion FCR was lower (P<0.05). The plasma campesterol:cholesterol ratio was inversely correlated (P<0.05) with plasma triacylglycerols (r =-0.346), RLP-C (r =-0.443), apoB-48 (r =-0.427) and plasma lathosterol:cholesterol ratio (r =-0.366); the campesterol:cholesterol ratio was also positively correlated with the remnant-like emulsion FCR (r = 0.398, P<0.05). In multiple regression analysis, the significant correlations between plasma campesterol:cholesterol ratio and plasma triacylglycerols, RLP-C, apoB-48 and FCR of the remnant-like emulsion were independent of age, dietary energy and plasma lathosterol. Our findings suggest that in subjects with the MS alterations in cholesterol absorption and synthesis may be closely linked with the kinetic defects in TRL metabolism.

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