The minor allele of the missense polymorphism Ser251Pro in perilipin 2 (PLIN2) disrupts an α‐helix, affects lipolysis, and is associated with reduced plasma triglyceride concentration in humans

2013 ◽  
Vol 27 (8) ◽  
pp. 3090-3099 ◽  
Author(s):  
Joëlle Magné ◽  
Anna Aminoff ◽  
Jeanna Perman Sundelin ◽  
Maria Nastase Mannila ◽  
Peter Gustafsson ◽  
...  
1988 ◽  
Vol 34 (12) ◽  
pp. 2456-2459 ◽  
Author(s):  
J S Cohn ◽  
J R McNamara ◽  
E J Schaefer

Abstract Lipoprotein cholesterol concentrations in plasma are routinely estimated by using the Friedewald formula, whereby very-low-density lipoprotein cholesterol (VLDL-C) is estimated to be one-fifth the plasma triglyceride concentration. Ordinarily, this formula is applied only to plasma sampled from patients in the fasted state. To determine whether lipoprotein cholesterol measurements are altered substantially in plasma sampled from nonfasting subjects, we obtained postprandial blood samples from 22 healthy subjects (nine men, 13 women, ages 22-79 years) fed a fat-rich meal (1 g fat per kilogram body wt.). The plasma triglyceride concentration increased postprandially in all subjects (233 +/- 16% of baseline at 3 h). The mean cholesterol concentration in plasma was essentially unchanged. High-density lipoprotein cholesterol (HDL-C) was significantly decreased (94 +/- 2% at 3 h, P less than 0.001). VLDL-C and low-density lipoprotein cholesterol (LDL-C), estimated by the Friedewald formula, were compared with measurements obtained by modified Lipid Research Clinics (LRC) methodology. As measured by either method, VLDL-C increased and LDL-C decreased significantly after the fat-rich meal. These postprandial changes were significantly greater (P less than 0.01) when estimated by the Friedewald formula than by LRC methodology. We conclude that (a) lipoprotein cholesterol concentrations measured in the fed subject differ significantly from those measured in the fasted subject, and (b) plasma must be obtained after at least a 12-h fast if an individual's risk of coronary heart disease is to be accurately assessed.


Metabolism ◽  
1979 ◽  
Vol 28 (5) ◽  
pp. 553-561 ◽  
Author(s):  
Alan Chait ◽  
John D. Brunzell ◽  
David G. Johnson ◽  
James W. Benson ◽  
Philip Werner ◽  
...  

Metabolism ◽  
1989 ◽  
Vol 38 (5) ◽  
pp. 484-490 ◽  
Author(s):  
Jeffrey S. Cohn ◽  
Judith R. McNamara ◽  
Stephen D. Krasinski ◽  
Robert M. Russell ◽  
Ernst J. Schaefer

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Nobutomo Ikarashi ◽  
Rumi Takeda ◽  
Kiyomi Ito ◽  
Wataru Ochiai ◽  
Kiyoshi Sugiyama

Acacia polyphenol (AP) extracted from the bark of the black wattle tree (Acacia mearnsii) is rich in unique catechin-like flavan-3-ols, such as robinetinidol and fisetinidol. In anin vitrostudy, we measured the inhibitory activity of AP on lipase and glucosidase. In addition, we evaluated the effects of AP on absorption of orally administered olive oil, glucose, maltose, sucrose and starch solution in mice. We found that AP concentration-dependently inhibited the activity of lipase, maltase and sucrase with an IC50of 0.95, 0.22 and 0.60 mg ml−1, respectively. In ICR mice, olive oil was administered orally immediately after oral administration of AP solution, and plasma triglyceride concentration was measured. We found that AP significantly inhibited the rise in plasma triglyceride concentration after olive oil loading. AP also significantly inhibited the rise in plasma glucose concentration after maltose and sucrose loading, and this effect was more potent against maltose. AP also inhibited the rise in plasma glucose concentration after glucose loading and slightly inhibited it after starch loading. Our results suggest that AP inhibits lipase and glucosidase activities, which leads to a reduction in the intestinal absorption of lipids and carbohydrates.


2007 ◽  
Vol 53 (9) ◽  
pp. 1706-1713 ◽  
Author(s):  
Mohammed K Azharuddin ◽  
Denis St J O’Reilly ◽  
Andrew Gray ◽  
Dinesh Talwar

Abstract Background: The plasma concentration of vitamin K1 (phylloquinone) is the most reliable index for assessing vitamin K status. Our aim was to analytically validate an HPLC method for quantifying phylloquinone in plasma and to examine the effect of plasma triglyceride concentration on the phylloquinone reference interval. We also examined the effect of acute-phase response on phylloquinone concentration in plasma. Methods: Phylloquinone was extracted from fasting plasma samples by deproteinization and C18 solid-phase extraction, separated by reversed-phase HPLC, and detected fluorometrically after postcolumn reduction with a platinum catalyst. We synthesized a novel internal calibrator, docosyl naphthoate. Results: The recovery of phylloquinone was >90%. Between-run imprecision was 8.7%–9.0%, and within-run imprecision was 3.8%–7.0%. The linearity was up to 44.8 nmol/L, limit of detection 0.08 nmol/L, and limit of quantification 0.14 nmol/L. The correlation between plasma phylloquinone and triglyceride concentrations was r = 0.7 in the reference population. The 95% reference interval for the phylloquinone:triglyceride ratio was 0.20 to 2.20 nmol/mmol. Plasma concentrations of C-reactive protein were significantly increased, whereas triglyceride and phylloquinone but not the phylloquinone:triglyceride ratio were transiently decreased >50% after surgery. Conclusion: Phylloquinone population reference intervals should be expressed as a ratio of the triglyceride concentration. Phylloquinone concentrations in plasma are decreased in acute-phase response and, unless corrected for plasma triglyceride concentration, are unlikely to be a reliable index of vitamin K status.


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