Hypolipidemic mechanisms of pectin and psyllium in guinea pigs fed high fat–sucrose diets: alterations on hepatic cholesterol metabolism

Background/Aims: Prenatal ethanol exposure (PEE) could induce intrauterine programming of hypothalamic-pituitary-adrenal axis-associated neuroendocrine metabolism, resulting in intrauterine growth retardation and susceptibility to adult hypercholesterolemia in offspring. This study aimed to analyse the effects and interactions of PEE, a post-weaning high-fat diet (HFD) and gender on the occurrence of adult hypercholesterolemia in offspring rats. Methods: Wistar female rats were treated with ethanol (4 g/kg.d) at gestational days 11-20. The offspring were given a normal diet or HFD after weaning, and the blood cholesterol metabolism phenotype and expression of hepatic cholesterol metabolism related genes were detected in 24-week-old offspring. Furthermore, the interactions among PEE, HFD, and gender on hypercholesterolemia occurrence were analysed. Results: PEE increased the serum total cholesterol (TCH) and low-density lipoprotein-cholesterol (LDL-C) levels and decreased the serum high-density lipoprotein-cholesterol (HDL-C) level in adult offspring rats; the changes in female offspring were greater than those in males. At the same time, the mRNA expression levels of hepatic cholesterol metabolic enzymes (apolipoprotein B (ApoB) and 7α-hydroxylase (CYP7A1))—were increased, while the mRNA expression levels of the scavenger receptor B1 (SR-B1) and LDL receptor (LDLR) were decreased. Furthermore, a three-way ANOVA showed there were interactions among PEE, post-weaning HFD and gender. For PEE offspring, a post-weaning HFD aggravated the elevated hepatic ApoB and CYP7A1 expression and reduced SR-B1 and LDLR expression; the changes in hepatic SR-B1 and CYP7A1 expression were greater in female HFD rats than in males. Conclusion: Our findings suggest that a post-weaning HFD could aggravate offspring hypercholesterolemia caused by PEE and that this mechanism might be associated with hepatic cholesterol metabolic disorders that are aggravated by a post-weaning HFD; hepatic cholesterol metabolism was more sensitive to neuroendocrine metabolic alterations by PEE and a post-weaning HFD in the female offspring than in the male offspring.

Download Full-text

Lime-treated corn husks lower plasma LDL cholesterol in guinea pigs by altering hepatic cholesterol metabolism

The Journal of Nutritional Biochemistry ◽

10.1016/s0955-2863(97)00062-4 ◽

1997 ◽

Vol 8 (8) ◽

pp. 479-486 ◽

Cited By ~ 12

Author(s):

Reyna Luz Vidal-Quintanar ◽

Laura Hernandez ◽

Karin Conde ◽

Marcela Vergara-Jimenez ◽

Maria Luz Fernandez

Keyword(s):

Guinea Pigs ◽

Ldl Cholesterol ◽

Cholesterol Metabolism ◽

Hepatic Cholesterol ◽

Lower Plasma

Download Full-text

Treadmill Exercise Training Modulates Hepatic Cholesterol Metabolism and Circulating PCSK9 Concentration in High-Fat-Fed Mice

Journal of Lipids ◽

10.1155/2013/908048 ◽

2013 ◽

Vol 2013 ◽

pp. 1-9 ◽

Cited By ~ 15

Author(s):

Shin Wen ◽

Kavita S. Jadhav ◽

David L. Williamson ◽

Todd C. Rideout

Keyword(s):

Exercise Training ◽

Treadmill Exercise ◽

Cholesterol Metabolism ◽

Hepatic Cholesterol ◽

High Fat

Download Full-text

PL-006 Expression of molecular markers of hepatic cholesterol metabolism are altered by a short-term high-fat diet

Exercise Biochemistry Review ◽

10.14428/ebr.v1i1.8103 ◽

2018 ◽

Vol 1 (1) ◽

Author(s):

Jean-Marc Lavoie

Keyword(s):

Lipid Accumulation ◽

High Fat Diet ◽

Metabolic Disorders ◽

Cholesterol Metabolism ◽

Plasma Cholesterol ◽

Hepatic Cholesterol ◽

High Fat ◽

Short Term ◽

Cholesterol Levels ◽

Ldl Particles

Objective Metabolic disorders are often associated with liver steatosis and increased plasma cholesterol levels. However, the link between excessive lipid accumulation and impairments in cholesterol metabolism remains uninvestigated in the liver. Hence, a short treatment with a high-fat diet (HFD) was previously shown to promote excessive lipid accumulation in liver prior to the development of metabolic disorders. The present study intended to characterize how increases in liver fat alter the expression of several key regulators of hepatic cholesterol metabolism in response to a short-term HFD. Methods Young Wistar rats were randomly submitted either to HFD (n = 8) or a regular chow diet (RCD; n = 8) for 14 days.Liver tissue and blood were sampled . Results Increases in triglycerides were highly significant (P< 0.01) in liver but marginal in plasma of HFD rats. In contrast, the HFD resulted in higher (P< 0.01) cholesterol levels in plasma but not in liver samples. Gene expression of key markers involved in cholesterol uptake (LDL particles) including low density lipoprotein receptor-related protein-1 (LRP-1) and protein convertase subtilisin/kexin type 9 (PCSK9) along with ATP-binding cassette, superfamily G, member 5 (ABCG5) involved in cholesterol exportation viabile ducts were found to be higher (P< 0.05) in response to the HFD. In contrast, expression of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), involved in cholesterol synthesis was down-regulated in liver Conclusions The data support the concept that excessive accumulation of lipids promptly alters the expression of key genes regulating cholesterol metabolism in liver. On a clinical point of view, this indicates that increases in plasma cholesterol occur after a short-term high fat diet.

Download Full-text