Associations Between Apolipoprotein-A5 Genotype, High-Fat Diet and Plasma Lipid Levels among HIV-infected Children Initiating Antiretroviral Therapy in India

The present study aimed to investigate whether olive leaf extract (OLE) prevents high-fat diet (HFD)-induced obesity in mice and to explore the underlying mechanisms. Mice were randomly divided into groups that received a chow diet (CD), HFD, or 0.15% OLE-supplemented diet (OLD) for 8 weeks. OLD-fed mice showed significantly reduced body weight gain, visceral fat-pad weights, and plasma lipid levels as compared with HFD-fed mice. OLE significantly reversed the HFD-induced upregulation of WNT10b- and galanin-mediated signaling molecules and key adipogenic genes (PPARγ, C/EBPα, CD36, FAS, and leptin) in the epididymal adipose tissue of HFD-fed mice. Furthermore, the HFD-induced downregulation of thermogenic genes involved in uncoupled respiration (SIRT1, PGC1α, and UCP1) and mitochondrial biogenesis (TFAM, NRF-1, and COX2) was also significantly reversed by OLE. These results suggest that OLE exerts beneficial effects against obesity by regulating the expression of genes involved in adipogenesis and thermogenesis in the visceral adipose tissue of HFD-fed mice.

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Anti-inflammatory Effect of Lactuca sativa L. Extract in Human Umbilical Vein Endothelial Cells and Improvement of Lipid Levels in Mice Fed a High-fat Diet

The Korean Journal of Food And Nutrition ◽

10.9799/ksfan.2016.29.6.998 ◽

2016 ◽

Vol 29 (6) ◽

pp. 998-1007 ◽

Cited By ~ 1

Author(s):

Jeon Hwang-Bo ◽

Kyung Ok Jang ◽

Hayoung Chung ◽

Jong-Hwa Park ◽

Tae Hoon Lee ◽

...

Keyword(s):

Endothelial Cells ◽

Lactuca Sativa ◽

High Fat Diet ◽

Umbilical Vein ◽

Lipid Levels ◽

High Fat ◽

Human Umbilical Vein ◽

Lactuca Sativa L ◽

Umbilical Vein Endothelial Cells ◽

Inflammatory Effect

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Abstract 15294: Activation of Mac-1 Integrin Prevents G-CSF Mediated Monocyte Mobilization and Atherosclerosis Severity in Hypercholesterolemic Mice

Circulation ◽

10.1161/circ.130.suppl_2.15294 ◽

2014 ◽

Vol 130 (suppl_2) ◽

Author(s):

Sina Rahimpour ◽

Annia Mesa ◽

Lei Song ◽

Natasha Fernandez ◽

Si M Pham ◽

...

Keyword(s):

High Fat Diet ◽

Plasma Lipid ◽

High Fat ◽

Once Daily ◽

Leukocyte Mobilization ◽

Sudan Iv ◽

Low Levels ◽

Atherosclerosis Development ◽

Excessive Number ◽

Atherosclerosis Severity

Background: Leukadherins (LA) are a novel family of Mac-1 agonists that increase cell adhesion and prevent leukocyte mobilization and tissue inflammation. This study brings new insights into how leukadherin LA1 protects hypercholesterolemic ApoE-null mice from excessive atherosclerosis development. Hypothesis: Activation of Mac-1 integrin with leukadherin LA1 retains monocytes in medullary and extramedullary centers and therefore, controls high fat diet induced monocytosis and atherosclerosis in ApoE-null mice. Methods and Results: Once daily administration of LA1 (10mg/kg) for 16 weeks significantly reduced atherosclerosis in the entire aorta and the aortic valve of high fat diet fed ApoE-null mice as determined by Sudan IV staining. The LA1 treatment had not effect on body weight or plasma lipid levels though it significantly reduced the number of circulating monocytes (Lin2- CD11c- CD11b+ by FACS). The remaining circulating monocytes in LA1-treated mice displayed low levels of Ly6C, a marker for inflammation. Interestingly, LA1 caused monocyte retention in the bone marrow (BM) and macrophages (F4/80+ by IHC) in the spleen of hypercholesterolemic mice, which account for the low numbers of monocytes seem in the circulation of these mice. On the other hand, the excessive number of BM monocytes didn’t compromise the number of hematopoietic (Lin- Sca+ c-Kit+) or myeloid (Lin- Sca- c-Kit+) progenitor cells. Finally, we assessed the effect of LA1 on systemic inflammatory mediators using multiplex immunoassay. The plasma levels of G-CSF, one of the main monocyte mobilization cytokines capable of promoting atherosclerosis in ApoE-null mice, were found reduced in a half in treated versus control mice. Conclusions: These data demonstrate that Mac-1 activation with LA1 significantly reduces atherosclerosis in hypercholesterolemic ApoE-null by impairing G-CSF mediated monocyte mobilization from medullary and extramedullary centers.

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