Effects of Resistant Starch on Gut Functions and Plasma Lipid Profiles in Rats Fed High Fat Diet

2002 ◽  
Vol 31 (2) ◽  
pp. 271-276 ◽  
Keyword(s):  
Resistant Starch ◽  
High Fat Diet ◽  
Plasma Lipid ◽  
Lipid Profiles ◽  
High Fat

scholarly journals Olive Leaf Extract Attenuates Obesity in High-Fat Diet-Fed Mice by Modulating the Expression of Molecules Involved in Adipogenesis and Thermogenesis

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Ying Shen ◽  
Su Jin Song ◽  
Narae Keum ◽  
Taesun Park
Keyword(s):  
Adipose Tissue ◽  
High Fat Diet ◽  
Leaf Extract ◽  
Body Weight Gain ◽  
Plasma Lipid ◽  
Epididymal Adipose Tissue ◽  
Chow Diet ◽  
Olive Leaf ◽  
High Fat ◽  
Olive Leaf Extract

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.

scholarly journals Resistant starch and exercise independently attenuate weight regain on a high fat diet in a rat model of obesity

2011 ◽  
Vol 8 (1) ◽  
pp. 49 ◽  
Author(s):  
Janine A Higgins ◽  
Matthew R Jackman ◽  
Ian L Brown ◽  
Ginger C Johnson ◽  
Amy Steig ◽  
...  
Keyword(s):  
Rat Model ◽  
Resistant Starch ◽  
High Fat Diet ◽  
Weight Regain ◽  
High Fat

scholarly journals Enhanced anti-obesity effects of complex of resistant starch and chitosan in high fat diet fed rats

2017 ◽  
Vol 157 ◽  
pp. 834-841 ◽  
Author(s):  
Xu Si ◽  
Padraig Strappe ◽  
Chris Blanchard ◽  
Zhongkai Zhou
Keyword(s):  
Resistant Starch ◽  
High Fat Diet ◽  
High Fat

Soyasaponins Reduce Inflammation and Improve Serum Lipid Profiles and Glucose Homeostasis in High Fat Diet-Induced Obese Mice

2018 ◽  
Vol 62 (19) ◽  
pp. 1800205 ◽  
Author(s):  
Qunying Xie ◽  
Xiangfu Gu ◽  
Junbin Chen ◽  
Minshun Liu ◽  
Fei Xiong ◽  
...  
Keyword(s):  
Glucose Homeostasis ◽  
High Fat Diet ◽  
Serum Lipid ◽  
Lipid Profiles ◽  
Obese Mice ◽  
High Fat

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

Circulation ◽  
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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