scholarly journals High Fat Relative To Low Fat Ground Beef Consumption Lowers Blood Pressure And Does Not Negatively Alter Arterial Stiffness

2020 ◽  
Vol 52 (7S) ◽  
pp. 235-235
Author(s):  
Jason R. Lytle ◽  
Karina L. Wilson ◽  
Sean T. Stanelle ◽  
Matthew B. Wofford ◽  
Rebecca M. Bonta ◽  
...  
Author(s):  
Simon Fryer ◽  
Keeron Stone ◽  
Craig Paterson ◽  
Meghan Brown ◽  
James Faulkner ◽  
...  

AbstractIndependently, prolonged uninterrupted sitting and the consumption of a meal high in saturated fats acutely disrupt normal cardiovascular function. Currently, the acute effects of these behaviors performed in combination on arterial stiffness, a marker of cardiovascular health, are unknown. This study sought to determine the effect of consuming a high-fat meal (Δ = 51 g fat) in conjunction with prolonged uninterrupted sitting (180 min) on measures of central and peripheral arterial stiffness. Using a randomized crossover design, 13 young healthy males consumed a high-fat (61 g) or low-fat (10 g) meal before 180 min of uninterrupted sitting. Carotid-femoral (cf) and femoral-ankle (fa) pulse wave velocity (PWV), aortic-femoral stiffness gradient (af-SG), superficial femoral PWV beta (β), and oscillometric pulse wave analysis outcomes were assessed pre and post sitting. cfPWV increased significantly more following the high-fat (mean difference [MD] = 0.59 m·s−1) meal than following the low-fat (MD = 0.2 m·s−1) meal, with no change in faPWV in either condition. The af-SG significantly decreased (worsened) (ηp2 = 0.569) over time in the high- and low-fat conditions (ratio = 0.1 and 0.1, respectively). Superficial femoral PWVβ significantly increased over time in the high- and low-fat conditions (ηp2 = 0.321; 0.8 and 0.4 m·s−1, respectively). Triglycerides increased over time in the high-fat trial only (ηp2 = 0.761). There were no significant changes in blood pressure. Consuming a high-fat meal prior to 180 min of uninterrupted sitting augments markers of cardiovascular disease risk more than consuming a low-fat meal prior to sitting.


2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Megha Murali ◽  
Carla Taylor ◽  
Peter Zahradka ◽  
Jeffrey Wigle

Background and Objective: Arterial stiffness is recognized as being an independent predictor of incipient vascular disease associated with obesity and metabolic syndrome. In obese subjects, the decrease in the plasma level of adiponectin, an anti-diabetic and anti-atherogenic adipokine, is well known. Hence the aim of our study was to examine the effect of loss of adiponectin on the development of arterial stiffness in response to a high fat diet. Methods and Results: Male 8-week old adiponectin knockout (APN KO) and C57BL/6 (control) mice were fed a high fat diet (60% Calories from fat) for 12 weeks to induce obesity and insulin resistance (n=10/group). APN KO and C57BL/6 mice were fed a low fat diet (10% Calories from fat) and used as lean controls (n=10/group). After 12 weeks on the high fat diet, the APN KO mice weighed significantly more than the C57BL/6 mice (45.1±1.3 g vs 40.1±1.1 g, p=0.0008) but there was no difference in the final weights between genotypes fed the low fat diet. APN KO mice on both high and low fat diets for 12 weeks developed insulin resistance as measured by oral glucose tolerance test (Area under curve (AUC) mmol/L х min = 437±70 and 438±57) as compared to the C57BL/6 mice fed low or high fat diets (AUC mmol/L х min = 251±27 and 245±43). Arterial stiffness was determined by Doppler pulse wave velocity analysis of the femoral artery. Pulse wave velocity was increased in APN KO mice fed a high fat diet relative to those fed the low fat diet (12.56±0.78 cm/s vs 9.47±0.95 cm/s, p=0.0035; n=8-10). Pulse wave velocity was not different between C57BL/6 control mice on the low or high fat diets (10.63±0.73 cm/s and 10.86±0.50 cm/s), thus revealing that only mice deficient in adiponectin developed arterial stiffness in response to high fat diet. Conclusions: Potentiation of the vascular stiffness in diet-induced obese APN KO mice indicates that adiponectin has a role in modulating vascular structure and the APN KO mouse models the vascular changes that occur in human obesity and metabolic disorders. Morphometric analysis of the aortic tissues for vessel thickness and expression of extracellular proteins will further validate the potential role of adiponectin on the maintenance of arterial elasticity in addition to its known effect on eNOS mediated vasoprotection.


2016 ◽  
Vol 94 (suppl_2) ◽  
pp. 62-62
Author(s):  
D. R. Reynolds ◽  
J. V. Cooper ◽  
B. R. Wiegand ◽  
Z. D. Callahan ◽  
A. B. Koc ◽  
...  
Keyword(s):  
High Fat ◽  
Low Fat ◽  

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1210-P
Author(s):  
RAYMOND TOWNSEND ◽  
MALA DHARMALINGAM ◽  
STEFANO GENOVESE ◽  
ANDREW STEELE ◽  
JOSE L. ARENAS ◽  
...  

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 723-P
Author(s):  
LINGWANG AN ◽  
DANDAN WANG ◽  
XIAORONG SHI ◽  
CHENHUI LIU ◽  
KUEICHUN YEH ◽  
...  

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