High Fat Diet versus Disturbed Blood Flow Conditions: Implications for Endothelial Glycocalyx Integrity and Pre‐Atherosclerotic Inflammation

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1 ◽  
Author(s):  
Ronodeep Mitra ◽  
Ju Qiao ◽  
Sudharsan Madhavan ◽  
Gerard O’Neil ◽  
Bailey Ritchie ◽  
...  
2015 ◽  
Vol 44 (8) ◽  
pp. 1105-1113
Author(s):  
Hyelin Jeon ◽  
Sungmin Kwak ◽  
Su-Jin Oh ◽  
Hyun Soo Nam ◽  
Doo Won Han ◽  
...  

2021 ◽  
pp. 0271678X2110034
Author(s):  
Gianna Huber ◽  
Mikolaj Ogrodnik ◽  
Jan Wenzel ◽  
Ines Stölting ◽  
Lukas Huber ◽  
...  

Angiotensin II receptor blockers (telmisartan) prevent rodents from diet-induced obesity and improve their metabolic status. Hyperglycemia and obesity are associated with reduced cerebral blood flow and neurovascular uncoupling which may lead to behavioral deficits. We wanted to know whether a treatment with telmisartan prevents these changes in obesity. We put young mice on high-fat diet and simultaneously treated them with telmisartan. At the end of treatment, we performed laser speckle imaging and magnetic resonance imaging to assess the effect on neurovascular coupling and cerebral blood flow. Different behavioral tests were used to investigate cognitive function. Mice developed diet-induced obesity and after 16, not 8 weeks of high-fat diet, however, the response to whisker pad stimulation was about 30% lower in obese compared to lean mice. Simultaneous telmisartan treatment increased the response again by 10% compared to obese mice. Moreover, telmisartan treatment normalized high-fat diet-induced reduction of cerebral blood flow and prevented a diet-induced anxiety-like behavior. In addition to that, telmisartan affects cellular senescence and string vessel formation in obesity. We conclude, that telmisartan protects against neurovascular unit impairments in a diet-induced obesity setting and may play a role in preventing obesity related cognitive deficits in Alzheimer’s disease.


2013 ◽  
Vol 305 (9) ◽  
pp. F1343-F1351 ◽  
Author(s):  
Anne-Emilie Declèves ◽  
Joshua J. Rychak ◽  
Dan J. Smith ◽  
Kumar Sharma

Obesity-related kidney disease occurs as a result of complex interactions between metabolic and hemodynamic effects. Changes in microvascular perfusion may play a major role in kidney disease; however, these changes are difficult to assess in vivo. Here, we used perfusion ultrasound imaging to evaluate cortical blood flow in a mouse model of high-fat diet-induced kidney disease. C57BL/6J mice were randomized to a standard diet (STD) or a high-fat diet (HFD) for 30 wk and then treated either with losartan or a placebo for an additional 6 wk. Noninvasive ultrasound perfusion imaging of the kidney was performed during infusion of a microbubble contrast agent. Blood flow within the microvasculature of the renal cortex and medulla was derived from imaging data. An increase in the time required to achieve full cortical perfusion was observed for HFD mice relative to STD. This was reversed following treatment with losartan. These data were concurrent with an increased glomerular filtration rate in HFD mice compared with STD- or HFD-losartan-treated mice. Losartan treatment also abrogated fibro-inflammatory disease, assessed by markers at the protein and messenger level. Finally, a reduction in capillary density was found in HFD mice, and this was reversed upon losartan treatment. This suggests that alterations in vascular density may be responsible for the elevated perfusion time observed by imaging. These data demonstrate that ultrasound contrast imaging is a robust and sensitive method for evaluating changes in renal microvascular perfusion and that cortical perfusion time may be a useful parameter for evaluating obesity-related renal disease.


2015 ◽  
Vol 36 (7) ◽  
pp. 1257-1270 ◽  
Author(s):  
Kristen L Zuloaga ◽  
Lance A Johnson ◽  
Natalie E Roese ◽  
Tessa Marzulla ◽  
Wenri Zhang ◽  
...  

Diabetes causes endothelial dysfunction and increases the risk of vascular cognitive impairment. However, it is unknown whether diabetes causes cognitive impairment due to reductions in cerebral blood flow or through independent effects on neuronal function and cognition. We addressed this using right unilateral common carotid artery occlusion to model vascular cognitive impairment and long-term high-fat diet to model type 2 diabetes in mice. Cognition was assessed using novel object recognition task, Morris water maze, and contextual and cued fear conditioning. Cerebral blood flow was assessed using arterial spin labeling magnetic resonance imaging. Vascular cognitive impairment mice showed cognitive deficit in the novel object recognition task, decreased cerebral blood flow in the right hemisphere, and increased glial activation in white matter and hippocampus. Mice fed a high-fat diet displayed deficits in the novel object recognition task, Morris water maze and fear conditioning tasks and neuronal loss, but no impairments in cerebral blood flow. Compared to vascular cognitive impairment mice fed a low fat diet, vascular cognitive impairment mice fed a high-fat diet exhibited reduced cued fear memory, increased deficit in the Morris water maze, neuronal loss, glial activation, and global decrease in cerebral blood flow. We conclude that high-fat diet and chronic hypoperfusion impair cognitive function by different mechanisms, although they share commons features, and that high-fat diet exacerbates vascular cognitive impairment pathology.


1997 ◽  
Vol 273 (6) ◽  
pp. R2040-R2045 ◽  
Author(s):  
Michael J. Glass ◽  
James P. Cleary ◽  
Charles J. Billington ◽  
Allen S. Levine

We tested whether carbohydrate source (corn starch, sucrose, Polycose) influences the choice between a high-fat and high-carbohydrate diet in spontaneously feeding rats and in rats stimulated to eat by neuropeptide Y (NPY) administration or food deprivation. Rats were tested under three diet options: 1) a high-fat diet versus a high-corn starch diet; 2) a high-fat diet versus a high-sucrose diet; and 3) a high-fat diet versus a high-Polycose diet. During daily and stimulated feeding rats ate more of the high-carbohydrate diet than the fat diet when the source of carbohydrate was sucrose or Polycose; however, when corn starch was provided as the carbohydrate source rats ate more of the high-fat diet. Food-deprived rats increased intake of both the high-fat and the high-carbohydrate diets, with the proportion of energy ingested from each of the diets resembling that noted during 3 days of spontaneous feeding. NPY-injected rats ate more of both the high-fat and high-carbohydrate diets during diet options 1 and 3, but not during option 2 when the high-sucrose and high-fat diets were offered concurrently. In that case, rats did not significantly increase their intake of the high-fat diet. Although carbohydrate source and NPY administration each influenced diet selection, altering the source of carbohydrate had a more marked effect.


2013 ◽  
Vol 38 (8) ◽  
pp. 836-843 ◽  
Author(s):  
Tianrun Li ◽  
Leiluo Geng ◽  
Xin Chen ◽  
Miranda Miskowiec ◽  
Xuan Li ◽  
...  

Nonalcoholic steatohepatitis (NASH) is a prevalent disease in countries around the world. The branched-chain amino acids (BCAAs) leucine, isoleucine, and valine cannot be synthesized by the body and have been shown to promote muscle buildup; thus, it is logical to suggest that BCAAs can reduce fat deposition in the body. We used gonadectomized rats fed a high-fat diet to investigate the effects of BCAAs on lipid metabolism over an 8-week experimental period. Body composition, tissue histology, plasma lipid indices, and hormone levels were examined. We demonstrated that the body weights of rats were not significantly decreased but the mesenteric fat was significantly decreased (p < 0.05) in BCAA-treated rats. In addition, BCAAs decreased plasma lipid levels and fat deposition in the liver. At week 4, when the untreated rats displayed macrovesicular steatosis, BCAA-treated rats had only macrovesicular droplets in their hepatocytes. At week 8, when the untreated rat livers displayed profound inflammation and cirrhosis, BCAA-treated rat livers remained in the macrovesicular stage of steatosis. BCAAs induced higher blood glucose and plasma insulin levels (p < 0.05). BCAAs also improved liver blood flow by increasing mean arterial blood pressure and decreasing portal pressure, which helped delay the change in blood flow pattern to that of cirrhosis. BCAAs also induced the skeletal muscle to express higher levels of branched-chain α-keto acid dehydrogenase E1α, which indicates an enhanced metabolic capacity of BCAAs in muscle tissue. This study clearly demonstrates the effects of BCAAs on the amelioration of fat deposition in rats fed a high-fat diet.


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