Obesity/overweight has been identified as a major risk factor for the development of vascular cognitive impairment with dementia; a form of dementia with a vascular origin. Obesity at young age increases the risk of cognitive impairment in later life that is associated with cerebral hypoperfusion. Reductions in the diameter of cerebral parenchymal arterioles (PAs) could reduce cerebral blood flow and lead to cognitive decline. In this study, we hypothesized that a high fat diet (HFD) would lead to a decline in cognition and inward remodeling of PAs. 3-week-old male and female Sprague Dawley rats were fed a HFD containing 36% fat or control diet containing 7.2% fat for 23-28 weeks. Data are presented as the mean ± SEM, HFD vs Control, n=3-16 in each group. At euthanasia, the male HFD group weighed more than its control while no significant differences were observed in the females (Male: 559±12.4g vs 475 ±9.12g, p=<0.0001, Female: 303±7.60g vs 264± 5.9g, p=0.474). HFD rats had more abdominal fat in both males and females (Male: 16.1 ± 0.957g vs 6.55 ±0.427g, p=<0.0001, Female: 13.2 ±1.55g vs 3.93 ± 1.08g, p=<0.0001). PAs were collected and their structure was assessed using pressure myography. In females, there was a significant decrease in outer and lumen diameter (p=0.0009, p=0.0007), in vessel area (p=0.0005), wall area (p=0.0028), and lumen area (p=0.0008) in PAs from the rats fed a HFD. Cognitive function was evaluated and there were no significant differences as well as no significant differences in blood flow, inflammation, neurogenesis, or synaptic markers. Thus, this HFD led to alterations in body weight and abdominal fat weight as well as PA structure in femaleswithout significantly affecting cognition.
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