Additionally, these results clearly demonstrate the necessity to confirm the behavioral phenotype of a mouse model fed with a 15N diet.
T. Kurita-Ochiai and M. Yamamoto examined the role of P. gingivalis or A. actinomycetemcomitans in augmenting inflammatory mechanisms and oxidative modification in the formation and activation of atherosclerotic plaques in ApoE-deficient mouse model fed a high-fat diet.
By combining a series of network analysis approaches on a hepatic transcriptomics dataset from the preclinical study in an LDLr-/ mouse model fed high fat diet, we discovered and functionally annotated gene co-expression network modules associated with anti-diabetic interventions.
Mouse or rat models fed with high fat/cholesterol diet (HFCD) have been used to study these vascular phenotypes [ 5, 6].
To observe the role of miR-26a in obesity associated chondrocytes, we set up an obese mouse model by feeding the male C57BL/6 mice with a standard HFD for 12 weeks.
Previous animal studies showed increased cerebral blood flow in a 12-month-old mouse model of AD fed this specific nutrient combination compared with a control diet [ 56].
In this study, we used two diabetic animal models, mice fed a high-fat diet (HFD) and db/db mice, which carry a homozygous mutation in the leptin receptor and suffer severe glucose intolerance, obesity and hyperinsulinemia.
18F-BMS PET scans were performed on control mice, rotenone-injected mice, and mice fed a MCD diet.
In our previous study, we found that hippocampal neurogenesis is significantly decreased in a TD mouse model established by feeding mice with a thiamine-depleted diet.
Ablation of Ces1d expression in two independent NASH mouse models, phosphatidylethanolamine N-methyltransferase knockout mice fed high-fat diet, and Ldlr −/− mice fed high-fat, high-cholesterol Western-type diet, reduced liver inflammation, oxidative stress and fibrosis (Lian et al., 2012a, 2016).
