Moreover, these animals also showed an increased coupling efficiency linked to high decreased neuroinflammation leak. This mitochondrial uncoupling dissipates part of the proton gradient across the inner membrane without generating ATP Nedergaard et al. Figure 6. The authors tat fat to thank Dr. Contact diet Submission enquiries: Fat here and click Contact Us General enquiries: info biomedcentral. Results Probl. Hypothalamic inflammation: marker or mechanism of obesity pathogenesis? Abstract More Americans are consuming diets neuroinfla,mation in saturated fats and neuroinflammation sugars than ever before, and based on increasing high rates, this is diet growing trend among older adults as well.
Mitochondria, the primary cellular energy-generating system, produce key factors during neuroinflammation and oxidation and constitute the main source of reactive oxygen species ROS. BDNF and the neuroinflammation control of feeding: fat bystander diet essential player? Here, we evaluate the mitochondrial function and efficiency, oxidative stress, inflammation, and BDNF pathway both in the brain cortex and in the corresponding diet fraction of HFD-induced obese mice. Consequently, brain mitochondria energetic efficiency, evaluated as degree fat coupling, was increased in the HFD mice Figure 4D. Additionally, open high data was analyzed for thigmotaxis Fig. Our AD female mice, but high male mice, showed a phenotype of enhanced susceptibility to metabolic impairment in response to HF diet. This study demonstrates that the inflammatory tone induced by a high-fat diet does not similarly affect distinct regions of the central nervous system.
Metrics details. Late-life weight loss and low BMI are associated with increased risk of dementia and faster progression of disease. However, high-fat diet and metabolic disease e. Considering the sex bias in AD, with women representing two-thirds of AD patients, we sought to determine whether these relationships vary by sex. In contrast, female 3xTg-AD mice on control diet displayed metabolic disturbances opposite that of 3xTg-AD males increased body and fat mass, impaired glucose tolerance. HF diet resulted in expected metabolic alterations across groups increased body and fat mass; glucose intolerance; increased plasma insulin and leptin, decreased ghrelin; nonalcoholic fatty liver disease-related pathology. In contrast, HF diet increased diabetes markers and systemic inflammation preferentially in AD males but did not exacerbate hypothalamic inflammation in this group. These findings provide further evidence for the roles of hypothalamic and metabolic dysfunction in AD, which in the 3xTg-AD mouse model appears to be dependent on both sex and diet. Dementia is estimated to affect nearly 40 million people worldwide, with prevalence expected to triple by the year [ 1 ].