A high fat diet alters metabolic and bioenergetic function in the brain: A magnetic resonance spectroscopy study

Raider, Kayla; Ma, Daifu; Harris, J. Ieuan; Fuentes, I.; Rogers, Robert S.; Wheatley, Joshua L.; Geiger, Paige C.; Choi, In‐Young; Brooks, William M.; Stanford, John A.

doi:10.1016/j.neuint.2016.04.008

Cited by 24 publications

(16 citation statements)

References 68 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…also on midlife intake). Our results point to reduction of fat intake in midlife and are in agreement with studies of Luchsinger et al [27], Laitinen et al [26] and with studies on rodents reported by Kadish et al [28] and Raider et al[29]. We propose only a modest shift in the consumption of fat, from the historical one, which we believe can reduce the AD susceptibility of a population, including also apolipoprotein E epsilon 4 allele carriers.…”

Section: Discussionsupporting

confidence: 93%

The Calculator of Anti-Alzheimer’s Diet. Macronutrients

2016

View full text Add to dashboard Cite

The opinions about optimal proportions of macronutrients in a healthy diet have changed significantly over the last century. At the same time nutritional sciences failed to provide strong evidence backing up any of the variety of views on macronutrient proportions. Herein we present an idea how these proportions can be calculated to find an optimal balance of macronutrients with respect to prevention of Alzheimer’s Disease (AD) and dementia. These calculations are based on our published observation that per capita personal income (PCPI) in the USA correlates with age-adjusted death rates for AD (AADR). We have previously reported that PCPI through the period 1925–2005 correlated with AADR in 2005 in a remarkable, statistically significant oscillatory manner, as shown by changes in the correlation coefficient R (Roriginal). A question thus arises what caused the oscillatory behavior of Roriginal? What historical events in the life of 2005 AD victims had shaped their future with AD? Looking for the answers we found that, considering changes in the per capita availability of macronutrients in the USA in the period 1929–2005, we can mathematically explain the variability of Roriginal for each quarter of a human life. On the basis of multiple regression of Roriginal with regard to the availability of three macronutrients: carbohydrates, total fat, and protein, with or without alcohol, we propose seven equations (referred to as “the calculator” throughout the text) which allow calculating optimal changes in the proportions of macronutrients to reduce the risk of AD for each age group: youth, early middle age, late middle age and late age. The results obtained with the use of “the calculator” are grouped in a table (Table 4) of macronutrient proportions optimal for reducing the risk of AD in each age group through minimizing Rpredicted−i.e., minimizing the strength of correlation between PCPI and future AADR.

show abstract

Section: Discussionsupporting

confidence: 93%

The Calculator of Anti-Alzheimer’s Diet. Macronutrients

2016

View full text Add to dashboard Cite

show abstract

“…This NAA increase may be linked to changes of osmolarity since the concentration of other major osmolites such as taurine and creatine was also observed. In rats under 60% HFD for 5 months, Raider et al (2016) have observed no changes in hippocampal NAA but reduced levels of myo-inositol, compared to controls. Hassan et al (2018) also observed HFDinduced metabolic changes in extracts from the prefrontal cortex, namely, higher relative concentrations of lactate, alanine, taurine, and myo-inositol, and lower GABA levels.…”

Section: Brain Metabolic Profilesmentioning

confidence: 74%

Brain Metabolism Alterations in Type 2 Diabetes: What Did We Learn From Diet-Induced Diabetes Models?

García-Serrano

Duarte

2020

Front. Neurosci.

View full text Add to dashboard Cite

Type 2 diabetes (T2D) is a metabolic disease with impact on brain function through mechanisms that include glucose toxicity, vascular damage and blood-brain barrier (BBB) impairments, mitochondrial dysfunction, oxidative stress, brain insulin resistance, synaptic failure, neuroinflammation, and gliosis. Rodent models have been developed for investigating T2D, and have contributed to our understanding of mechanisms involved in T2D-induced brain dysfunction. Namely, mice or rats exposed to diabetogenic diets that are rich in fat and/or sugar have been widely used since they develop memory impairment, especially in tasks that depend on hippocampal processing. Here we summarize main findings on brain energy metabolism alterations underlying dysfunction of neuronal and glial cells promoted by diet-induced metabolic syndrome that progresses to a T2D phenotype.

show abstract

“…This is likely due to the distinct study designs, diet compositions, fat origin, age and/or species. Recent studies do not find HFD-induced increased levels of GFAP in the rat hippocampus (Raider et al, 2016; Ribeiro et al, 2018). In contrast, Tarantini et al found that mice exposed to a 60%-fat diet from 3 to 8 months of age show mild behavior deficits and neuroinflammation, which are exacerbated by exposure to a cellular stress induced by deletion of the transcription factor nrf2 that regulates the expression of antioxidant proteins, thus protecting against oxidative damage (Tarantini et al, 2018).…”

Section: Discussionmentioning

confidence: 88%

Neurochemical Modifications in the Hippocampus, Cortex and Hypothalamus of Mice Exposed to Long-Term High-Fat Diet

et al. 2019

View full text Add to dashboard Cite

Metabolic syndrome and diabetes impact brain function and metabolism. While it is well established that rodents exposed to diets rich in saturated fat develop brain dysfunction, contrasting results abound in the literature, likely as result of exposure to different high-fat diet (HFD) compositions and for varied periods of time. In the present study, we investigated alterations of hippocampal-dependent spatial memory by measuring Y-maze spontaneous alternation, metabolic profiles of the hippocampus, cortex and hypothalamus by 1H magnetic resonance spectroscopy (MRS), and levels of proteins specific to synaptic and glial compartments in mice exposed for 6 months to different amounts of fat (10, 45, or 60% of total energy intake). Increasing the dietary amount of fat from 10 to 45% or 60% resulted in obesity accompanied by increased leptin, fasting blood glucose and insulin, and reduced glucose tolerance. In comparison to controls (10%-fat), only mice fed the 60%-fat diet showed increased fed glycemia, as well as plasma corticosterone that has a major impact on brain function. HFD-induced metabolic profile modifications measured by 1H MRS were observed across the three brain areas in mice exposed to 60%- but not 45%-fat diet, while both HFD groups displayed impaired hippocampal-dependent memory. HFD also affected systems involved in neuro- or gliotransmission in the hippocampus. Namely, relative to controls, 60%-fat-fed mice showed reduced SNAP-25, PSD-95 and syntaxin-4 immunoreactivity, while 45%-fat-fed mice showed reduced gephyrin and syntaxin-4 immunoreactivity. For both HFD levels, reductions of the vesicular glutamate transporter vGlut1 and levels of the vesicular GABA transporter were observed in the hippocampus and hypothalamus, relative to controls. Immunoreactivity against GFAP and/or Iba-1 in the hypothalamus was higher in mice exposed to HFD than controls, suggesting occurrence of gliosis. We conclude that different levels of dietary fat result in distinct neurochemical alterations in the brain.

show abstract

A high fat diet alters metabolic and bioenergetic function in the brain: A magnetic resonance spectroscopy study

Cited by 24 publications

References 68 publications

The Calculator of Anti-Alzheimer’s Diet. Macronutrients

The Calculator of Anti-Alzheimer’s Diet. Macronutrients

Brain Metabolism Alterations in Type 2 Diabetes: What Did We Learn From Diet-Induced Diabetes Models?

Neurochemical Modifications in the Hippocampus, Cortex and Hypothalamus of Mice Exposed to Long-Term High-Fat Diet

Contact Info

Product

Resources

About