Effect of dietary fat and the circadian clock on the expression of brain-derived neurotrophic factor (BDNF)

Genzer, Yoni; Dadon, Maayan; Burg, Chen; Chapnik, Nava; Froy, Oren

doi:10.1016/j.mce.2016.04.015

Cited by 43 publications

(31 citation statements)

References 32 publications

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“…As well as the brain, expression of proBDNF, BDNF, and its receptor TrkB has been reported in the liver and muscle [42][43][44][45], although the functional role of proBDNF-BDNFTrkB signaling in these tissues is not fully understood. The high expression of BDNF and TrkB proteins in the livers suggests neurotrophic support for autonomic innervation of this organ [43,44].…”

Section: Discussionmentioning

confidence: 99%

Brain-derived neurotrophic factor-TrkB signaling in the medial prefrontal cortex plays a role in the anhedonia-like phenotype after spared nerve injury

Fang

Yang

et al. 2018

Eur Arch Psychiatry Clin Neurosci

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Although depressive symptoms including anhedonia (i.e., loss of pleasure) frequently accompany pain, little is known about the risk factors contributing to individual differences in pain-induced anhedonia. In this study, we examined if signaling of brain-derived neurotrophic factor (BDNF) and its receptor tropomyosin-receptor-kinase B (TrkB) contribute to individual differences in the development of neuropathic pain-induced anhedonia. Rats were randomly subjected to spared nerved ligation (SNI) or sham surgery. The SNI rats were divided into two groups based on the results of a sucrose preference test. Rats with anhedonia-like phenotype displayed lower tissue levels of BDNF in the medial prefrontal cortex (mPFC) compared with rats without anhedonia-like phenotype and sham-operated rats. In contrast, tissue levels of BDNF in the nucleus accumbens (NAc) of rats with an anhedonia-like phenotype were higher compared with those of rats without anhedonia-like phenotype and sham-operated rats. Furthermore, tissue levels of BDNF in the hippocampus, L2-5 spinal cord, muscle, and liver from both rats with or without anhedonia-like phenotype were lower compared with those of sham-operated rats. A single injection of 7,8-dihydroxyflavone (10 mg/kg; TrkB agonist), but not ANA-12 (0.5 mg/kg; TrkB antagonist), ameliorated reduced sucrose preference and reduced BDNF-TrkB signaling in the mPFC in the rats with anhedonia-like phenotype. These findings suggest that reduced BDNF-TrkB signaling in the mPFC might contribute to neuropathic pain-induced anhedonia, and that TrkB agonists could be potential therapeutic drugs for pain-induced anhedonia.

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Section: Discussionmentioning

confidence: 99%

Brain-derived neurotrophic factor-TrkB signaling in the medial prefrontal cortex plays a role in the anhedonia-like phenotype after spared nerve injury

Fang

Yang

et al. 2018

Eur Arch Psychiatry Clin Neurosci

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“…In that study, the rs6265 variant and other two different SNPs were associated with weight regain. Although BDNF expression is mediated by dietary fat [30], the effect of fat intake on metabolic changes and its relationship with variants of the BDNF gene has not been evaluated. In a mouse model [30], when combined with high-fat diet, it leads to a unique metabolic state in which AMPK is activated, mTOR is downregulated, and the levels of mature BDNF are high.…”

Section: Discussionmentioning

confidence: 99%

“…Although BDNF expression is mediated by dietary fat [30], the effect of fat intake on metabolic changes and its relationship with variants of the BDNF gene has not been evaluated. In a mouse model [30], when combined with high-fat diet, it leads to a unique metabolic state in which AMPK is activated, mTOR is downregulated, and the levels of mature BDNF are high. In a recent human study, McCaffery et al [31] demonstrated with the strength of independent replication that another genetic variant of the BDNF gene (rs2030323) was associated with 100-150 greater total calorie intake per allele, independent of macronutrient distribution.…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular Risk Factors and Insulin Resistance after Two Hypocaloric Diets with Different Fat Distribution in Obese Subjects: Effect of the rs10767664 Gene Variant in Brain-Derived Neurotrophic Factor

Luis

Romero²,

Izaola³

et al. 2017

Lifestyle Genomics

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Background: The role of brain-derived neurotrophic factor (BDNF) variants on change in body weight and cardiovascular risk factors after weight loss remains unclear in obese patients. Objective: Our aim was to analyze the effects of the rs10767664 BDNF gene polymorphism on body weight, cardiovascular risk factors, and serum adipokine levels after a high monounsaturated fatty acids (MUFAs) hypocaloric diet (diet M) versus a high polyunsaturated fatty acids (PUFAs) hypocaloric diet (diet P). Methods: A Caucasian population of 361 obese patients was enrolled. Subjects who met the inclusion criteria were randomly allocated to one of two diets for a period of 3 months. Results: Two hundred and sixteen subjects (59.8%) had the genotype AA (wild-type group), and 145 (40.2%) patients had the genotypes AT (122 patients, 33.8%) or TT (23 patients, 6.4%) (mutant-type group). After weight loss with diet P and diet M and in both genotype groups, body mass index, weight, fat mass, waist circumference, systolic blood pressure, serum leptin levels, low-density lipoprotein cholesterol, and total cholesterol decreased in a significant way. Secondary to weight loss with diet M and only in the wild-type group, insulin levels (-2.1 ± 2.0 vs. -0.7 ± 2.9 IU/L, p < 0.05) and homeostatic model assessment of insulin resistance (-0.7 ± 0.9 vs. -0.3 ± 1.0 U, p < 0.05) decreased. Conclusion: Our data show that the rs10767664 variant of the BDNF gene modifies insulin resistance and insulin levels after weight loss with a hypocaloric diet enriched with MUFAs.

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“…A KD, but not a high fat or a low fat diet, led to a circadian shift in the expression of brain and liver BDNF, suggesting that a KD might impact (i) circadian activities, and (ii) the expression of BDNF [37]. However, the significance of neurotrophic factors as possible mediators of KD therapy are not yet clear, because in healthy rats a KD reduced BDNF levels in striatum, but not hippocampus, whereas the astrocyte neurotrophic cytokine S100β was not affected in the brain [38].…”

Section: Neurotrophic Factorsmentioning

confidence: 99%

New insights into the mechanisms of the ketogenic diet

Boison

2017

Current Opinion in Neurology

209

150

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Purpose of review High-fat, low-carbohydrate ketogenic diets (KDs) have been used for almost a century for the treatment of epilepsy. Used traditionally for the treatment of refractory pediatric epilepsies, in recent years the use of KDs has experienced a revival to include the treatment of adulthood epilepsies as well as conditions ranging from autism to chronic pain and cancer. Despite the ability of KD therapy to suppress seizures refractory to antiepileptic drugs and reports of lasting seizure freedom, the underlying mechanisms are poorly understood. This review explores new insights into mechanisms mobilized by KD therapies. Recent findings KDs act through a combination of mechanisms, which are linked to the effects of ketones and glucose restriction, and to interactions with receptors, channels, and metabolic enzymes. Decanoic acid, a component of medium chain triclycerides, contributes to seizure control through direct AMPA receptor inhibition, whereas drugs targeting lactate dehydrogenase reduce seizures through inhibition of a metabolic pathway. KD therapy also affects DNA methylation, a novel epigenetic mechanism of the diet. Summary KD therapy combines several beneficial mechanisms that provide broad benefits for the treatment of epilepsy with the potential to not only suppress seizures but also to modify the course of the epilepsy.

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Effect of dietary fat and the circadian clock on the expression of brain-derived neurotrophic factor (BDNF)

Cited by 43 publications

References 32 publications

Brain-derived neurotrophic factor-TrkB signaling in the medial prefrontal cortex plays a role in the anhedonia-like phenotype after spared nerve injury

Brain-derived neurotrophic factor-TrkB signaling in the medial prefrontal cortex plays a role in the anhedonia-like phenotype after spared nerve injury

Cardiovascular Risk Factors and Insulin Resistance after Two Hypocaloric Diets with Different Fat Distribution in Obese Subjects: Effect of the rs10767664 Gene Variant in Brain-Derived Neurotrophic Factor

New insights into the mechanisms of the ketogenic diet

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