Cover Story Current Issue

Evolutionary forces have wired our brains to prefer and consume energy-dense foods to aid in our survival. While effective during periods of limited access, the ubiquitous nature of high-fat food sources in society leads to obesity and numerous related health complications. Exacerbating this drive to consume more energy-dense, palatable foods is a devaluation of less appetitive, nutritionally-balanced foods. While this preference for calorically-rich foods is well known, significant gaps exist in our understanding of how this develops and leads to devaluation.

Laboratory mice are typically provided with ad libitum access to a well-balanced standard chow diet (SD) in which the macronutrient composition has been formulated for optimal growth. Introduction to ad libitum high fat diet (HFD), but not a high-sucrose diet, leads to rapid weight gain, at least in part due to excessive caloric intake. Interestingly, when mice are given a choice between ad libitum access to both SD and HFD, they strongly prefer consumption of the latter at the expense of the former. While this predilection for HFD over SD during prolonged exposure is well described, how rapidly this transition occurs under physiological or artificial hunger is less known. Removal of HFD from mice given the choice between HFD and SD, akin to a strict human diet, results in rapid weight loss due to the self-restricted consumption of SD. Additionally, mice fed a HFD will forgo SD consumption even in states of physiological or artificially-induced caloric deprivation. While this SD devaluation is robustly conserved between sex and subject and independent of fat mass accrual, the causative nature of this phenomenon is not well understood.

Full text

 

Current Issue

Time-restricted feeding prevents memory impairments induced by obesogenic diet consumption, via hippocampal thyroid hormone signaling

Jean-Christophe Helbling, Rachel Ginieis, Pierre Mortessagne, Mariano Ruiz-Gayo, ... Marie-Pierre Moisan

 

Objective

The early consumption of calorie-rich diet disrupts circadian rhythms and has adverse effects on memory, yet the effects of time-restricted feeding (TRF) and the underlying molecular mechanisms are unknown. Here, we set out to identify the behavioral and molecular circadian rhythms disruptions generated by juvenile obesogenic diet consumption and their restoration by TRF in male mice.

Methods

Metabolic rhythms were measured by indirect calorimetry and memory performances by behavioral tasks. Hippocampal translatome (pS6_TRAP), enrichment and co-regulated gene network analyses were conducted to identify the molecular pathways involved in memory impairments and their restoration by TRF. Differential exon usage analyses, mass spectrometry and pharmacological intervention were used to confirm thyroid hormone signaling involvement.

Results

We show that four weeks of TRF restore the rhythmicity of metabolic parameters and prevents memory impairments in mice fed a high fat-high sucrose (HFS) diet since weaning, independently of body fat levels. Hippocampal translatome and differential exon usage analyses indicate that impaired memory of mice under ad libitum HFS diet is accompanied by reduced thyroid hormone signaling and altered expression of astrocytic genes regulating glutamate neurotransmission. TRF restored the diurnal expression variation of part of these genes and intra-hippocampal infusion of T3, the active form of thyroid hormone, rescues memory performances and astrocytic gene expression of ad libitum HFS diet-fed mice.

Conclusions

Thus, thyroid hormones contribute to the TRF positive effects on both metabolism and memory in mice fed an obesogenic diet, highlighting this nutritional approach as a powerful tool in addressing obesity brain comorbidities and paving the way for further mechanistic studies on hippocampal thyroid signaling.

 

 

Articles in Press

Time-restricted feeding prevents memory impairments induced by obesogenic diet consumption, via hippocampal thyroid hormone signaling

Jean-Christophe Helbling, Rachel Ginieis, Pierre Mortessagne, Mariano Ruiz-Gayo, ... Marie-Pierre Moisan

 

Objective

The early consumption of calorie-rich diet disrupts circadian rhythms and has adverse effects on memory, yet the effects of time-restricted feeding (TRF) and the underlying molecular mechanisms are unknown. Here, we set out to identify the behavioral and molecular circadian rhythms disruptions generated by juvenile obesogenic diet consumption and their restoration by TRF in male mice.

Methods

Metabolic rhythms were measured by indirect calorimetry and memory performances by behavioral tasks. Hippocampal translatome (pS6_TRAP), enrichment and co-regulated gene network analyses were conducted to identify the molecular pathways involved in memory impairments and their restoration by TRF. Differential exon usage analyses, mass spectrometry and pharmacological intervention were used to confirm thyroid hormone signaling involvement.

Results

We show that four weeks of TRF restore the rhythmicity of metabolic parameters and prevents memory impairments in mice fed a high fat-high sucrose (HFS) diet since weaning, independently of body fat levels. Hippocampal translatome and differential exon usage analyses indicate that impaired memory of mice under ad libitum HFS diet is accompanied by reduced thyroid hormone signaling and altered expression of astrocytic genes regulating glutamate neurotransmission. TRF restored the diurnal expression variation of part of these genes and intra-hippocampal infusion of T3, the active form of thyroid hormone, rescues memory performances and astrocytic gene expression of ad libitum HFS diet-fed mice.

Conclusions

Thus, thyroid hormones contribute to the TRF positive effects on both metabolism and memory in mice fed an obesogenic diet, highlighting this nutritional approach as a powerful tool in addressing obesity brain comorbidities and paving the way for further mechanistic studies on hippocampal thyroid signaling.

 

 

You are what you eat

Here is a video of Vimeo. When the iframes is activated, a connection to Vimeo is established and, if necessary, cookies from Vimeo are also used. For further information on cookies policy click here.

Auf Werbeinhalte, die vor, während oder nach Videos von WEBSITE-URL eingeblendet werden, hat WEBSITE-URL keinen Einfluss. Wir übernehmen keine Gewähr für diese Inhalte. Weitere Informationen finden Sie hier.