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Short-term consumption of ultra-processed diets impairs the sense of smell and brain physiology [Brain]

ABSTRACT: Short-term consumption of ultra-processed diets impairs the sense of smell and brain physiology [Brain]

PROVIDER: PRJNA900858 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22266700_1.fastq.gz	Fastqsanger.gz
	SRR22266700_2.fastq.gz	Fastqsanger.gz
	SRR22266701_1.fastq.gz	Fastqsanger.gz
	SRR22266701_2.fastq.gz	Fastqsanger.gz
	SRR22266702_1.fastq.gz	Fastqsanger.gz

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Short-term consumption of ultra-processed diets impairs the sense of smell and brain physiology [Brain]

Project description:Considering the present scenario of fast-paced life, the major shifts in eating culture in the last five decades, and the crucial role of smell in food intake, it is thus crucial to map and better understand the effects of ultra-processed diets - especially under short-term regimens - on our brain metabolism and sense of smell. To address this question, we used mice to investigate the effects of the short-term consumption of three diets varying in macronutrient composition and origin (one whole-grain-based and two ultra-processed synthetic diets) on the transcriptional profiles of the olfactory mucosa and different brain regions.

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Short-term consumption of ultra-processed diets impairs the sense of smell and brain physiology

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Short-term consumption of ultra-processed diets impairs the sense of smell and brain physiology

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Sense-antisense transcript comparison in mouse brain and kidney

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Ultra-Processed Foods drive Intestinal Barrier permeability increasing Microvascular Disease risk

Project description:Abstract: Our intake of ultra-processed foods has dramatically increased over the past few decades in line with the prevalence of obesity and diabetes, key risk factors for microvascular diseases such as chronic kidney disease (CKD). The extent to which long-term intake of highly processed food influences CKD outcome is unclear. Here, we show in rodent models that a highly processed diet drives intestinal barrier permeability and an increased risk of CKD. Inhibition of the advanced glycation pathway, which generates Maillard reaction products within foods upon thermal processing, reversed kidney injury. Consequently, a highly processed diet leads to innate immune complement activation and local kidney inflammation via the potent proinflammatory effector molecule complement 5a (C5a). C5a receptor inhibition ameliorated albuminuria. In a mouse model of diabetes, a high resistant starch fiber diet led to a redistribution of the gut commensal consortium, prevented impaired gut barrier function and decreased the severity of kidney injury via suppression of complement. These results provide mechanistic insight into the role of highly processed foods on inflammation and chronic disease risk. One Sentence Summary: Ultra-processed diets promote chronic kidney disease

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Short-term consumption of highly processed diets varying in macronutrient content impair the sense of smell and brain metabolism in mice.

Project description:ObjectiveFood processing greatly contributed to increased food safety, diversity, and accessibility. However, the prevalence of highly palatable and highly processed food in our modern diet has exacerbated obesity rates and contributed to a global health crisis. While accumulating evidence suggests that chronic consumption of such foods is detrimental to sensory and neural physiology, it is unclear whether its short-term intake has adverse effects. Here, we assessed how short-term consumption (<2 months) of three diets varying in composition and macronutrient content influence olfaction and brain metabolism in mice.MethodsThe diets tested included a grain-based standard chow diet (CHOW; 54% carbohydrate, 32% protein, 14% fat; #8604 Teklad Rodent diet , Envigo Inc.), a highly processed control diet (hpCTR; 70% carbohydrate, 20% protein, 10% fat; #D12450B, Research Diets Inc.), and a highly processed high-fat diet (hpHFD; 20% carbohydrate, 20% protein, 60% fat; #D12492, Research Diets Inc.). We performed behavioral and metabolic phenotyping, electro-olfactogram (EOG) recordings, brain glucose metabolism imaging, and mitochondrial respirometry in different brain regions. We also performed RNA-sequencing (RNA-seq) in the nose and across several brain regions, and conducted differential expression analysis, gene ontology, and network analysis.ResultsWe show that short-term consumption of the two highly processed diets, but not the grain-based diet, regardless of macronutrient content, adversely affects odor-guided behaviors, physiological responses to odorants, transcriptional profiles in the olfactory mucosa and brain regions, and brain glucose metabolism and mitochondrial respiration.ConclusionsEven short periods of highly processed food consumption are sufficient to cause early olfactory and brain abnormalities, which has the potential to alter food choices and influence the risk of developing metabolic disease.

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Project description:Olfaction is fundamental for survival but there is little known about the connection between smell perception and metabolism. In this study we implemented IGF1R knockout mice in the olfactory sensory neurons, by olfactory marker protetin (OMP) Cre specific recombination, and investigated metabolic parameters, smell perception and transcriptome sequencing. We could demonstrate that IGF1R knockout in the olfactory sensory neurons results in enhanced smell perception, insulin resistance under normal chow diet conditions and increased adiposity in mice fed control diet. Transcriptome analysis of the olfactory epithelium revealed differential expression of markers for mature and immature olfactory sensory neurons, being down-regulated and up- regulated respectively, pointing to differentiation-dependent changes that result in increased olfactory perception. Collectively, this study provides evidence that enhanced smell perception can result in insulin resistance and increased adiposity.

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