Lifestyle Genomics最新文献

Background: Precision nutrition is based on the integration of individual's phenotypical and biological characteristics including genetic variants, epigenetic marks, gut microbiota profiles, and metabolite fingerprints as well as medical history, lifestyle practices, and environmental and cultural factors. Thus, nutriomics areas including nutrigenomics, nutrigenetics, nutriepigenetics, nutrimetabolomics, and nutrimetagenomics have emerged to comprehensively understand the complex interactions between nutrients, diet, and the human body's molecular processes through precision nutrition.

Summary: This document from the Ibero-American Network of Nutriomics and Precision Nutrition (RINN22; https://rinn22.com/) provides a comprehensive overview of the concepts of precision nutrition approaches to guide their application in clinical and public health as well as establish the position of RINN22 regarding the current and future state of precision nutrition.

Key messages: The progress and participation of nutriomics to precision nutrition is an essential pillar for addressing diet-related diseases and developing innovative managing strategies, which will be promoted by advances in bioinformatics, machine learning, and integrative software, as well as the description of specific novel biomarkers. In this context, synthesizing and critically evaluating the latest developments, potential applications, and future needs in the field of nutrition is necessary with a holistic perspective, incorporating progress in omics technologies aimed at precision nutrition interventions. This approach must address and confront healthy, social, food security, physically active lifestyle, sanitation, and sustainability challenges with preventive, participatory, and predictive strategies of personalized, population, and planetary nutrition for a precision tailored health.

Introduction: Excess fructose intake has been linked to increased risk of dyslipidemia, insulin resistance, hyperuricemia, inflammation, and obesity. In this human study, we investigated if serum C-reactive protein (CRP) concentrations change after fructose consumption, and whether genetic variants and obesity status influence this change.

Methods: Blood was drawn before and at four time points after administration of a fructose load (n = 57). Serum concentrations of CRP were measured, and 11 single nucleotides polymorphisms (SNPs) (rs1205, rs1417938, rs1470515, rs3093068, rs6588158, rs16842568, rs2259820, rs157581, rs2794521, rs3093062, rs17700633), previously associated with serum CRP were genotyped and assessed for their association with CRP levels.

Results: Participants identifying as White (n = 37) had higher mean CRP levels across all time points compared to those identifying as Black (n = 20). Participants with obesity (body mass index ≥30 kg/m2) (n = 25) were younger and had higher mean CRP levels throughout the study period compared to those without (n = 32). All SNPs were in Hardy-Weinberg equilibrium and their effect allele frequencies ranged between 11 and 96%. Baseline CRP was associated with CRP SNPs rs1417938 and rs2794521 (p < 0.005); rs2794521 was also associated with CRP response to fructose challenge (p < 0.005). The variability in response to fructose and genetic associations was mainly observed in individuals without obesity. Obesity status was associated with early changes in CRP (0-30 min and 30-60 min) whereas CRP SNPs were associated with later changes (60-120 min and 120-180 min).

Conclusion: Changes in serum CRP were associated with obesity status or SNPs based on the time elapsed since fructose ingestion. Larger studies are needed to confirm and validate these associations.

Reviewers:

Introduction: Prior work in predominantly European ancestry populations has explained how the risk associated with demographic, lifestyle, and health factors differs with underlying genetic susceptibility to type 2 diabetes (T2D), but less is known about these relationships in Black Americans.

Methods: We used covariate-adjusted logistic regression models of T2D to examine interactions between a published trans-ancestry derived T2D polygenic risk score (PRS) and various demographic, lifestyle, and health-related factors among 28,251 self-identified Black Americans from six cohort studies.

Results: The results are generally consistent with prior work in White populations. The PRS showed a significant interaction with body mass index, with a greater effect on T2D risk in individuals who were leaner (pinteraction = 0.038).

Conclusion: These results contribute to understanding the relationship between genetics and other T2D risk factors in Black Americans who have a high burden of T2D, potentially informing targeted prevention strategies.

In the article by Sierra-Ruelas et al. entitled "Uncoupling Proteins Variants Are Linked to Hypercholesterolemia and Abdominal Obesity in Metabolically Unhealthy Women" [Lifestyle Genomics. 2025;18:27-35; https://doi.org/10.1159/000543484], there is an error introduced during production which resulted in the different superscript letters (b, c and d) in Table 1 being changed to the same superscript "a" value.The original article has been updated.

Olfactory dysfunction (OD) is not uncommon following viral infection. Herein, we explore the interplay of host genetics with viral correlates in coronavirus disease 2019 (COVID-19)- and long COVID-related OD, and its diagnosis and treatment that remain challenging. Two genes associated with olfaction, UGT2A1 and UGT2A2, appear to be involved in COVID-19-related anosmia, a hallmark symptom of acute infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), particularly in the early stages of the pandemic. SARS-CoV-2 infects olfactory support cells, sustentacular and Bowman gland cells, that surround olfactory sensory neurons (OSNs) in the olfactory epithelium (OE) where the initial step of odor detection takes place. Anosmia primarily arises from the infection of support cells of the OE, followed by the deciliation and disruption of OE integrity, typically without OSN infection. Through the projected axons of OSNs, the virus could theoretically reach the olfactory bulb and brain, but current evidence points against this route. Intriguingly, SARS-CoV-2 infection of support cells leads to profound alterations in the nuclear architecture of OSNs, leading to the downregulation of odorant receptor-related genes, e.g., of Adcy3. Viral factors associated with the development of OD include spike protein aminoacidic changes, e.g., D614G, the first substitution that was selected early during SARS-CoV-2 evolution. More recent variants of the Omicron family are less likely to cause OD compared to Delta or Alpha, although OD has been associated with a milder disease course. OD is one of the most prevalent post-acute neurologic symptoms of SARS-CoV-2 infection. The tens of millions of people worldwide who have lingering problems with OD wait eagerly for effective new treatments that will restore their sense of smell which adds value to their quality of life.

Introduction: Obesity, characterized by excess adipose tissue, is a major public health problem worldwide. Brown adipose tissue (BAT) and beige adipose tissue participate in thermogenesis through uncoupling protein 1 (UCP1). Polyphenols including those from Calafate (a native polyphenol-rich Patagonian berry), are considered as potential anti-obesity compounds due to their pro-thermogenic characteristics. However, polyphenols are mainly metabolized by the gut microbiota (GM) that may influence their bioactivity and bioavailability. The aim of this study was to determine the impact of dietary administration with a Calafate polyphenol-rich extract on thermogenic activity of BAT and beige adipose tissue and GM composition.

Methods: Eight-week-old C57BL6 mice (n = 30) were divided into 4 groups to receive for 24 weeks a control diet (C), a high-fat diet alone (HF), or high-fat diet supplemented with Calafate extract (HFC) or the same high-fat diet supplemented with Calafate extract but treated with antibiotics (HFCAB) from week 19-20. Administration with Calafate extract (50 mg/kg per day) was carried out for 3 weeks from week 21-23 in the HFC and HFCAB groups. After euthanasia, gene expression of thermogenic markers was analyzed in BAT and inguinal white adipose tissue (iWAT). Transmission electron microscopy was performed to assess mitochondrial morphology and cristae density in BAT. GM diversity and composition were characterized by deep sequencing with the MiSeq Illumina platform.

Results: Calafate extract administration had no effect on weight gain in mice fed a high-fat diet. However, it prevented alterations in mitochondrial cristae induced by HFD and increased Dio2 expression in BAT and iWAT. The intervention also influenced the GM composition, preventing changes in specific bacterial taxa induced by the high-fat diet. However, the antibiotic treatment prevented in part these effects, suggesting the implications of GM.

Conclusion: These results suggest that the acute administration of a Calafate extract modulates the expression of thermogenic markers, prevents alterations in mitochondrial cristae and intestinal microbiota in preclinical models. The study highlights the complex interaction between polyphenols, thermogenesis, and the GM, providing valuable insights into their potential roles in the treatment of obesity-related metabolic diseases.