bims-minfam Biomed News
on Inflammation and metabolism in ageing and cancer
Issue of 2022‒12‒11
eight papers selected by
Ayesh Seneviratne
Western University


  1. J Prev Med Hyg. 2022 Jun;63(2 Suppl 3): E36-E43
      The Mediterranean diet is the most well-known and researched dietary pattern worldwide. It is characterized by the consumption of a wide variety of foods, such as extra-virgin olive oil (EVOO), legumes, cereals, nuts, fruits, vegetables, dairy products, fish, and wine. Many of these foods provide several phytonutrients, among which polyphenols and vitamins play an important role. Data from several studies have strongly established that nutrition is a key factor in promoting a healthy lifestyle and preventing many chronic diseases. In particular, a large number of studies have established the protective effects of the Mediterranean diet against several chronic diseases, among which are diabetes, cardiovascular diseases, cancer, aging disorders, and against overall mortality. Animal and human translational studies have revealed the biological mechanisms regulating the beneficial effects of the traditional Mediterranean diet. Indeed, several studies demonstrated that this nutritional pattern has lipid-lowering, anticancer, antimicrobial, and anti-oxidative effects. Moreover, the Mediterranean diet is considered environmentally sustainable. In this review, we describe the composition of the Mediterranean diet, assess its beneficial effects, and analyze their epigenomic, genomic, metagenomic, and transcriptomic aspects. In the future it will be important to continue exploring the molecular mechanisms through which the Mediterranean diet exerts its protective effects and to standardize its components and serving sizes to understand more precisely its effects on human health.
    Keywords:  Anticancer effects; Antidiabetic effects; Antimicrobial effects; Mediterranean diet; Modification of hormone release
    DOI:  https://doi.org/10.15167/2421-4248/jpmh2022.63.2S3.2745
  2. J Prev Med Hyg. 2022 Jun;63(2 Suppl 3): E142-E149
      Precision nutrition is an emerging branch of nutrition science that aims to use modern omics technologies (genomics, proteomics, and metabolomics) to assess an individual's response to specific foods or dietary patterns and thereby determine the most effective diet or lifestyle interventions to prevent or treat specific diseases. Metabolomics is vital to nearly every aspect of precision nutrition. It can be targeted or untargeted, and it has many applications. Indeed, it can be used to comprehensively characterize the thousands of chemicals in foods, identify food by-products in human biofluids or tissues, characterize nutrient deficiencies or excesses, monitor biochemical responses to dietary interventions, track long- or short-term dietary habits, and guide the development of nutritional therapies. Indeed, metabolomics can be coupled with genomics and proteomics to study and advance the field of precision nutrition. Integrating omics with epidemiological and clinical data will begin to define the beneficial effects of human food metabolites. In this review, we present the metabolome and its relationship to precision nutrition. Moreover, we describe the different techniques used in metabolomics and present how metabolomics has been applied to advance the field of precision nutrition by providing notable examples and cases.
    Keywords:  Food metabolome; Mediterranean diet; Metabolomics; NMR; Precision nutrition
    DOI:  https://doi.org/10.15167/2421-4248/jpmh2022.63.2S3.2755
  3. Front Endocrinol (Lausanne). 2022 ;13 1091358
      
    Keywords:  T2DM; aging; diabetes; elderly; insulin
    DOI:  https://doi.org/10.3389/fendo.2022.1091358
  4. J Intern Med. 2022 Dec 09.
      Diet is one of the most important exposures that may affect health throughout life span. Investigations on dietary patterns rather than single food components are gaining in popularity because they take the complexity of the whole dietary context into account. Adherence to such dietary patterns can be measured by using metabolomics, which allows measurements of thousands of molecules simultaneously. Derived metabolite signatures of dietary patterns may reflect the consumption of specific groups of foods or their constituents originating from the dietary pattern per se, or the physiological response toward the food-derived metabolites, their interaction with endogenous metabolism, and exogenous factors such as gut microbiota. Here, we review and discuss blood metabolite fingerprints of healthy dietary patterns. The plasma concentration of several food-derived metabolites-such as betaines from whole grains and n - 3 polyunsaturated fatty acids and furan fatty acids from fish-seems to consistently reflect the intake of common foods of several healthy dietary patterns. The metabolites reflecting shared features of different healthy food indices form biomarker panels for which specific, targeted assays could be developed. The specificity of such biomarker panels would need to be validated, and proof-of-concept feeding trials are needed to evaluate to what extent the panels may mediate the effects of dietary patterns on disease risk indicators or if they are merely food intake biomarkers. Metabolites mediating health effects may represent novel targets for precision prevention strategies of clinical relevance to be verified in future studies.
    Keywords:  biomarkers; healthy dietary patterns; metabolomics; plasma; serum
    DOI:  https://doi.org/10.1111/joim.13596
  5. Aging Dis. 2022 Dec 01. 13(6): 1664-1714
      According to the cell centric hypotheses, the deficits that drive aging occur within cells by age dependent progressive damage to organelles, telomeres, biologic signaling pathways, bioinformational molecules, and by exhaustion of stem cells. Here, we amend these hypotheses and propose an eco-centric model for geroplasticity (aging plasticity including aging reversal). According to this model, youth and aging are plastic and require constant maintenance, and, respectively, engage a host of endogenous rejuvenating (rejuvenins) and gero-inducing [geriatrin] factors. Aging in this model is akin to atrophy that occurs as a result of damage or withdrawal of trophic factors. Rejuvenins maintain and geriatrins adversely impact cellular homeostasis, cell fitness, and proliferation, stem cell pools, damage response and repair. Rejuvenins reduce and geriatrins increase the age-related disorders, inflammatory signaling, and senescence and adjust the epigenetic clock. When viewed through this perspective, aging can be successfully reversed by supplementation with rejuvenins and by reducing the levels of geriatrins.
    Keywords:  balance; geriatrins; geroplasticity; rejuvenins
    DOI:  https://doi.org/10.14336/AD.2022.0414
  6. Age Ageing. 2022 Dec 05. pii: afac285. [Epub ahead of print]51(12):
      Multimorbidity has increased in prevalence world-wide. It is anticipated to affect over 1 in 6 of the UK population by 2035 and is now recognised as a global priority for health research. Genomic medicine has rapidly advanced over the last 20 years from the first sequencing of the human genome to integration into clinical care for rarer conditions. Genetic studies help identify new disease mechanisms as they are less susceptible to the bias and confounding that affects epidemiological studies, as genetics are assigned from conception. There is also genetic variation in the efficacy of medications and the risk of side effects, pharmacogenetics. Genomic approaches offer the potential to improve our understanding of mechanisms underpinning multiple long-term conditions/multimorbidity and guide precision approaches to risk, diagnosis and optimisation of management. In this commentary as part of the Age and Ageing 50th anniversary commentary series, we summarise genomics and the potential utility of genomics in multimorbidity.
    Keywords:  genetic; genomic; older people; personalised; precision
    DOI:  https://doi.org/10.1093/ageing/afac285
  7. Cell Rep. 2022 Dec 06. pii: S2211-1247(22)01657-6. [Epub ahead of print]41(10): 111774
      Mitochondrial damage causes mitochondrial DNA (mtDNA) release to activate the type I interferon (IFN-I) response via the cGAS-STING pathway. mtDNA-induced inflammation promotes autoimmune- and aging-related degenerative disorders. However, the global picture of inflammation-inducing mitochondrial damages remains obscure. Here, we have performed a mitochondria-targeted CRISPR knockout screen for regulators of the IFN-I response. Strikingly, our screen reveals dozens of hits enriched with key regulators of cristae architecture, including phospholipid cardiolipin and protein complexes such as OPA1, mitochondrial contact site and cristae organization (MICOS), sorting and assembly machinery (SAM), mitochondrial intermembrane space bridging (MIB), prohibitin (PHB), and the F1Fo-ATP synthase. Disrupting these cristae organizers consistently induces mtDNA release and the STING-dependent IFN-I response. Furthermore, knocking out MTX2, a subunit of the SAM complex whose null mutations cause progeria in humans, induces a robust STING-dependent IFN-I response in mouse liver. Taken together, beyond revealing the central role of cristae architecture to prevent mtDNA release and inflammation, our results mechanistically link mitochondrial cristae disorganization and inflammation, two emerging hallmarks of aging and aging-related degenerative diseases.
    Keywords:  CP: Cell biology; CP: Molecular biology; MICOS; Metaxin2; OPA1; SAM; cGAS-STING; cristae architecture; inflammation; mtDNA release; type I interferon response
    DOI:  https://doi.org/10.1016/j.celrep.2022.111774