PMC:7335494 / 41913-43495 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7335494","sourcedb":"PMC","sourceid":"7335494","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7335494","text":"In healthy subjects, even one MD-style meal was shown to reduce the expression of pro-inflammatory molecules (De Lorenzo et al., 2017), with no differences between sexes regarding effects on systemic inflammatory status (Bedard et al., 2015). In elderly individuals, a MD intervention lead to lower glycoxidative impairment (Lopez-Moreno et al., 2018) and inflammatory response (Camargo et al., 2012; Yubero-Serrano et al., 2012), paralleled to a diet based on saturated fatty acids (Fig. 2 ).\nFig. 2 Diets rich in proteins, lipids and carbohydrates induce the production of pro-inflammatory molecules that lead to the activation of several inflammatory pathways including JAK/STAT pathway, NF-Kβ pathway and MAPK kinase cascade. These pathways lead to oxidative stress, as wells as, COX-2, TNF-α, and interleukins production via transcriptional regulation ultimately leading to chronic inflammation. Oxidative stress either directly or via metabolic dysfunctions causing e.g insulin resistance, as well as the rest of the inflammatory molecules as a result of unhealthy diet promote the onset of several chronic diseases including CVD, neurodegenerative diseases, autoimmunity, pulmonary diseases and are-related frailty; (NF-kβ – nuclear factor kappa-light-chain-enhancer of activated B cells heterodimer, consisting of p50, p65 and IkBα proteins; STAT3 – Signal transducer and activator of transcription 3; ERK/MAPK – mitogen-activated protein kinases; JNK – c-Jun N-terminal kinases; COX-2 – cyclooxygenase 2; TNF-α – Tumour necrosis factor alpha; IL-1/6/8 – interleukin 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