Dietary polyphenols are studied as potential adjuncts for type 2 diabetes (T2D), although many reviews still rely on an antioxidant framework that does not adequately reflect human exposure. This review organises the evidence around two metabolite waves, namely early postprandial phase-II conjugates produced by host enzymes within 0 to 4 h of a polyphenol-rich meal, and microbiome-derived catabolites including urolithins and γ-valerolactones that peak at 6 to 24 h. This biphasic interpretation is advanced as a hypothesis-generating framework rather than as an established explanation, and it offers a testable account of why polyphenol effects may be meal-contingent, metabotype-dependent and heterogeneous across clinical trials. Using randomised controlled trials and meta-analyses published between 2015 and 2025, we review the human evidence for anthocyanins, catechins, stilbenes, cocoa flavanols and olive phenolics, with briefer coverage of isoflavones, curcuminoids and ellagitannins. Anthocyanins show the most consistent glycaemic signal, with a best available pooled estimate of about 0.3% for HbA1c (−0.31%, median exposure eight weeks) derived from trials that did not verify metabolite exposure, an effect that is modest and lies at the lower bound of what is generally regarded as clinically meaningful. Green tea catechins and high-phenolic extra-virgin olive oil are associated with comparable postprandial gains, whereas cocoa flavanols and resveratrol more reliably improve vascular and inflammatory intermediates than glycaemia itself. Most interventions were well tolerated at the nutritional doses tested. Polyphenols are better regarded as meal-timed dietary adjuncts to standard T2D care than as primary glycaemic agents.
Celia María Curieses Andrés, J. M. Pérez de la Lastra, Elena Bustamante Munguira et al.· Nutrients· 0 citations
Cellular redox regulation is increasingly recognised as a spatially organised network in which oxidant production, thiol buffering, and selective signalling operate within compartment-specific microdomains rather than as uniform cellular processes. However, peptide-mediated mechanisms that actively define these local redox environments have not previously been integrated into a unified conceptual framework. This review introduces the concept of peptide redox networks, defined as peptide or protein systems whose local abundance, oxidation state, or proteolytic processing directly determines the amplitude, spatial confinement, or propagation of redox signalling within specific cellular microdomains. We evaluate the evidence supporting this framework and discuss its implications for mechanistic research and clinical translation. We synthesise current knowledge on glutathione, histidine-containing dipeptides, mitochondria-targeted peptides, and mitochondrial-derived peptides as complementary regulators of cellular redox homeostasis. Particular emphasis is placed on compartment-specific redox set points, NADPH-dependent buffering, ferroptosis vulnerability, mitochondrial quality control, and regulated thiol signalling. We further examine recent advances in redox proteomics, isotope tracing, and proteoform-aware analytical strategies, highlighting methodological challenges that influence data interpretation. Based on these considerations, we propose operational criteria for defining peptide redox network components, establish minimum reporting recommendations to improve reproducibility, and identify experimental approaches capable of distinguishing adaptive redox regulation from irreversible oxidative dysfunction. Peptide redox networks provide an integrative framework that links compartmental redox biology with peptide-mediated regulation across multiple physiological and pathological contexts. Adoption of standardised analytical approaches together with mechanistically defined network criteria should improve reproducibility, facilitate biomarker development, and accelerate the translation of peptide-based redox interventions into precision medicine.
J. M. Pérez de la Lastra, Celia María Curieses Andrés, E. B. Munguira et al.· International Journal of Pep...· 0 citations
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