Biology subjects

Gradillas, A.

Publications and source records attributed to Gradillas, A..

2 recordsLinked to original sources

bioRxiv2025

A lipidomic exploration of the effects of high-intensity interval exercise in healthy men after metformin intake

We have previously found that high-intensity interval exercise (HIIE) affected metformin pharmacokinetics, causing higher maximal plasma concentration compared with rest. In this scenario, changes in individual lipids could play an important role. The prolonged responses of the lipidome to HIIE have not been explored. Thus, this study aimed to explore differences in the plasma lipidomic profiles between HIIE and rest, both under metformin treatment. Nine healthy males participated in two sessions where they received 1,000 mg of metformin. In session A, they performed HIIE at an average intensity of 67% of maximum heart rate for a total duration of 76 min, whereas in session B they rested. Plasma was collected before taking metformin and during each session (in total 14 time points spanning 12 h). Samples were analysed through lipidomics using mass spectrometry. Paired Wilcoxon tests between sessions were applied for statistics. We found several variations in the lipid profiles due to HIIE, which persisted until 4 h post-exercise. The main discriminant lipid classes were fatty acids, acyl carnitines, glycerophosphocholins, sphingomyelins, and triglycerides. These changes were followed in time up to 12 h, showing the effect of the meals taken during the session. We hypothesize the changes are a synergic effect of HIIE and metformin in the lipidome with the effect of HIIE being the predominant. These findings provide important insights into the dynamic and complex physiological response of humans to intensive exercise under metformin intake.

systems biology↗

bioRxiv2023

Allergic inflammation triggers dyslipidemia via IgG signalling

BackgroundAllergic diseases begin early in life and are often chronic, thus creating an inflammatory environment that may precede or exacerbate other pathologies. In this regard, allergy has been associated to metabolic disorders and with a higher risk of cardiovascular disease, but the underlying mechanisms remain incompletely understood. MethodsWe used a murine model of allergy and atherosclerosis, different diets and sensitization methods, and cell-depleting strategies to ascertain the contribution of acute and late phase inflammation to dyslipidemia. Untargeted lipidomic analyses were applied to define the lipid fingerprint of allergic inflammation at different phases of allergic pathology. Expression of genes related to lipid metabolism was assessed in liver and adipose tissue at different times post-allergen challenge. Also, changes in serum triglycerides (TG) were evaluated in a group of 59 patients [≥]14 days after the onset of an allergic reaction. ResultsWe found that allergic inflammation induces a unique lipid signature that is characterized by increased serum TG and changes in the expression of genes related to lipid metabolism in liver and adipose tissue. Alterations in blood TGs following an allergic reaction are independent of T-cell-driven late phase inflammation. On the contrary, the IgG-mediated alternative pathway of anaphylaxis is sufficient to induce a TG increase and a unique lipid profile. Lastly, we demonstrated an increase in serum TG in 59 patients after undergoing an allergic reaction. ConclusionOverall, this study reveals that IgG-mediated allergic inflammation regulates lipid metabolism.

immunology↗