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María Insenser

Researcher at University of Alcalá

Publications -  43
Citations -  1735

María Insenser is an academic researcher from University of Alcalá. The author has contributed to research in topics: Polycystic ovary & Adipose tissue. The author has an hindex of 19, co-authored 38 publications receiving 1346 citations. Previous affiliations of María Insenser include Carlos III Health Institute & Complutense University of Madrid.

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Postprandial inflammatory responses after oral glucose, lipid and protein challenges: Influence of obesity, sex and polycystic ovary syndrome.

TL;DR: Glucose ingestion, as opposed to lipid and protein intake, results into the largest increase in leukocyte gene expression of inflammatory mediators, suggesting a compensatory mechanisms against postprandial inflammation that may be blunted in obesity.
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Proteomics and genomics: A hypothesis-free approach to the study of the role of visceral adiposity in the pathogenesis of the polycystic ovary syndrome.

TL;DR: The present manuscript reviews the hypothesis‐free approaches – such as genomics and proteomics – that have been used recently to study PCOS, focusing on studies from the group addressing the gene expression profiles and the proteome of visceral adipose tissue of morbidly obese women presenting with or without PCOS.
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Application of proteomics to the study of polycystic ovary syndrome.

TL;DR: Review of proteomic studies conducted to date that addressed different aspects of the pathogenesis of polycystic ovary syndrome revealed that PCOS associates changes in protein expression in several acute-phase response proteins.
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Proteomic analysis of adipose tissue: informing diabetes research

TL;DR: This review has summarized the studies conducting adipose tissue proteomics in subjects with diabetes and insulin resistance, and discussed the proteins identified in these studies as candidates to exert important roles in these disorders.
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Circulating adiponectin increases in obese women after sleeve gastrectomy or gastric bypass driving beneficial metabolic changes but with no relationship with carotid intima-media thickness.

TL;DR: RYGB induces a higher increase in adiponectin than SG, which parallels SHBG, the reduction of fasting insulin and insulin resistance, and no association was found with carotid intima-media, lipid profiles or blood pressure.