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Roger Maldonado-Ruiz

Researcher at Universidad Autónoma de Nuevo León

Publications -  13
Citations -  186

Roger Maldonado-Ruiz is an academic researcher from Universidad Autónoma de Nuevo León. The author has contributed to research in topics: Offspring & Medicine. The author has an hindex of 6, co-authored 9 publications receiving 113 citations.

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Microglia activation due to obesity programs metabolic failure leading to type two diabetes.

TL;DR: This review will cover the most significant advances that explore the molecular signals during microglia activation and inflammatory stage in the brain in the context of obesity, and its influence on the development of metabolic syndrome and type two diabetes.
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Maternal Overnutrition Programs Central Inflammation and Addiction-Like Behavior in Offspring.

TL;DR: The most relevant scientific reports about the impact of hypercaloric nutritional fetal programming on central and peripheral inflammation and its effects on addictive behavior of the offspring are reviewed.
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Central Modulation of Neuroinflammation by Neuropeptides and Energy-Sensing Hormones during Obesity.

TL;DR: The role of lipotoxicity associated with positive energy balance during obesity in proinflammatory response in microglia, B and T lymphocytes, and its modulation by neuropeptides is discussed.
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Priming of Hypothalamic Ghrelin Signaling and Microglia Activation Exacerbate Feeding in Rats’ Offspring Following Maternal Overnutrition

TL;DR: It is found that programmed offspring by CAF diet exhibits overfeeding after fasting and peripheral ghrelin administration, which correlates with an increase in the hypothalamic Iba-1 microglia marker and c-Fos cell activation.
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Fetal Programming by Methyl Donors Modulates Central Inflammation and Prevents Food Addiction-Like Behavior in Rats.

TL;DR: The in vivo and in vitro data suggest that fetal programming by methyl donors actively decreases addiction-like behavior to palatable food in the offspring, which correlates with a decrease in NAc shell methylome, expression of pro-inflammatory cytokine genes, and activity of phagocytic microglia.