Browsing by Author "Tapia, Gladys"

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    Exercise Induces an Augmented Skeletal Muscle Mitochondrial Unfolded Protein Response in a Mouse Model of Obesity Produced by a High-Fat Diet
    (2023) Apablaza, Pia; Borquez, Juan Carlos; Mendoza, Rodrigo; Silva, Monica; Tapia, Gladys; Espinosa, Alejandra; Troncoso, Rodrigo; Videla, Luis A.; Juretic, Nevenka; del Campo, Andrea
    Increase in body fat contributes to loss of function and changes in skeletal muscle, accelerating sarcopenia, a phenomenon known as sarco-obesity or sarcopenic obesity. Studies suggest that obesity decreases the skeletal muscle (SM)'s ability to oxidize glucose, increases fatty acid oxidation and reactive oxygen species production, due to mitochondrial dysfunction. Exercise improves mitochondrial dysfunction in obesity; however, it is not known if exercise regulates the mitochondrial unfolded protein response (UPRmt) in the SM. Our study aimed to determine the mito-nuclear UPRmt in response to exercise in a model of obesity, and how this response is associated with the improvement in SM functioning after exercise training. C57BL/6 mice were fed a normal diet and high-fat diet (HFD) for 12 weeks. After 8 weeks, animals were subdivided into sedentary and exercised for the remaining 4 weeks. Grip strength and maximal velocity of mice submitted to HFD improved after training. Our results show an increase in the activation of UPRmt after exercise while in obese mice, proteostasis is basally decreased but shows a more pronounced increase with exercise. These results correlate with improvement in the circulating triglycerides, suggesting mitochondrial proteostasis could be protective and could be related to mitochondrial fuel utilization in SM.
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    Higher hepatic advanced glycation end products and liver damage markers are associated with nonalcoholic steatohepatitis
    (2022) Priken, Kathleen; Tapia, Gladys; Cadagan, Cynthia; Quezada, Nicolas; Torres, Javiera; D'Espessailles, Amanda; Pettinelli, Paulina
    Advanced glycation end products (AGEs) may be associated with nonalcoholic fatty liver disease (NAFLD) from stimulation of oxidative stress, inflammation, and fibrosis. We hypothesized that patients with NAFLD would have a lower concentration of soluble AGEs receptor and higher quantity of serum and liver AGEs and an increase in hepatic smooth muscle actin alpha (alpha-SMA) and transforming growth factor beta 1 (TGF-beta 1) compared with a control group. We compared the presence of hepatic and serum AGEs, AGE soluble receptor (sRAGE), and markers associated with hepatic damage between NAFLD patients and controls without disease. Histological characteristics, plasma biochemical parameters, serum AGEs, serum receptor sRAGE, and liver proteins (alpha-SMA, TGF-beta 1, AGEs, immunohistochemistry) were assessed in participants aged 18 to 65 years, with NAFLD (simple steatosis [SS]: n = 7; steatohepatitis [NASH]: n = 15) and controls (n = 11). NASH patients presented higher glycated hemoglobin levels (%) (5.7; 5.4-6.3) compared with SS (5.4; 5.2-5.7) and controls (5.4; 5.3-5.5). The NAFLD activity score (NAS) for NASH patients was 4.9 +/- 1.3; for SS patients, 2.0 +/- 1.0. NASH patients showed higher hepatic AGEs, TGF-beta 1, and alpha-SMA compared with SS and control groups. The NAS score indicates that patients with 5 to 8 had higher hepatic AGEs, TGF-beta 1, and alpha-SMA compared with a NAS of 1 to 4 and 0. For alpha-SMA, a NAS of 1 to 4 was higher than NAS 0. No difference was found in serum AGEs and sRAGE between groups. Higher hepatic AGEs, TGF-beta 1, and alpha-SMA were observed with increasing disease severity (according to NAS); therefore, endogenous liver AGEs may participate in hepatic damage progression. (C) 2022 Elsevier Inc. All rights reserved.
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    Rol de la microbiota intestinal en el desarrollo del hígado graso no alcohólico
    (Sociedad Médica de Santiago, 2021) Tumani Karmy, María Fernanda; Tapia, Gladys; Aguirre, Carolina; Obregón, Ana María; Pettinelli, Paulina
    Non-alcoholic fatty liver disease (NAFLD) encompasses a wide spectrum of hepatic pathologies ranging from simple steatosis (SS) to hepatocellular carcinoma. Intestinal microbiota (IM) is composed of trillions of microorganisms existing in the gut. It has 150 times more genes than the host. Changes in the composition and function of the IM are associated with different diseases, including NAFLD. In this condition, IM could have a pathogenic role through different mechanisms such as energy salvaging from food, an inflammatory stimulus, a modulation of the innate immune system, regulation of bile acid turnover, alteration of choline metabolism and increasing endogenous ethanol levels. This review is an update on the role of the intestinal microbiota in NAFLD and the possible mechanisms involved.
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    Role of dietary α- and γ-tocopherol from Rosa mosqueta oil in the prevention of alterations induced by high-fat diet in a murine model
    (2018) Tapia, Gladys; Silva, David; Romero, Nalda; Pettinelli Rocha, Paulina Pilar; Dossi, Camila G.; De Miguel, Manuel; González-Mañán, Daniel