Browsing by Author "Rigotti Rivera, Attilio"

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    Deficiency of Niemann-Pick C1 protein protects against diet-induced gallstone formation in mice
    (2010) Morales France, María Gabriela; Amigo Böker, Ludwig Peter; Balboa Castillo, Elisa Ivana; Acuña Aravena, Mariana Loreto; Castro, Juan; Molina, Héctor; Miquel P., Juan Francisco; Nervi, Flavio; Rigotti Rivera, Attilio; Zanlungo Matsuhiro, Silvana
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    Increased statin eligibility based on ACC/AHA versus NCEP guidelines for high cholesterol management in Chile
    (2016) Echeverría, G.; Dussaillant, C.; Villarroel del Pino, Luis A.; Rigotti Rivera, Attilio
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    Isolation and Purification of Human Biliary Vesicles With Potent Cholesterol Nucleation-Promoting Activity
    (1992) Brandan, Enrique; Miquel P., Juan Francisco; Nervi, Flavio; Rigotti Rivera, Attilio
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    Lipoprotein receptor SR-B1 deficiency enhances adipose tissue inflammation and reduces susceptibility to hepatic steatosis during diet-induced obesity in mice
    (2020) Rivera Vega, Katherine Solange; Rigotti Rivera, Attilio; Pontificia Universidad Católica de Chile. Facultad de Medicina
    Obesity is a worldwide epidemic associated with excessive lipid accumulation in adipose and non-adipose tissues, including the liver, an early feature in the development of non-alcoholic fatty liver disease (NAFLD). Several studies have linked NAFLD with a deranged high-density lipoprotein (HDL) metabolism. Scavenger receptor class B type 1 (SR-B1) is the major membrane HDL receptor and is involved in reverse cholesterol, but its role in obesity and NAFLD development is unclear. The aim of this thesis was to determine the effects of SR-B1 deficiency on plasma metabolic parameters and fat deposition in adipose tissue and liver during obesity. Male SR-B1 knock-out (SR-B1-/-) mice and wild-type (WT) littermates were fed for 12 weeks with a high-fat diet (HFD) to induce obesity. At the end of the intervention SR-B1-/- mice fed a HFD exhibited significantly increased levels of plasma total cholesterol, triglycerides (TG) and TNF-α, in association with hypertrophied adipocytes and macrophage-containing crown-like structures (CLS) in adipose tissue, compared to WT obese mice. Remarkably, obese SR-B1-/- mice exhibited attenuated liver TG content, dysregulation in hepatic gene expression profile, increased hepatic TG secretion, and altered hepatic fatty acid (FA) composition, compared to WT mice. These results provide the basis for further elucidation of SR-B1 role in obesity and fatty liver disease, two major worldwide public health issues that increase the risk of advanced chronic disease and mortality in the general population.Obesity is a worldwide epidemic associated with excessive lipid accumulation in adipose and non-adipose tissues, including the liver, an early feature in the development of non-alcoholic fatty liver disease (NAFLD). Several studies have linked NAFLD with a deranged high-density lipoprotein (HDL) metabolism. Scavenger receptor class B type 1 (SR-B1) is the major membrane HDL receptor and is involved in reverse cholesterol, but its role in obesity and NAFLD development is unclear. The aim of this thesis was to determine the effects of SR-B1 deficiency on plasma metabolic parameters and fat deposition in adipose tissue and liver during obesity. Male SR-B1 knock-out (SR-B1-/-) mice and wild-type (WT) littermates were fed for 12 weeks with a high-fat diet (HFD) to induce obesity. At the end of the intervention SR-B1-/- mice fed a HFD exhibited significantly increased levels of plasma total cholesterol, triglycerides (TG) and TNF-α, in association with hypertrophied adipocytes and macrophage-containing crown-like structures (CLS) in adipose tissue, compared to WT obese mice. Remarkably, obese SR-B1-/- mice exhibited attenuated liver TG content, dysregulation in hepatic gene expression profile, increased hepatic TG secretion, and altered hepatic fatty acid (FA) composition, compared to WT mice. These results provide the basis for further elucidation of SR-B1 role in obesity and fatty liver disease, two major worldwide public health issues that increase the risk of advanced chronic disease and mortality in the general population.
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    Npc1 deficiency in the C57BL/6J genetic background enhances Niemann–Pick disease type C spleen pathology
    (2011) Parra Cares, Julio Alejandro; Klein, Andres D.; Castro, Juan Francisco; Morales France, María Gabriela; Mosqueira Montero, Matías José; Valencia Araya, Ilse; Cortés Mora, Víctor Antonio; Rigotti Rivera, Attilio; Zanlungo Matsuhiro, Silvana
    Niemann–Pick type C (NPC) disease is an autosomal recessive neurovisceral lipid storage disorder. The affected genes are NPC1 and NPC2. Mutations in either gene lead to intracellular cholesterol accumulation. There are three forms of the disease, which are categorized based on the onset and severity of the disease: the infantile form, in which the liver and spleen are severely affected, the juvenile form, in which the liver and brain are affected, and the adult form, which affects the brain. In mice, a spontaneous mutation in the Npc1 gene originated in the BALB/c inbred strain mimics the juvenile form of the disease. To study the influence of genetic background on the expression of NPC disease in mice, we transferred the Npc1 mutation from the BALB/c to C57BL/6J inbred background. We found that C57BL/6J-Npc1−/− mice present with a much more aggressive form of the disease, including a shorter lifespan than BALB/c-Npc1−/− mice. Surprisingly, there was no difference in the amount of cholesterol in the brains of Npc1−/− mice of either mouse strain. However, Npc1−/− mice with the C57BL/6J genetic background showed striking spleen damage with a marked buildup of cholesterol and phospholipids at an early age, which correlated with large foamy cell clusters. In addition, C57BL/6J Npc1−/− mice presented red cell abnormalities and abundant ghost erythrocytes that correlated with a lower hemoglobin concentration. We also found abnormalities in white cells, such as cytoplasmic granulation and neutrophil hypersegmentation that included lymphopenia and atypias. In conclusion, Npc1 deficiency in the C57BL6/J background is associated with spleen, erythrocyte, and immune system abnormalities that lead to a reduced lifespan.
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    Race and sex differences in HDL peroxide content among American adults with and without type 2 diabetes
    (2022) Flaherty, Shelby M.; Wood, Elizabeth K.; Ryff, Carol D.; Love, Gayle D.; Kelesidis, Theodoros; Berkowitz Fiebich, Loni; Echeverría Errázuriz, Guadalupe; Rivera Vega, Katherine Solange; Rigotti Rivera, Attilio; Coe, Christopher L.
    Background: High-density lipoprotein (HDL) plays a critical role in protection against atherosclerosic and cardiovascular disease (ASCVD). In addition to contributing to clearing excess vascular cholesterol, HDL particles exhibit antioxidative functions, helping to attenuate adverse effects of oxidized low-density lipoproteins. However, these beneficial properties can be undermined by oxidative stress, inflammation, and unhealthy lifestyles and diet, as well as influenced by race and sex. Thus, when assessing cardiovascular risk, it is important to consider multifactorial aspects of HDL, including antioxidant activity rather than just total amount and type of HDL-cholesterol (HDL-C) particles. Because prior research showed HDL peroxide content (HDLperox) can be inversely associated with normal anti-oxidant HDL activity, elevated HDLperox may serve as a bioindicator of HDL dysfunction. Methods: In this study, data from a large national cohort of Americans was utilized to determine the impact of sex, race, and diabetes status on HDLperox in middle-aged and older adults. A previously developed cell-free fluorometric method was utilized to quantify HDLperox in serum depleted of apo-B containing lipoproteins. Results: In keeping with predictions, white men and diabetics exhibited HDLperox in the atypical upper range, suggestive of less functional HDL. White men had higher HDLperox levels than African American males (13.46 ± 6.10 vs. 10.88 ± 5.81, p < .001). There was also a significant main effect of type 2 diabetes (F(1,1901) = 14.9, p < .0001). Overall, African Americans evinced lower HDLperox levels, despite more obesity (10.3 ± 4.7 vs.11.81 ± 5.66 for Whites) suggesting that other aspects of lipid metabolism and psychosocial factors account for the higher prevalence of ASCVD in African Americans. Conclusion: This research helps to provide a more comprehensive understanding of HDL function in a racially and metabolically diverse adult population. HDLperox content was significantly different in adults with type 2 diabetes, and distinctive in nondiabetic White males, and suggests other processes account for the higher prevalence of ASCVD among African Americans.
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    Recursos psicosociales positivos y salud cardiovascular
    (2014) Nitsche, M.; Bitrán Carreño, Marcela; Pedrals, Nuria; Echeverría Errázuriz, Guadalupe; Rigotti Rivera, Attilio
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    Standardization of the Food Composition Database Used in the Latin American Nutrition and Health Study (ELANS)
    (2015) Kovalskys, Irina; Fisberg, Mauro; Gómez, Georgina; Rigotti Rivera, Attilio; Cortés, Lilia Yadira; Yepez, Martha Cecilia; Pareja, Rossina G.; Herrera Cuenca, Marianella; Zimberg, Ioná Z.; Tucker, Katherine L.; Koletzko, Berthold; Pratt, Michael