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ABSTRACT: The twenty-first century arrived in the middle of a global epidemic of metabolic syndrome (MS) and type 2 diabetes mellitus (DM2). It is generally accepted that an excess of nutrients linked to a low physical activity triggers the problem. However, the molecular features that interact to develop the MS are not clear. In an effort to understand and control them, they have been extensively studied, but this goal has not been achieved yet. Nonhuman animal models have been used to explore diet and genetic factors in which experimental conditions are controlled. For example, only one factor in the diet, such as fats or carbohydrates can be modified to better understand a single change that would be impossible in humans. Most of the studies have been done in rodents. However, it is difficult to directly compare them, because experiments are different in more than one variable; genetic strains, amount, and the type of fat used in the diet and sex. Thus, the only possible criteria of comparison are the relevance of the observed changes. We review different animal models and add some original observations on short-term changes in metabolism and beta cells in our own model of adult Wistar rats that are not especially prone to get fat or develop DM2, treated with 20% sucrose in drinking water. One early change observed in pancreatic beta cells is the increase in GLUT2 expression that is located to the membrane of the cells. This change could partially explain the presence of insulin hypersecretion and hyperinsulinemia in these rats. Understanding early changes that lead to MS and in time to pancreatic islet exhaustion is an important biomedical problem that may contribute to learn how to prevent or even reverse MS, before developing DM2. © 2011 IUBMB IUBMB Life, 2011
International Union of Biochemistry and Molecular Biology Life 09/2011; 63(10):831 - 839. · 3.51 Impact Factor
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Gabriela Gutierrez-Reyes,
Maria del Carmen Garcia de Leon,
Gustavo Varela-Fascinetto,
Pedro Valencia,
Ruy Pérez Tamayo,
Claudia Gonzalez Rosado,
Blanca Farfan Labonne,
Norma Morales Rochilin,
Rosalinda Martinez Garcia,
Jonathan Aguirre Valadez,
Gabriela Togno Latour,
Dana Lau Corona, Guillermo Robles Diaz,
Albert Zlotnik,
David Kershenobich
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ABSTRACT: Senescent cells occur in adults with cirrhotic livers independent of the etiology.
Investigate the presence rate of cellular senescence and expression of cell cycle check points in livers from children with end stage disease.
Livers of five children aged three years or less undergoing liver transplantation due to tyrosinemia (n = 1), biliary atresia (n = 2), or fulminant hepatitis (n = 2) were analyzed for senescence associated beta-galactosidase (SA-betagal) activity and p16INK4a, p21cip1 and p53. All livers displayed positive cellular staining for SA-betagal in the canals of Hering and interlobular biliary ducts. In the presence of cirrhosis (3/5 cases) SA-betagal was found at the cholangioles and hepatocytes surrounding the regenerative nodules. Children with fulminant hepatic failure without cirrhosis had significant ductular transformation with intense SA-betagal activity. No SA-betagal activity was evident in the fibrous septa. Staining for p53 had a similar distribution to that observed for SA-betagal. Staining for p16(INK4a) and p21(cip1) was positive in the explanted liver of the patient with tyrosinemia, in the hepatocytes, the canals of Hering, cholangioles and interlobular bile ducts. In the livers with fulminant hepatitis, p21(cip1) staining occurred in the areas of ductular transformation and in the interlobular bile ducts.
Cellular senescence in livers of children with end stage disease is associated with damage rather than corresponding to an age dependent phenomenon. Further studies are needed to support the hypothesis that these senescence markers correlate with disease progression.
PLoS ONE 01/2010; 5(4):e10231. · 4.09 Impact Factor
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Eduardo Ferat-Osorio,
Isabel Wong-Baeza,
Noemí Esquivel-Callejas,
Silvia Figueroa-Figueroa,
Andrés Duarte-Rojo,
Gilberto Guzmán-Valdivia-Gómez,
Heriberto Rodea-Rosas,
Rubén Torres-González,
Patricio Sánchez-Fernández,
Lourdes Arriaga-Pizano,
Constantino López-Macías, Guillermo Robles-Díaz,
Armando Isibasi
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ABSTRACT: Acute pancreatitis (AP) is usually a mild and self-limiting disease, but some patients develop a severe form that is associated with high mortality. In AP, local inflammation is followed first by the systemic inflammatory response syndrome and then by the compensatory anti-inflammatory response syndrome, which is defined by low human leukocyte antigen (HLA)-DR expression on monocytes, increased concentration of the anti-inflammatory cytokine IL-10, and decreased monocyte function. Our aim was to measure the expression of triggering receptor expressed on myeloid cells (TREM)-1 (a proposed marker of infection or inflammation) and HLA-DR on monocytes, and the serum concentrations of IL-6 (a proinflammatory cytokine) and IL-10 in patients with AP to determine whether these markers can identify patients at high risk of developing severe AP or infection.
Fifty healthy volunteers, 18 patients with mild AP, and 11 patients with severe AP were included in this study. Samples were taken at admission and one and three days later. TREM-1 and HLA-DR expression was evaluated by flow cytometry, and soluble TREM-1, IL-6 and IL-10 concentrations were measured by ELISA.
TREM-1 expression was higher in patients with AP than in healthy volunteers, but there was no difference between patients with mild and severe AP. TREM-1 expression was not associated with mortality or with the presence of infection. Soluble TREM-1 concentration in serum was higher in non-survivors than in survivors. HLA-DR expression was lower and IL-6 concentration higher in patients with severe AP and in infected patients.
Increased TREM-1 expression was associated with the presence of inflammation but not infection in AP. In patients with AP, low HLA-DR expression and high IL-6 concentration could predict severity and infection in samples taken shortly after admission.
Critical care (London, England) 06/2009; 13(3):R69. · 4.61 Impact Factor
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Maria del Carmen Garcia de Leon Mendez,
Gabriela Gutierrez-Reyes, Guillermo Robles Diaz,
Angelica Cuapio-Gomez,
Claudia I. Gonzalez-Rosado,
Mario T. Mendoza Carrasco,
Yesika Oliva-Fuentes,
Gabriela Togno-Latour,
Eusebio Tello-Montes,
Irmgard Montfort-Happel,
Ruy Perez-Tamayo,
David Kershenobich
Gastroenterology. 04/2008; Volume 134(Issue 4-134):Pages A-794-A-795.
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ABSTRACT: Endocrine pancreatic tumors (EPTs) are rare lesions with varying biological behavior. Establishing malignancy is a challenge for clinicians and pathologists.
To establish the role of proliferative, apoptotic, angiogenic, and hormonal markers as predictors of malignancy in EPTs.
Paraffin-embedded EPT samples were studied for prognostic markers.
Twenty-one consecutive patients with a diagnosis of EPT.
The proliferative fraction (topoisomerase IIalpha), microvascular density (CD34), vascular endothelial growth factor expression, and estrogen receptor-beta (ERbeta) expression were studied by immunohistochemistry on all EPTs. Apoptosis was also assessed with terminal deoxynucleotidyl transferase nick-end labeling.
We identified 13 benign and 8 malignant tumors. Topoisomerase IIalpha was significantly increased in malignant tumors (P =.001), while there were no differences in apoptosis, microvascular density, or vascular endothelial growth factor expression in association with malignancy. No correlation could be identified between microvascular density and vascular endothelial growth factor expression, and ERbeta was not detected. A receiver operating characteristic curve for topoisomerase IIalpha disclosed that above a labeling index of 13, the test had 88% sensitivity and 100% specificity for predicting malignancy.
Cellular proliferation measured with topoisomerase IIalpha is a simple prognostic marker for malignancy in EPTs, unlike apoptosis, angiogenesis, or the presence of ERbeta, which were not associated with malignant behavior. These findings designate a defined field for future research on endocrine pancreatic carcinogenesis and a possible target for chemotherapeutic agents.
Archives of pathology & laboratory medicine 05/2004; 128(4):426-9. · 2.58 Impact Factor
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ABSTRACT: To report a case of an isolated pancreatic metastasis from a primary cecum carcinoma.
Carcinoma of the colon and rectum commonly metastasizes to distant sites such as liver, lung, bone, brain, and ovaries. Only a few cases of pancreatic metastasis from a primary colonic carcinoma had been reported. Metastasic lesions to the pancreas are found only in 3% to 12% of autopsies from advanced malignancies. Primary tumors that commonly metastasize to the pancreas are lung and kidney. Most of the patients with metastatic lesions to pancreas also had extrapancreatic metastatic disease.
We report a case of a 86-year-old woman with a single pancreatic metastasis from a primary cecum carcinoma resected 8 months before.
The finding of an isolated metastasis to the pancreatic body from a primary cecum adenocarcinoma is extremely rare.
Current Surgery 61(3):328-30.
