Severity of non-alcoholic fatty liver disease is associated with high systemic levels of tumor necrosis factor alpha and low serum interleukin 10 in morbidly obese patients
Por:
Paredes-Turrubiarte, Gabriela, Gonzalez-Chavez, Antonio, Perez-Tamayo, Ruy, Salazar-Vazquez, Beatriz Y., Hernandez, Vito S., Garibay-Nieto, Nayeli, Manuel Fragoso, Jose, Escobedo, Galileo
Publicada:
1 may 2016
Resumen:
Morbid obesity has been shown to increase the risk to develop hepatic
steatosis, also referred to as non-alcoholic fatty liver disease
(NAFLD). Emerging evidence suggests that the severity of NAFLD may
associate with increased serum levels of inflammatory markers as well as
decreased concentration of mediators with anti-inflammatory actions,
such as tumor necrosis factor alpha (TNF-alpha) and interleukin (IL) 10,
respectively. We thus examined the serum levels of TNF-alpha and IL-10
in 102 morbidly obese women and men (body mass index > 40 kg/m(2)),
exhibiting different grades of NAFLD. Blood glucose, glycated
hemoglobin, insulin, the homeostatic model assessment of insulin
resistance (HOMA-IR), total cholesterol, triglycerides, high- and
low-density lipoproteins, parameters of liver function, TNF-alpha, and
IL-10 were measured in each subject. The stage of NAFLD was estimated by
abdominal ultrasound imaging. In comparison with morbidly obese subjects
without steatosis, morbidly obese patients with NAFLD showed increased
age (39.23 +/- 9.80 years), HOMA-IR (6.74 +/- 1.62), total cholesterol
(219.7 +/- 9.58 mg/dl), aspartate aminotransferase (36.25 +/- A 3.24
UI/l), gamma-glutamyl transpeptidase (37.12 +/- 3.41 UI/l), and
TNF-alpha (37.41 +/- 1.72 pg/ml) as well as decreased serum levels of
IL-10 (61.05 +/- 2.43 pg/ml). Interestingly, the systemic levels of
TNF-alpha increased, while IL-10 decreased in accordance with the
severity of NAFLD, which supports a role for systemic inflammatory
mediators in promoting steatosis progression. Further clinical
prospective studies need to be addressed to elucidate the role of
TNF-alpha and IL-10 in the development of NAFLD while also establishing
their clinical utility in the assessment of morbidly obese patients at
higher risk to develop severe steatosis.
Filiaciones:
Paredes-Turrubiarte, Gabriela:
Gen Hosp Mexico Dr Eduardo Liceaga, Dept Internal Med, Mexico City 06720, DF, Mexico
Gonzalez-Chavez, Antonio:
Gen Hosp Mexico Dr Eduardo Liceaga, Dept Internal Med, Mexico City 06720, DF, Mexico
Perez-Tamayo, Ruy:
Univ Nacl Autonoma Mexico, Unit Expt Med, Sch Med, Gen Hosp Mexico Dr Eduardo Liceaga, Mexico City 06720, DF, Mexico
Salazar-Vazquez, Beatriz Y.:
Univ Nacl Autonoma Mexico, Unit Expt Med, Sch Med, Gen Hosp Mexico Dr Eduardo Liceaga, Mexico City 06720, DF, Mexico
Hernandez, Vito S.:
Univ Nacl Autonoma Mexico, Dept Physiol, Sch Med, Mexico City 04510, DF, Mexico
Garibay-Nieto, Nayeli:
Gen Hosp Mexico Dr Eduardo Liceaga, Dept Human Genet, Mexico City 06720, DF, Mexico
Manuel Fragoso, Jose:
Natl Inst Cardiol Ignacio Chavez, Dept Mol Biol, Mexico City 14080, DF, Mexico
Escobedo, Galileo:
Univ Nacl Autonoma Mexico, Unit Expt Med, Sch Med, Gen Hosp Mexico Dr Eduardo Liceaga, Mexico City 06720, DF, Mexico
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