TY - JOUR
T1 - Metformin influences on respiratory system in obese mice induced by postnatal overnutrition
AU - Dias, Maycon Daniel
AU - Goulart, Melissa
AU - Dalécio, Cecilia
AU - Enes-Marques, Silvia
AU - Salles, Évila da Silva Lopes
AU - Venâncio, Marina
AU - Pereira, Elisângela Monteiro
AU - Paffaro, Valdemar Antonio
AU - Incerpi, Erika Kristina
AU - Soncini, Roseli
N1 - Funding Information:
Our work was partially supported by the Minas Gerais Research Foundation (FAPEMIG, process number APQ-01887-13 ) and Federal University of Alfenas, Minas Gerais ( UNIFAL-MG ). Additionally, we appreciate all technical support and animal care involved.
Publisher Copyright:
© 2017 Elsevier B.V.
PY - 2018/1
Y1 - 2018/1
N2 - Many studies have confirmed the merits of metformin to treat type 2 diabetes, but few studies have addressed its effect on the respiratory system. Moreover, vascular endothelial growth factor (VEGF) is critical to many lung functions. In this way, we evaluated the metformin impact on the lung in treated obese Swiss mice, induced by postnatal overnutrition. Glucose and insulin were detected and the insulin resistance index (HOMA) was calculated; inflammatory cells and nitrite/nitrate concentration (NOx) was quantified from bronchoalveolar lavage, collagen and lung VEGF-a was analysed in the lung tissue and lung mechanics were evaluated by methacholine-induced bronchoconstriction. Values of glucose, insulin, HOMA; VEGF-a and collagen demonstrate the partial ability of metformin to improve the effects of obesity. However, metformin is ineffective in re-establishing the inflammation, shows no effects on NOx and does not restore bronchoconstriction in obese mice. In conclusion, metformińs beneficial effects on lung are questionable in the postnatal overnutrition model of obesity.
AB - Many studies have confirmed the merits of metformin to treat type 2 diabetes, but few studies have addressed its effect on the respiratory system. Moreover, vascular endothelial growth factor (VEGF) is critical to many lung functions. In this way, we evaluated the metformin impact on the lung in treated obese Swiss mice, induced by postnatal overnutrition. Glucose and insulin were detected and the insulin resistance index (HOMA) was calculated; inflammatory cells and nitrite/nitrate concentration (NOx) was quantified from bronchoalveolar lavage, collagen and lung VEGF-a was analysed in the lung tissue and lung mechanics were evaluated by methacholine-induced bronchoconstriction. Values of glucose, insulin, HOMA; VEGF-a and collagen demonstrate the partial ability of metformin to improve the effects of obesity. However, metformin is ineffective in re-establishing the inflammation, shows no effects on NOx and does not restore bronchoconstriction in obese mice. In conclusion, metformińs beneficial effects on lung are questionable in the postnatal overnutrition model of obesity.
KW - Airway resistance
KW - Bronchoconstriction
KW - Insulin
KW - Obesity
KW - Vascular endothelial growth factor
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U2 - 10.1016/j.resp.2017.09.010
DO - 10.1016/j.resp.2017.09.010
M3 - Article
C2 - 28963087
AN - SCOPUS:85030317963
SN - 1569-9048
VL - 247
SP - 96
EP - 102
JO - Respiratory Physiology and Neurobiology
JF - Respiratory Physiology and Neurobiology
ER -
