Diana Vega-Galaviz1, Georgina Del Vecchyo-Tenorio1,2, Raúl Alcántara-Suárez1, Lucia A Méndez-García1, Ana L Sánchez-Del Real1, Rafael Villalobos-Molina3,4, José M Fragoso5, Sonia León-Cabrera6, Pedro Ostoa-Saloma7, Ruy Pérez-Tamayo2, Galileo Escobedo1. 1. Laboratory for Proteomics & Metabolomics, Research Division, General Hospital of Mexico 'Dr. Eduardo Liceaga', 06720 Mexico City, Mexico. 2. Unidad de Investigación en Medicina Experimental, Facultad de Medicina, Universidad Nacional Autónoma de México, Mexico City, Mexico. 3. Unidad de Biomedicina, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México, Mexico. 4. Departamento de Bioquímica, Facultad de Medicina, Universidad Nacional Autónoma de México, Mexico City, Mexico. 5. Departamento de Biología Molecular, Instituto Nacional de Cardiología 'Ignacio Chávez', Mexico City, Mexico. 6. Carrera de Médico Cirujano, Unidad de Biomedicina, Facultad de Estudios Superiores-Iztacala, Universidad Nacional Autónoma de México, Avenida de los Barrios 1, Los Reyes Iztacala 54090, Mexico. 7. Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, Mexico.
Abstract
Aim: Glucose intolerance associates with M1/M2 macrophage unbalance. We thus wanted to examine the effect of M2 macrophage administration on mouse model of glucose intolerance. Materials & methods: C57BL/6 mice fed a high-fat diet (HFD) for 12 weeks and then received thrice 20 mg/kg streptozotocin (HFD-GI). Bone marrow-derived stem cells were collected from donor mice and differentiated/activated into M2 macrophages for intraperitoneal administration into HFD-GI mice. Results: M2 macrophage treatment abolished glucose intolerance independently of obesity. M2 macrophage administration increased IL-10 in visceral adipose tissue and serum, but showed no effect on serum insulin. While nitric oxide synthase-2 and arginase-1 remained unaltered, M2 macrophage treatment restored AKT phosphorylation in visceral adipose tissue. Conclusion: M2 macrophage treatment abolishes glucose intolerance by increasing IL-10 and phosphorylated AKT.
Aim: Glucose intolerance associates with M1/M2 macrophage unbalance. We thus wanted to examine the effect of M2 macrophage administration on mouse model of glucose intolerance. Materials & methods: C57BL/6 mice fed a high-fat diet (HFD) for 12 weeks and then received thrice 20 mg/kg streptozotocin (HFD-GI). Bone marrow-derived stem cells were collected from donormice and differentiated/activated into M2 macrophages for intraperitoneal administration into HFD-GI mice. Results: M2 macrophage treatment abolished glucose intolerance independently of obesity. M2 macrophage administration increased IL-10 in visceral adipose tissue and serum, but showed no effect on serum insulin. While nitric oxide synthase-2 and arginase-1 remained unaltered, M2 macrophage treatment restored AKT phosphorylation in visceral adipose tissue. Conclusion: M2 macrophage treatment abolishes glucose intolerance by increasing IL-10 and phosphorylated AKT.
Authors: Marcos Andre Rodrigues da Costa Santos; Jhenifer Santos Dos Reis; Carlos Antonio do Nascimento Santos; Kelli Monteiro da Costa; Pedro Marçal Barcelos; Karen Queiroz de Oliveira Francisco; Pedro Antônio Guimarães Notaroberto Barbosa; Emanuelle Damasceno Souza da Silva; Celio Geraldo Freire-de-Lima; Alexandre Morrot; Debora Decote-Ricardo; Israel Diniz-Lima; Jose Osvaldo Previato; Lucia Mendonca-Previato; Leonardo Marques da Fonseca; Leonardo Freire-de-Lima Journal: Immunol Res Date: 2022-10-05 Impact factor: 4.505
Authors: Sandra Pereira; Daemon L Cline; Melissa Chan; Kalin Chai; Ji Soo Yoon; Shannon M O'Dwyer; Cara E Ellis; Maria M Glavas; Travis D Webber; Robert K Baker; Suheda Erener; Scott D Covey; Timothy J Kieffer Journal: Sci Rep Date: 2021-09-15 Impact factor: 4.379