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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Resilient hepatic mitochondria! function and lack of iNOS dependence in diet-induced insulin resistance

Full text
Author(s):
Kakimoto, Pamela A. [1] ; Chausse, Bruno [1, 2] ; Caldeira da Silva, Camille C. [1] ; Donato Junior, Jose Prime [3] ; Kowaltowski, Alicia J. [1]
Total Authors: 5
Affiliation:
[1] Univ Sao Paulo, Inst Quim, Dept Bioquim, Sao Paulo - Brazil
[2] Heidelberg Univ, Inst Physiol & Pathophysiol, Heidelberg - Germany
[3] Univ Sao Paulo, Inst Ciencia Biomed, Dept Fisiol & Biofis, Sao Paulo - Brazil
Total Affiliations: 3
Document type: Journal article
Source: PLoS One; v. 14, n. 2 FEB 4 2019.
Web of Science Citations: 1
Abstract

Obesity-derived inflammation and metabolic dysfunction has been related to the activity of the inducible nitric oxide synthase (iNOS). To understand the interrelation between metabolism, obesity and NO., we evaluated the effects of obesity-induced NO. signaling on liver mitochondrial function. We used mouse strains containing mitochondrial nicotinamide transhydrogenase activity, while prior studies involved a spontaneous mutant of this enzyme, and are, therefore, more prone to oxidative imbalance. Wild-type and iNOS knockout mice were fed a high fat diet for 2, 4 or 8 weeks. iNOS knockout did not protect against diet induced metabolic changes. However, the diet decreased fatty-acid oxidation capacity in liver mitochondria at 4 weeks in both wild-type and knockout groups; this was recovered at 8 weeks. Interestingly, other mitochondrial functional parameters were unchanged, despite significant modifications in insulin resistance in wild type and iNOS knockout animals. Overall, we found two surprising features of obesity-induced metabolic dysfunction: (i) iNOS does not have an essential role in obesity-induced insulin resistance under all experimental conditions and (ii) liver mitochondria are resilient to functional changes in obesity-induced metabolic dysfunction. (AU)

FAPESP's process: 13/07937-8 - Redoxome - Redox Processes in Biomedicine
Grantee:Ohara Augusto
Support Opportunities: Research Grants - Research, Innovation and Dissemination Centers - RIDC
FAPESP's process: 17/18972-0 - Multi-user equipment approved in grant 17/02983-2: minispec LF50 body composition mice analyzer
Grantee:Jose Donato Junior
Support Opportunities: Multi-user Equipment Program
FAPESP's process: 15/25862-0 - Hepatic bioenergetics and redox signaling in obesity murine model: integrative analysis of nutritional, hormonal, and inflammatory stimuli
Grantee:Pâmela Aiako Hypólito Brito Kakimoto
Support Opportunities: Scholarships in Brazil - Doctorate (Direct)
FAPESP's process: 15/07670-7 - Study of the metabolic reprograming sustaining microglial activation to inflammatory profiles
Grantee:Bruno Chausse de Freitas
Support Opportunities: Scholarships in Brazil - Post-Doctoral