| Literature DB >> 29247431 |
Gabriela Silva1, Cleber Ferraresi2,3, Rodrigo Teixeira de Almeida1, Mariana Lopes Motta1, Thiago Paixão1, Vinicius Oliveira Ottone1, Ivana Alice Fonseca1, Murilo Xavier Oliveira4, Etel Rocha-Vieira1, Marco Fabrício Dias-Peixoto1, Elizabethe Adriana Esteves1, Cândido Celso Coimbra1,5, Fabiano Trigueiro Amorim1,6, Flávio de Castro Magalhães7.
Abstract
Obesity represents a continuously growing global epidemic and is associated with the development of type 2 diabetes mellitus. The etiology of type 2 diabetes is related to the resistance of insulin-sensitive tissues to its action leading to impaired blood glucose regulation. Photobiomodulation (PBM) therapy might be a non-pharmacological, non-invasive strategy to improve insulin resistance. It has been reported that PBM therapy in combination with physical exercise reduces insulin resistance. Therefore, the aim of this study was to investigate the effects of PBM therapy on insulin resistance in obese mice. Male Swiss albino mice received low-fat control diet (n = 16, LFC) or high-fat diet (n = 18, HFD) for 12 weeks. From 9th to 12th week, the mice received PBM therapy (LASER) or Sham (light off) treatment and were allocated into four groups: LFC Sham (n = 8), LFC PBM (n = 8), HFD Sham (n = 9), and HFD PBM (n = 9). The PBM therapy was applied in five locations: to the left and right quadriceps muscle, upper limbs and center of the abdomen, during 40 s at each point, once a day, 5 days a week, for 4 weeks (780 nm, 250 mW/cm2, 10 J/cm2, 0.4 J per site; 2 J total dose per day). Insulin signaling pathway was evaluated in the epididymal adipose tissue. PBM therapy improved glucose tolerance and phosphorylation of Akt (Ser473) and reversed the HFD-induced reduction of GLUT4 content and phosphorylation of AS160 (Ser588). Also, PBM therapy reversed the increased area of epididymal and mesenteric adipocytes. The results showed that chronic PBM therapy improved parameters related to obesity and insulin resistance in HFD-induced obesity in mice.Entities:
Keywords: Glucose intolerance; Insulin resistance; Insulin signaling; Low-level laser therapy; Type 2 diabetes mellitus
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Year: 2017 PMID: 29247431 DOI: 10.1007/s10103-017-2408-2
Source DB: PubMed Journal: Lasers Med Sci ISSN: 0268-8921 Impact factor: 3.161