GH ameliorates impaired glucose tolerance in obese mice by modifying the visceral fat condition through adiponectin
Y Okamoto, M Fukushima, S Ishii, M Okamoto, H Katsumata & S Minami
Objectives: Secretion of GH, a pituitary and anabolic hormone that reduces visceral fat, is diminished in obese or elderly subjects. The reduced GH may induce visceral fat accumulation and subsequently accelerate metabolic syndrome in these population. In the present study, we sought the effect of chronic GH supplement on visceral fat and glucose metabolism in diet-induced obese (DIO) mice.
Methods and results: Male obese mice (C57BL/6, 12 weeks old) under high fat/high sucrose (HF/HS) diet were treated with daily injection of GH (5 μg/g body weight, n=6) or PBS (control, n=6) for 6 weeks. GH markedly reduced the mass of epididymal fat (Epi; PBS: 1.68±0.14 vs GH: 1.13±0.04 g, P<0.0001) and increased that of skeletal (gastrocnemius) muscle (PBS: 0.31±0.01 vs GH: 0.36±0.02 g, P<0.0001). Intra-peritoneal glucose tolerance test (IPGTT) demonstrated that GH dramatically ameliorated the impaired glucose tolerance (IGT) in the DIO mice. Real-time quantitative PCR analyses with Epi showed that GH significantly increased the expressions of adiponectin (40.8%, P<0.05), anti-inflammatory M2 macrophage markers (IL10: 66.4%, P<0.05; CD206: 41.4%, P<0.01), anti-oxidant enzyme (glutathione peroxidase: 36.6%, P<0.05) compared with control. Moreover, GH lowered the plasma levels of thiobarbituric acid reactive substance (TBARS), an oxidative stress marker, by 22.1% (PBS: 4.48±0.23 vs GH: 3.49±0.17 μM, P<0.05), in the DIO mice. However, in adipoectin-deficient mice under HF/HS diet, GH supplement neither changed the mass of Epi and skeletal muscle, nor modified IGT.
Conclusion: Chronic GH supplement mitigates IGT in DIO mice by modifying visceral fat mass, inflammation and oxidative stress likely through adiponectin.
Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.
Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.