OBJECTIVE: Obesity commonly causes hepatic lipid accumulation that may favor oxidative stress and inflammation with negative clinical impact. Acylated ghrelin (A-Ghr) modulates body lipid distribution and metabolism, and it may exert antioxidant effects in vitro as well as systemic anti-inflammatory effects in vivo. The impact of A-Ghr on liver triglyceride content, redox state and inflammation markers in diet-induced obesity was investigated. DESIGN AND METHODS: A-Ghr (200-μg/injection: HFG) or saline (HF) were administered subcutaneously twice-daily for 4 days to 12-week-old male rats fed a high-fat diet for 1 month (n = 8-10/group). RESULTS: Compared to lean animals, liver triglyceride accumulation occurred in HF despite enhanced phosphorylation of the lipid oxidation regulator AMPK and preserved mitochondrial enzyme activities. High triglycerides were accompanied by pro-oxidant changes in redox state and proinflammatory changes in NF-kB and TNF-alpha. A-Ghr limited liver triglyceride excess (P < 0.05 HF > HFG > Control) with concomitant activation of glutathione peroxidase and normalized redox state and cytokines. A-Ghr-induced liver changes were associated with higher plasma adiponectin and lower circulating fatty acids (P < 0.05 HFG vs. HF). CONCLUSIONS: A-Ghr limits liver triglyceride accumulation and normalizes tissue redox state and inflammation markers in diet-induced obese rats. These results suggest a favorable impact of A-Ghr on hepatic complications of diet-induced obesity.

Acylated Ghrelin Limits Fat Accumulation and Improves Redox State and Inflammation Markers in the Liver of High-Fat-Fed Rats.

BARAZZONI, ROCCO;SEMOLIC, ANNA MARIA;ZANETTI, MICHELA;GUARNIERI, GIANFRANCO
2014

Abstract

OBJECTIVE: Obesity commonly causes hepatic lipid accumulation that may favor oxidative stress and inflammation with negative clinical impact. Acylated ghrelin (A-Ghr) modulates body lipid distribution and metabolism, and it may exert antioxidant effects in vitro as well as systemic anti-inflammatory effects in vivo. The impact of A-Ghr on liver triglyceride content, redox state and inflammation markers in diet-induced obesity was investigated. DESIGN AND METHODS: A-Ghr (200-μg/injection: HFG) or saline (HF) were administered subcutaneously twice-daily for 4 days to 12-week-old male rats fed a high-fat diet for 1 month (n = 8-10/group). RESULTS: Compared to lean animals, liver triglyceride accumulation occurred in HF despite enhanced phosphorylation of the lipid oxidation regulator AMPK and preserved mitochondrial enzyme activities. High triglycerides were accompanied by pro-oxidant changes in redox state and proinflammatory changes in NF-kB and TNF-alpha. A-Ghr limited liver triglyceride excess (P < 0.05 HF > HFG > Control) with concomitant activation of glutathione peroxidase and normalized redox state and cytokines. A-Ghr-induced liver changes were associated with higher plasma adiponectin and lower circulating fatty acids (P < 0.05 HFG vs. HF). CONCLUSIONS: A-Ghr limits liver triglyceride accumulation and normalizes tissue redox state and inflammation markers in diet-induced obese rats. These results suggest a favorable impact of A-Ghr on hepatic complications of diet-induced obesity.
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11368/2691817
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