AIM:To explore the therapeutic role of globular adiponectin (gAd) in high-fat diet/streptozotocin (STZ)-induced type 2 diabetic rats with nonalcoholic fatty liver disease (NAFLD). METHODS:Seven rats were fed a basic diet (normal control group; NC) during the experiment. Experimental rats (14 rats) were given a high-fat diet for 4 wk and were then injected with STZ to induce type 2 diabetes mellitus (T2DM) and NAFLD. Half of the T2DM/NAFLD rats were randomly injected intraperitoneally with gAd for 7 d (gAd-treated group), while the other 7 rats (T2DM/NAFLD group) received 0.9% saline. Plasma biochemical parameters and insulin concentrations were measured. Liver histopathology was examined RANDOMIZED CONTROLLED TRIAL 14950October 28, 2014|Volume 20|Issue 40| WJG|www.wjgnet.com by hematoxylin-eosin staining. Insulin receptor expression in the liver was analyzed by immunohistochemical staining, Western blot and quantitative real-time reverse transcription polymerase chain reaction analysis. RESULTS:Compared to the control group, the T2DM/ NAFLD group had increased levels of glucolipid and decreased levels of insulin. Plasma glucose and lipid levels were decreased in the gAd-treated group, while serum insulin levels increased. The expression of insulin receptor in the T2DM/NAFLD group increased compared with the NC group, and gAd downregulated insulin receptor expression in the livers of T2DM/NAFLD rats. Steatosis of the liver was alleviated in the gAd-treated group compared to the T2DM/NAFLD group (NAS 1.39 ± 0.51 vs 1.92 ± 0.51, P < 0.05). CONCLUSION:Globular adiponectin exerts beneficial effects in T2DM rats with NAFLD by promoting insulin secretion, mediating glucolipid metabolism, regulating insulin receptor expression and alleviating hepatic steatosis.© 2014 Baishideng Publishing Group Inc. All rights reserved.Key words: Adiponectin; Insulin secretion; Insulin receptor; Steatosis Core tip: Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease and is closely associated with obesity and type 2 diabetes mellitus (T2DM). Adiponectin is a fat-derived hormone with anti-diabetic properties, and evidence indicates that adiponectin plays a protective role in NAFLD. Our study focused on the beneficial roles of adiponectin in T2DM rats with NAFLD as a potential therapeutic target. The findings demonstrated that adiponectin exerts its beneficial effects in T2DM rats with NAFLD by promoting insulin secretion, mediating glucolipid metabolism, regulating insulin receptor expression and alleviat- where they were housed in individual cages maintained under ambient temperature (25 ℃ ± 2 ℃) with a 12/12 h light/dark cycle and ad libitum access to water and food. The rats were randomly assigned to three groups: an NC group, comprising normal control rats (n = 7); a T2DM/NAFLD group, comprising type 2 diabetic rats with NAFLD (n = 7); and a gAd-treated group, comprising type 2 diabetic rats with NAFLD that were treated with gAd (n = 7). After a week of acclimation, the T2DM rats were ad...

Aims. To evaluate the effects of globular adiponectin (gAd) on treatment of type 2 diabetic rats combined with NAFLD. Materials and Methods. Twenty-one male wistar rats were fed with normal diet (7 rats) or high fat diet (HFD) (14 rats) for 4 weeks, and then HFD-fed rats were injected with streptozotocin (STZ) to induce type 2 diabetes mellitus (T2DM). Half of T2DM rats were randomly injected with gAd intraperitoneally for 7 days. The expressions of adiponectin receptors (adipoR1/R2) in liver and skeletal muscle tissues were detected through western blotting or RT-qPCR, respectively. Results. Globular adiponectin alleviated the hepatic steatosis and increased insulin secretion. In liver, both the protein and mRNA expressions of adipoR2 in T2DM group decreased (P < 0.05, resp.) in contrast to NC group and increased (P < 0.05 and P < 0.001, resp.) after gAd treatment. But the protein and mRNA expressions of adipoR1 increased (P < 0.05, resp.) in T2DM group and no change was found in the gAd-treated group. In skeletal muscle, the protein and mRNA expressions of adipoR1 and adipoR2 were upregulated in T2DM group and were downregulated after gAd treatment. Conclusions. Globular adiponectin could ameliorate the hepatic steatosis and vary the expressions of adiponectin receptors in liver and skeletal muscle by stimulating insulin secretion.

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