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Abstract
Astragalus polysaccharide (APS) is an important bioactive component of Astragalus membranaceus which is used as an anti-diabetes herb in traditional Chinese medicine. The objective of this study was to investigate the effects and mechanisms of APS on insulin-sensitizing of adipocytes. Mouse 3T3-L1 preadipocytes were used as a model. The results showed that APS increased preadipocytes proliferation in a dose dependent manner, and 0.1 μg/mL APS sufficiently increased Proliferating Cell Nuclear Antigen (PCNA) content (p < 0.01). Moreover, APS enhanced intracellular lipid accumulation and mRNA expression of proliferator-activated receptor γ (PPARγ, p < 0.01), CCAAT/enhancer binding protein α (C/EBPα, p < 0.01) and fatty acid binding protein (aP2, p < 0.01). As expected, corresponding protein contents were elevated. Importantly, APS increased 2-(N-(7-Nitrobenz-2-oxa-1,3-diazol-4-yl)Amino)-2-Deoxyglucose (2-NBDG) uptake (p < 0.01). Meanwhile, both mRNA and protein content of glucose transporter 4 (Glut4) were elevated by APS (p < 0.01). The APS treatment enhanced tyrosine phosphorylation of insulin receptor substrate 1 (IRS1, p < 0.05) and phosphor-Akt content (p < 0.01). Besides, phosphorylated AMP-activated protein kinase (AMPK) content was increased in the APS treated cells (p < 0.01). Taken together, APS improved insulin sensitivity by enhancing glucose uptake, possibly through AMPK activation. These results suggested that APS might be a therapeutic candidate for insulin resistance.
Highlights
Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder, and its prevalence has been increasing steadily worldwide [1]
These results suggested that Astragalus polysaccharide (APS) might be a therapeutic candidate for insulin resistance
The effects of APS on cellular cytotoxicity were determined by a Lactate dehydrogenase (LDH)
Summary
Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder, and its prevalence has been increasing steadily worldwide [1]. T2DM patients have a lower insulin utilization ability in metabolic organs and tissues, leading to high blood glucose levels and other complications, such as obesity, hypertension, atherosclerosis, liver failure, and certain cancers [2]. Insulin resistance (IR) refers to the reduced biological efficacy of insulin on effector organs. IR and the consequences of declined glucose uptake and elimination in surrounding tissues, including the liver, skeletal muscle, and adipose tissues, are the main contributors of the T2DM pathogenesis [3]. Therapeutic agents that improve the insulin sensitivity have received considerable attention.
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