Abstract
This study aimed to investigate the expression of C1q/TNF-related protein-3 (CTRP3) in rats at different pathogenic stages of type 2 diabetes mellitus (T2DM) and the impacts of glucagon-like peptide-1 (GLP-1) receptor agonist on it. Male wistar rats were fed with high-fat diet for 10 weeks to induce insulin resistance (IR) and then were given low-dose streptozotocin (STZ) intraperitoneal injection to induce T2DM. Exendin-4 (Ex-4), a GLP-1 receptor agonist, was subcutaneous injected to the IR rats and T2DM rats for 4 weeks. The expression of CTRP3 mRNA and protein in epididymis adipose tissue of rats at the stage of IR was lower significantly than that of normal control (NC) rats and decreased more when they were at the stage of overt T2DM (all P < 0.05 or P < 0.01). After the treatment with Ex-4, the mRNA and protein expressions of CTRP3 were increased by 15.5% (P < 0.01) and 14.8% (P < 0.05), respectively, in IR rats and increased by 20.6% (P < 0.01) and 16.5% (P < 0.05), respectively, in T2DM rats. Overall, this study found that the expression of CTRP3 in visceral adipose tissue was progressively decreased in a T2DM rat model from the pathogenic stage of IR to overt diabetes, while Ex-4 treatment increased its expression in such animals.
Highlights
Type 2 diabetes mellitus (T2DM) is a chronic disease characterized by insulin resistance and pancreatic islet beta cells dysfunction
Many studies have shown that rats fed with high-fat diet develop insulin resistance but not frank hyperglycemia or diabetes, indicating that high-fat diet might be a good way to initiate insulin resistance which is one of the important features and motivators of T2DM [15]
It is well known that high-dose STZ severely impairs insulin secretion, mimicking type 1 diabetes mellitus, and low-dose STZ after high-fat diet feeding induces a mild damage to beta cells on the background of insulin resistance, which is similar to the features of T2DM pathogenesis [16]
Summary
Type 2 diabetes mellitus (T2DM) is a chronic disease characterized by insulin resistance and pancreatic islet beta cells dysfunction. The T2DM pathogenesis represents the combined effects of genetics, nutrition, and lifestyle and involves both gene-gene and gene-environment interactions [1]. It is well known that white adipose tissue is serving as a long-term energy store and as an active endocrine organ that secretes a number of bioactive molecules called adipokines [3]. In addition to being important regulators of adipose tissue development and function, adipokines have significant impacts on glucose metabolism in various tissues [4]. Abnormal expression and secretion of some adipokines in adiposity are strongly associated with the development and progression of insulin resistance and pancreatic islet beta cell dysfunction, which gradually and lead to the pathogenesis of T2DM
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