Protective role of adiponectin against testicular impairment in high-fat diet/streptozotocin-induced type 2 diabetic mice

• Published in: Biochimie 2020-01, Vol.168, p.41-52
• Main Authors: Choubey, Mayank, Ranjan, Ashutosh, Bora, Puran S., Krishna, Amitabh
• Format: Article
• Language: English
• Subjects: Adiponectin; Adiponectin - pharmacology; Animals; Antioxidants; Antioxidants - pharmacology; Diabetes Mellitus, Experimental - drug therapy; Diabetes Mellitus, Experimental - pathology; Glucose - metabolism; Glucose Transport Proteins, Facilitative - metabolism; Insulin resistance; Lactic Acid - metabolism; Male; Mice; Oxidative Stress - drug effects; Receptor, Insulin - metabolism; Testicular impairment; Testis - drug effects; Testosterone - blood; Type 2 diabetes
• ISSN: 0300-9084; 1638-6183
• DOI: 10.1016/j.biochi.2019.10.014

Type 2 diabetes (T2D) is the most common endocrine and metabolic disorder, leading to reproductive impairments and infertility in male. Our recent study showed crucial role of adiponectin in the regulation of testicular functions, and the circulating level of adiponectin declines in diabetes. The current study thus aimed to examine the efficacy of adiponectin in improving testicular dysfunction in high-fat diet/streptozotocin-induced T2D mice. T2D was induced in pre-pubertal mice fed with high-fat diet for ∼10 weeks followed by a single dose of streptozotocin. T2D mice showed presence of increased body mass, hyperglycemia, hyperinsulinemia, insulin resistance, increased oxidative stress, and declined serum testosterone compared to vehicle-treated control mice. The spermatogenic, steroidogenic, metabolic, and antioxidative parameters were evaluated in T2D mice treated with adiponectin for both two and four weeks. The exogenous administration of adiponectin to T2D mice showed enhanced serum testosterone and expression of testicular steroidogenic markers proteins, insulin receptor and GLUT8 proteins, increase in intra-testicular concentrations of glucose and lactate and activity of LDH and antioxidant enzymes compared to the levels in untreated T2D mice. This suggests that treatment of adiponectin effectively improves testicular functions by increasing expression of insulin receptor-mediated increased transport of energy substrate (glucose and lactate) and a marked reduction in oxidative stress are the possible mechanism by which adiponectin effectively improves testicular function in T2D mice. •HFD/STZ-induced T2D mice exhibited marked decline in the expression of testicular adiponectin and its receptors proteins.•Adiponectin regulates glucose and lactate homeostasis and reduces apoptosis in the testis of HFD/STZ-induced T2D mice.•Adiponectin treatment ameliorates testicular steroidogenesis, metabolism, oxidative stress, and apoptosis in T2D mice.