Intracerebroventricular injection of adiponectin regulates locomotor activity in rats

Abstract

Enhancing exercise motivation is the best way to prevent obesity and diabetes. In this study, we examined whether adiponectin affects locomotion activity in Wister and Spontaneously-Running Tokushima-Shikoku (SPORTS) rats using two types of behavioral assays: home cage and wheel running activity. SPORTS rats were established from an original line from Wister strain that had shown high level of wheel running activity in our laboratory. Injection of adiponectin into the lateral ventricle of Wister rats and SPORTS rats decreased home cage activity, but no change was observed in the food intake and oxygen consumption. This result indicates the possibility that adiponectin can reduce non-exercise activity thermogenesis (NEAT) and physical activity via the central nervous system. In contrast, injection of adiponectin did not change wheel running activity in SPORTS rats. We produced hypothalamus-destructed model rat using monosodium glutamate (MSG) to elucidate the regulation site of adiponectin. Injection of adiponectin into MSG-treated SPORTS rats did not change amount of home cage activity and food intake, suggesting that adiponectin action on home cage activity was in the hypothalamic area. These results suggest that adiponectin regulates locomotion activity through mediobasal hypothalamus.

Adiponectin Protects against Glutamate‐Induced Excitotoxicity via Activating SIRT1‐Dependent PGC‐1α Expression in HT22 Hippocampal Neurons

“…Even though human-derived APN has been successfully synthesized, it is hard to investigate its neuroprotective effects through intravenous injection, as its relatively large size prevents it from passing through the blood-brain barrier. Due to this setback, APN knockout mice, adenovirus-mediated supplementation of APN, and intracerebroventricular injection of APN have been the primary methods of previous research [17, 20, 21]. In the present study, we used a variant of APN peptide that was synthesized according to the APN amino acid sequence and has been shown to simulate APN function.…”

Acute physical exercise increases the adaptor protein APPL1 in the hypothalamus of obese mice

“…All these actions were dependent on AdipoR1, since inhibition of this receptor, and not of AdipoR2, completely reversed the effects described above. On the order hand, another previous study [3] using rats as animal model indicated other central effects of adiponectin on spontaneous activity, showing that these central effects might depend on the species since in our study the analyses were performed with Swiss mice. Additionally, in our study, there was no difference in the hypothalamic content of APPL2, a protein with a counter-regulatory effect on the insulin pathway [32].…”

“…The hypothalamus receives peripheral stimuli during the food intake and thermogenesis regulation [2]. Among these stimuli, we can highlight the action of adipokines and hormones (adiponectin and leptin) for adequate energy metabolism regulation [2,3].…”

“…However, Coope and colleagues showed that AdipoR1 mediates the anorectic and insulin/leptin-like actions of adiponectin in the hypothalamus of Wistar rats [2]. In parallel, a previous study indicated other central effects of adiponectin on energy balance by regulating locomotor activity in rats [3]. Therefore, the molecular pathway underlying the anorectic effect of adiponectin is not yet fully elucidated.…”

“…Although the role of adiponectin in the central nervous system (CNS) has been previously explored [2,3], the effects of obesity and exercise on hypothalamic APPL1 protein levels are not known. Here we hypothesized that APPL1 might be crucial in the control of food intake.…”