Low-protein diet enhances adiponectin secretion in rats

ABSTRACT

Previous studies including ours have shown that a low-protein diet up-regulates insulin signaling in the liver and muscle and induces fatty liver in rats. Adiponectin is known as an insulin-sensitizing adipocytokine. We, therefore, examined the effect of a low-protein diet on the adiponectin levels in rats. The low-protein diet significantly increased serum adiponectin level. However, mRNA and protein levels of adiponectin in white adipose tissue (WAT) were not changed by the low-protein diet. Since it is known that oligomerization is important to control serum adiponectin level, we examined the population of adiponectin oligomeric forms in WAT and found that low-protein diet did not change it. Despite these events, the amount of its secretion was significantly increased in the adipocytes isolated from WAT of low-protein diet-fed rats. These results indicate that a low-protein diet enhances adiponectin secretion, which is not due to the increased intracellular amount and oligomerization of adiponectin.

Graphical abstract

Low-protein diet enhance adiponectin secretion, which is not due to the increased intracellular amount and oligomerization of adiponectin. These events could contribute to the enhancement of insulin sensitivity induced by a low-protein diet.

KEYWORDS:

• Low-protein diet
• adiponectin
• secretion
• white adipose tissue

Author contributions

Takashi Yagi conducted the experiments, analyzed the data, and wrote the manuscript. Yuka Toyoshima designed the study, conducted the experiments, analyzed the data, and wrote the manuscript. Reiko Tokita and Yusuke Taguchi conducted the experiments and analyzed the data. Yoshihisa Okamoto, Shin-Ichiro Takahashi, Hisanori Kato, and Shiro Minami wrote the manuscript. All authors discussed the data and reviewed the manuscript.

Acknowledgments

We thank Ms. Kanako Oki for her help with animal care. We are grateful for the discussions with Dr. Oksana Gavrilova (NIDDK, NIH) during the preparation of this manuscript. This work was partially supported by Grant-in-Aid for Young Scientist to Y. T. (JP25850095) from the Japan Society for Promotion of Science and by a grant to S. M. from Boehringer Ingelheim, Ono Pharmaceuticals, and Kyowa-Kirin.

Disclosure statement

No potential conflict of interest was reported by the authors.