TY - JOUR
T1 - Similar metabolic responses to calorie restriction in lean and obese Zucker rats
AU - Chiba, Takuya
AU - Komatsu, Toshimitsu
AU - Nakayama, Masahiko
AU - Adachi, Toshiyuki
AU - Tamashiro, Yukari
AU - Hayashi, Hiroko
AU - Yamaza, Haruyoshi
AU - Higami, Yoshikazu
AU - Shimokawa, Isao
N1 - Funding Information:
We are grateful to Dr. Masashi Tanaka (Tokyo Metropolitan Institute of Gerontology) for helpful discussion. We are also grateful to the staff at the Biomedical Research Center at Center for Frontier Life Sciences, Nagasaki University, for technical assistance and animal care. We thank Yutaka Araki and Yuko Moriyama for technical assistance. We acknowledge the editorial support of Dr. Gregor Stewart. This work was supported in part by a Grant-in-Aid for Young Scientists (B) from the Japan Society for the Promotion of Science Nos. 17790269 and 20790306 (T.C.), the Japan Health Foundation (T.C.), and Nagasaki University, Japan (T.C.).
PY - 2009/10/15
Y1 - 2009/10/15
N2 - Calorie restriction (CR), which is thought to be largely dependent on the neuroendocrine system modulated by insulin/insulin-like growth factor-I (IGF-I) and leptin signaling, decreases morbidity and increases lifespan in many organisms. To elucidate whether insulin and leptin sensitivities are indispensable in the metabolic adaptation to CR, we investigated the effects of CR on obese Zucker (fa/fa) rats and lean control (+/+) rats. CR did not fully improve insulin resistance in (fa/fa) rats. Nonetheless, CR induced neuropeptide Y (NPY) expression in the hypothalamic arcuate nucleus and metabolism related gene expression changes in the liver in (fa/fa) rats and (+/+) rats. Up-regulation of NPY augmented plasma corticosterone levels and suppressed pituitary growth hormone (GH) expression, thereby modulating adipocytokine production to induce tissue-specific insulin sensitivity. Thus, central NPY activation via peripheral signaling might play a crucial role in the effects of CR, even in insulin resistant and leptin receptor deficient conditions.
AB - Calorie restriction (CR), which is thought to be largely dependent on the neuroendocrine system modulated by insulin/insulin-like growth factor-I (IGF-I) and leptin signaling, decreases morbidity and increases lifespan in many organisms. To elucidate whether insulin and leptin sensitivities are indispensable in the metabolic adaptation to CR, we investigated the effects of CR on obese Zucker (fa/fa) rats and lean control (+/+) rats. CR did not fully improve insulin resistance in (fa/fa) rats. Nonetheless, CR induced neuropeptide Y (NPY) expression in the hypothalamic arcuate nucleus and metabolism related gene expression changes in the liver in (fa/fa) rats and (+/+) rats. Up-regulation of NPY augmented plasma corticosterone levels and suppressed pituitary growth hormone (GH) expression, thereby modulating adipocytokine production to induce tissue-specific insulin sensitivity. Thus, central NPY activation via peripheral signaling might play a crucial role in the effects of CR, even in insulin resistant and leptin receptor deficient conditions.
KW - Glucose and lipid metabolism
KW - Hypothalamus
KW - Neuroendocrine
KW - Oxidative stress
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U2 - 10.1016/j.mce.2009.05.001
DO - 10.1016/j.mce.2009.05.001
M3 - Article
C2 - 19446600
AN - SCOPUS:67651172791
SN - 0303-7207
VL - 309
SP - 17
EP - 25
JO - Molecular and Cellular Endocrinology
JF - Molecular and Cellular Endocrinology
IS - 1-2
ER -