- Growth Hormone-Releaser Diet Attenuates Cognitive Dysfunction in Klotho Mutant Mice via Insulin-Like Growth Factor-1 Receptor Activation in a Genetic Aging Model
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Seok Joo Park, Yoon Hee Chung, Jeong Hyun Lee, Duy-Khanh Dang, Yunsung Nam, Ji Hoon Jeong, Yong Sun Kim, Toshitaka Nabeshima, Eun-Joo Shin, Hyoung-Chun Kim
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Endocrinol Metab. 2014;29(3):336-348. Published online September 25, 2014
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DOI: https://doi.org/10.3803/EnM.2014.29.3.336
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- Background
It has been recognized that a defect in klotho gene expression accelerates the degeneration of multiple age-sensitive traits. Accumulating evidence indicates that aging is associated with declines in cognitive function and the activity of growth hormone (GH)/insulin-like growth factor-1 (IGF-1). MethodsIn this study, we examined whether a GH-releaser diet could be effective in protecting against cognitive impairment in klotho mutant mice. ResultsThe GH-releaser diet significantly induced the expression of IGF-1 and IGF-1 receptors in the hippocampus of klotho mutant mice. Klotho mutant mice showed significant memory impairments as compared with wild-type mice. In addition, the klotho mutation significantly decreased the expression of cell survival/antiapoptotic factors, including phospho-Akt (p-Akt)/phospho-glycogen synthase kinase3β (p-GSK3β), phospho-extracellular signal-related kinase (p-ERK), and Bcl-2, but significantly increased those of cell death/proapoptotic factors, such as phospho-c-jun N-terminal kinase (p-JNK), Bax, and cleaved caspase-3 in the hippocampus. Treatment with GH-releaser diet significantly attenuated both decreases in the expression of cell survival/antiapoptotic factors and increases in the expression of cell death/proapoptotic factors in the hippocampus of klotho mutant mice. In addition, klotho mutation-induced oxidative stress was significantly attenuated by the GH-releaser diet. Consequently, a GH-releaser diet significantly improved memory function in the klotho mutant mice. GH-releaser diet-mediated actions were significantly reversed by JB-1, an IGF-1 receptor antagonist. ConclusionThe results suggest that a GH-releaser diet attenuates oxidative stress, proapoptotic changes and consequent dysfunction in klotho mutant mice by promoting IGF-1 expression and IGF-1 receptor activation.
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Citations
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- A Case of McCunt-Albright Syndrome Associated with Acremegaly and Fibrous Dysplasia.
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Jung Guk Kim, Sung Woo Ha, Sang Won Chung, Seong Mo Koo, Jae Tae Lee, Kyu Bo Lee, Yong Sun Kim, Sam Kwon, Bo Wan Kim
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J Korean Endocr Soc. 1998;13(1):108-114. Published online January 1, 2001
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- Acromegaly and hyperprolactinemia have been described in association with polyostotic fibrous dysplasia. The pathogenic mechanisms of this endocrinopathy are not clear. We experienced a 19-year-old male with hypersecretion of GH, hyperprolactinemia and fibrous dysplasia. He was referred for evaluation of suspected acromegaly. He had no skin pigmentation. Plasma GH, PRL, somatomedin-C, LH, FSH, testosterone, estradiol, progesterone, T3, T4, TSH and cortisol were measured. Among those, the levels of plasma GH, PRL and somatomedin-C were high. Serum alkaline phosphatase was increased. OGTT did not suppress plasma OH concentration and GH showed paradoxical response to TRH and LHRH. GH was suppressed after a test-dose of somatastatin and bromocriptine. Brain MRI demonstrated a mass lesion in sella turcica and another mass lesions in nasal cavity and posterior occipital bone. Whole body bone scan revealed increased uptake in skull, nasal bone, both 9th posterior rib, both femurs, both tibias, left scapular and pelvic bone. These fmdings were consistent with bone tumor such as fibrous dysplasia. We report a case with incomplete MeCune-Albright syndrome including acromegaly, hyperprolactinemia and polyostotic fibrous dysplasia.
- Slow virus and endocrine disease.
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Yong Sun Kim, Eun Kyoung Choi, I Carp Richar
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J Korean Endocr Soc. 1993;8(1):6-14. Published online January 1, 2001
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