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Endocrinol Metab : Endocrinology and Metabolism


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Jin Young Kim  (Kim JY) 3 Articles
Adrenal gland
Highly Palatable Food during Adolescence Improves Anxiety-Like Behaviors and Hypothalamic-Pituitary-Adrenal Axis Dysfunction in Rats that Experienced Neonatal Maternal Separation
Jong-Ho Lee, Jin Young Kim, Jeong Won Jahng
Endocrinol Metab. 2014;29(2):169-178.   Published online June 26, 2014
  • 3,502 View
  • 34 Download
  • 20 Web of Science
  • 18 Crossref
AbstractAbstract PDFPubReader   

This study was conducted to examine the effects of ad libitum consumption of highly palatable food (HPF) during adolescence on the adverse behavioral outcome of neonatal maternal separation.


Male Sprague-Dawley pups were separated from dam for 3 hours daily during the first 2 weeks of birth (maternal separation, MS) or left undisturbed (nonhandled, NH). Half of MS pups received free access to chocolate cookies in addition to ad libitum chow from postnatal day 28 (MS+HPF). Pups were subjected to behavioral tests during young adulthood. The plasma corticosterone response to stress challenge was analyzed by radioimmunoassay.


Daily caloric intake and body weight gain did not differ among the experimental groups. Ambulatory activities were decreased defecation activity and rostral grooming were increased in MS controls (fed with chow only) compared with NH rats. MS controls spent less time in open arms, and more time in closed arms during the elevated plus maze test, than NH rats. Immobility duration during the forced swim test was increased in MS controls compared with NH rats. Cookie access normalized the behavioral scores of ambulatory and defecation activities and grooming, but not the scores during the elevated plus maze and swim tests in MS rats. Stress-induced corticosterone increase was blunted in MS rats fed with chow only, and cookie access normalized it.


Prolonged access to HPF during adolescence and youth partly improves anxiety-related, but not depressive, symptoms in rats that experienced neonatal maternal separation, possibly in relation with improved function of the hypothalamic-pituitary-adrenal (HPA) axis.


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    Proceedings of the Nutrition Society.2020; 79(1): 113.     CrossRef
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    Daniel Wang, Jessica L. S. Levine, Victor Avila-Quintero, Michael Bloch, Arie Kaffman
    Translational Psychiatry.2020;[Epub]     CrossRef
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  • Animal models of gastrointestinal and liver diseases. Animal models of visceral pain: pathophysiology, translational relevance, and challenges
    Beverley Greenwood-Van Meerveld, Dawn K. Prusator, Anthony C. Johnson
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  • Articles in 'Endocrinology and Metabolism' in 2014
    Won-Young Lee
    Endocrinology and Metabolism.2015; 30(1): 47.     CrossRef
  • Anxiolytic efficacy of repeated oral capsaicin in rats with partial aberration of oral sensory relay to brain
    Young-Jun Choi, Jin Young Kim, Wei-Peng Jin, Yoon-Tae Kim, Jong-Ho Lee, Jeong Won Jahng
    Archives of Oral Biology.2015; 60(7): 989.     CrossRef
  • Anti-Anxiety Effect of Schisandra chinensis Baill Lignans on Mice in Elevated Plus Maze Test
    Tao Jiang, Xin Tian Fan, Chun Mei Wang, Li Mei Chen, Jing Hui Sun, Wei Jing Sun, Jian Guang Chen, He Li
    Applied Mechanics and Materials.2014; 675-677: 1580.     CrossRef
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KAL Gene and GnRH Receptor Gene Analysis in Patients with Kallmann's Syndrome.
Ki Hyun Park, Hyoung Jin Mo, Jin Young Kim, Jeong Yeon Kim, Sang Wook Bae, Byung Seok Lee, In Kyu Kim, Sei Kwang Kim, Kyung Ah Kim, Yong Ho Ahn
J Korean Endocr Soc. 1999;14(4):645-656.   Published online January 1, 2001
  • 1,066 View
  • 19 Download
AbstractAbstract PDF
Kallmann's syndrome is related to the defect in migration of olfactory neuron and GnRH neuron from the olfactory placode to the brain and it represents hypogonadism with anosmia or hyposmia. There are 3 modes of transmission in Kallmann's syndrome: X-linked, autosomal recessive and autosomal dominant. X-linked form is the most common. KAL gene is responsible for the X-linked form of Kallmann's syndrome and it had been localized to Xp22.3. The intron-exon organization had been determined and KAL gene mutation had also been identified in familial Kallmann's syndrome and it is very rare and shows heterogeneity. Furthermore, in the sporadic cases, KAL gene mutation is more rare. METHODS: In order to investigate the KAL gene mutation and the regulation of the gene expression in Kallmann's syndrome, we examined genomic DNA of 35 patients with sporadic Kallmann's syndrome. In the exon 3, 4, 5, 6, 7, 8, 9, 10, 11, 12 of KAL gene and 1, 2, 3 of GnRH receptor gene, the mutations were analyzed by PCR-based DNA sequencing. RESULTS: In our study, the mutation of KAL gene and GnRH receptor gene was not identified in the studied exons that were known as preferable sites of the mutation. CONCLUSION: The mutation of KAL gene and GnRH receptor gene is rare, and it might be needed to investigate mutations in other genes or in other part of the KAL gene such as intron or promoter region.
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A Case of Delayed Puberty due to Hypoplasia of Anterior Pituitary Gland with Pituitary Stalk Agenesis and Ectopic Neurohypophysis.
Seung Yong Shin, Jin Young Kim, Seung Jae Yoon, Sung Ki Kim, Seong Bin Hong, Yeo Joo Kim, Moon Suk Nam, Mi Rim Kim, Yong Seong Kim
J Korean Endocr Soc. 1999;14(3):578-586.   Published online January 1, 2001
  • 1,135 View
  • 28 Download
AbstractAbstract PDF
Hypopituitarism is not a common cause of delayed puberty, however it should always be considered, especially if there are such signs as severe dwarfism, dollish face, truncal obesity, small hands and feet, and microgenitalia. Either congenital or acquired, hypopituitarism can be resulted from hypothalamic and hypophyseal lesions. The clinical feature can be diverse depending on age of the patients, rate of progression, degree of hormone deficiency and characteristics of the lesion. The recent high interest in delayed puberty and the improved detection of hypothalamic hypophyseal lesions using combined pituitary fuction stimulation test, brain CT and MRJ, has made the differential diagnosis of hypopituitarism possible as the cause of delayed puberty. MRI has shown hypophyeal hypoplasia accompanied by anterior pituitary hypoplasia and ectopic neurohypophysis in some of the patients with hypopituitasm, and although the anatomical abnormality around the hypophysis in these patients is considered the reason for hypopituitarism, the pathogensis of which has not yet to be known. We, here, report a case of delayed puberty by hypopituitarism due to hypoplasia of anterior pituitary gland, pituitary stalk agenesis and ectopic neurohypophysis with brief review of the litereature.
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