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Original Articles
The Effect of Leptin Level Fluctuations by a Repeated Fasting/Refeeding on the Leptin Sensitivity in OLETF Rats.
Sung Chul Park, Yong Hoon Park, So Young Park, Jong Yeon Kim, Yoon Ki Park, Tae Hyung Lee, Kyu Chang Won, Yong Woon Kim
J Korean Endocr Soc. 2008;23(5):310-318.   Published online October 1, 2008
DOI: https://doi.org/10.3803/jkes.2008.23.5.310
  • 2,631 View
  • 33 Download
  • 4 Crossref
AbstractAbstract PDF
BACKGROUND
Leptin resistance is a common feature in obese subjects and animals, and this is commonly accompanied with hyperleptinemia. We speculated that one of the causes of leptin resistance is a persistently elevated leptin concentration and then we hypothesized that fluctuations of serum leptin would increase leptin sensitivity in the leptin-resistant state. METHODS: We used a repeated fasting and refeeding (RFR) protocol to produce fluctuation in leptin levels in 7 month-old Otsuka Long-Evans Tokushima Fatty (OLETF) rats and Long-Evans Tokushima Otsuka (LETO) rats, We then measured the leptin sensitivity following an intracerebroventricular (i.c.v.) infusion of leptin. RESULTS: The OLETF rats exhibited severe visceral fat deposition, hyperleptinemia and leptin resistance. However, in the OLETF-RFR rats, the anorexic effect following i.c.v. leptin infusion was restored. Moreover, the visceral fat mass and serum leptin levels decreased, while the serum adiponectin levels were elevated in the OLETF-RFR rats compared to the OLETF-Control rats. The leptin receptor content in the hypothalamus increased in the OLETF-RFR rats compared to the OLETF-Control rats, and the leptin receptor content in the OLETF-RFR rats decreased compared to that in the the LETO-Control rats. CONCLUSION: These results suggest that the intermittent suppression of the serum leptin level reversed the leptin resistance in OLEFT rats, and this may have occurred due to an increased number of leptin receptors in the hypothalamus.

Citations

Citations to this article as recorded by  
  • Reduced Striatal Dopamine Transporter Availability and Heightened Response to Natural and Pharmacological Stimulation in CCK-1R-Deficient Obese Rats
    Sevag Hamamah, Andras Hajnal, Mihai Covasa
    International Journal of Molecular Sciences.2023; 24(11): 9773.     CrossRef
  • Improvement of Leptin Resistance
    Yong Woon Kim
    Yeungnam University Journal of Medicine.2013; 30(1): 4.     CrossRef
  • The Effect of Food Restriction on Appetite Regulating Hormones and Adiponectin Activity
    Ki Hoon Kim, Hyun Kook Kim
    Korean Journal of Nutrition.2012; 45(1): 5.     CrossRef
  • The Effect of Leptin Level Fluctuations by a Repeated Fasting/Refeeding on the Leptin Sensitivity in OLETF Rats
    Min Seon Kim
    Journal of Korean Endocrine Society.2008; 23(5): 298.     CrossRef
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Fos Expression Induced by Combined Injection of Leptin and Cholecystokinin in the Rat Brain.
Young Uck Kim, Kyung Suk You, Ho Suck Kang, Choon Hee Chung, Tae Sun Hwang
J Korean Endocr Soc. 2002;17(4):486-500.   Published online August 1, 2002
  • 1,282 View
  • 19 Download
AbstractAbstract PDF
BACKGROUND
Several studies have reported that cholecystokinin (CCK), a short-term meal related satiety signal, and leptin, long-term signal for controlling feeding behaviour and body weight, act synergistically to inhibit food intake. However the mechanism and neuroanatomical basis for this response remain unclear. To clarify the neuronal mechanisms underlying the synergistic interaction between leptin and CCK, we examined the neuron activated by single or combined injection of leptin and CCK in fasted rats using immunohistochemistry for Fos. The expression of Fos can be used to trace neuronal activation pathways. METHODS: The rats were divided into 4 groups; Tris solution-saline, Tris solution-CCK, leptin-saline, leptin-CCK. Rats were received a single intracerebroventricular injection of either 3mul Tris solution or 3microgram leptin, and a single intraperitoneal injection of either 2mul saline or 2microgram/kg sulfated CCK-8. The changes of the Fos expression were investigated in the paraventricular nucleus (Pa), retrochiasmatic area (RCh), lateral hypothalamic nucleus (LH), central nucleus of amygdala(Ce), supraoptic nucleus (SO), arcuate nucleus (Arc), ventromedial hypothalamic nucleus(VMH),dorsomedial hypothalamic nucleus (DM), ventral premammillary nucleus (PMV), superior lateral subdivision of parabrachial nucleus (LPBS), external lateral subdivision of parabrachial nucleus (LPBE), supragenual nucleus (SGe), area postrema (AP), medial area (SolM) and commissural area (SolC) of nucleus of the solitary tract nuclei. RESULTS: CCK increased the Fos expression in the Pa, RCh, LH, Ce, SO, Arc, VMH, DM, PMV, LPBS, LPBE and SolM. Leptin increased the Fos expression in the Pa, RCh, LH, SO, Arc, VMH, DM, PMV, LPBS, LPBE, SGe, AP and SolM. Injections of leptin and CCK significantly enhanced the Fos expression in the Pa, RCh, VMH, DM, LPBS, and SolM compared with those induced by leptin or CCK alone. CONCLUSION: Our results suggest that the Pa, RCh, VMH, DM, LPBS and SolM may be essential sites mediating the synergistic effect of leptin and CCK to regulate food intake.
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Changes in Plasma Leptin Levels Relating to Short-Term Thyroid Manipulation in Rats.
Min Seon Kim, Cho Ya Yoon, Young Min Cho, Hye Seung Jung, Chan Soo Shin, Kyong Soo Park, Seong Yeon Kim, Bo Youn Cho, Hong Kyu Lee, Stephen R Bloom
J Korean Endocr Soc. 2002;17(2):197-205.   Published online April 1, 2002
  • 1,341 View
  • 21 Download
AbstractAbstract PDF
BACKGROUND
Leptin, an adipocyte derived hormone, and thyroid hormone have similar effects on energy homeostasis, such that a shortage of both hormones is associated with decreased energy expenditure and increased body weight. Therefore, for the maintenance of energy homeostasis may require a close interaction between leptin and thyroid hormone. This study was performed to investigate the change in plasma leptin levels relating to short-term thyroid manipulation causing no significant change in body weight. METHODS: Hypothyroidism was induced by surgical thyroidectomy and hyperthyroidism by subcutaneous injection of 50 g of L-T3/100 g body weight/day, for 5 days, in 6~8 weeks old male Wistar rats. Body weights and food intakes were monitored daily until sacrifice. Plasma samples were collected, and the thyroid stimulating hormone (TSH), free triiodothyronine (T3) and leptin levels measured. The plasma leptin levels in rats with hypothyroidism and hyperthyroidism were compared with those of body weights at death and food intakes during the study, atched controls. RESULTS: The rats treated with L-T3 consumed equal amount of food as freely fed, rats but their final body weights were significantly lower (L-T3 treated 220.0 +/- 1.8 vs. freely fed 226.0 +/- 2.0 g, p<0.05). There was no difference in food intake during study, and final body weight, between the thyroidectomised rats and their paired controls (thyroidectomised 220.4 +/- 1.7 vs. paired 223.9 +/- 4.7 g, P=NS). Plasma leptin levels in the L-T3 treated rats were significantly lower than those in freely fed rats (L-T3 treated 1.7 +/- 0.1 vs. freely fed 4.8 +/- 0.2 ng/ml, p<0.005). Conversely, the thyroidectomised rats had higher plasma leptin levels, compared to those of their paired controls (thyroidectomised 4.8 +/- 0.3 vs. paired 1.7 +/- 0.1 ng/ml, p<0.005). CONCLUSION: The Plasma leptin levels in the rats were decreased by short term hyperthyroidism, while they were increased by short term hypothyroidism. These findings suggest that thyroid hormones may affect the production or secretion of leptin
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Endocrinol Metab : Endocrinology and Metabolism
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