Shigeki Kobayashi

Kitasato University, Edo, Tōkyō, Japan

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Publications (6)9.79 Total impact

  • Nihon Chikusan Gakkaiho 01/2012; 83(4):357-362. DOI:10.2508/chikusan.83.357
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    ABSTRACT: This study was conducted to examine the contributions of central and peripheral leptin to hyperphagia in lactation. Lactating rats were mated at 7-8 weeks of age and housed singly with their litters. In experiment 1, food intakes were significantly (P<0.01) greater (350% on average) in lactation than in non-lactation throughout a day. Cerebrospinal fluid (CSF) leptin levels remained constant despite plasma leptin levels being significantly (P<0.05) greater in non-lactation than in lactation. In experiment 2, CSF leptin levels were not altered by i.v. injections of leptin (0.2 and 0.4 mg/kg body weight) despite that plasma leptin levels were dose dependently (P<0.01) increased. Moreover, i.v. administration of leptin significantly (P<0.05) decreased food intake in non-lactating rats but not in lactating rats. In experiment 3, nocturnal food intakes were temporarily (P<0.05) reduced in non-lactating and lactating rats. I.c.v. administration of a leptin antagonist (15 μg) blocked the reductions of food intakes. I.c.v. administration of leptin (10 μg) significantly (P<0.05) decreased cumulative food intakes during 24 h in both the physiological states. In conclusion, this study has presented new evidence that the hyperphagia of lactating rats could be partly due to depressed sensitivity of neurons contacting blood leptin. In contrast, the responsiveness of leptin receptors contacting CSF leptin may not differ between non-lactating and lactating rats. Furthermore, the levels of CSF leptin remained constant independent of those of blood leptin. Therefore, the expression of hypothalamic leptin receptors contacting CSF could be involved in the difference in food intake between non-lactating and lactating rats.
    Journal of Endocrinology 10/2010; 207(1):105-11. DOI:10.1677/JOE-09-0463 · 3.59 Impact Factor
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    ABSTRACT: This study was conducted to investigate effects of glucagon intracerebroventricularly administered on feed intake and endocrine changes in sheep. Four male sheep (48-55 kg BW) were used. The animals were acclimatized to be fed alfalfa hay cubes at 12.00 hour. Human glucagon (40 and 80 microg/0.5 mL) was injected into the lateral ventricle at 12.00 hour. Blood samples were taken every 10 min from 30 min before to 180 min after the glucagon injection. Soon after the injection, the animals were given alfalfa hay cubes, and the amounts of the feed eaten within 2 h were measured. Feed intakes were significantly (P < 0.05) suppressed by 80 microg of glucagon. Plasma glucose levels in control animals were gradually decreased after the feeding, whilst those in glucagon-treated animals were temporarily elevated just after the feeding and then kept higher than control levels. Plasma insulin was abruptly elevated after the feeding and was maintained at higher levels than before the feeding in all treatments. Plasma NEFA concentrations were decreased after the feeding in all treatments. A tendency of increase in plasma cortisol levels occurred in glucagon-injected animals. The present study provides the first evidence that glucagon directly acts on the brain, then inhibiting feeding behavior and inducing endocrine responses in ruminants.
    Animal Science Journal 12/2009; 80(6):686-90. DOI:10.1111/j.1740-0929.2009.00685.x · 1.04 Impact Factor
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    ABSTRACT: The present study was conducted to investigate roles of ghrelin in glucose-induced insulin secretion in fasting- and meal-fed state in sheep. Castrated Suffolk rams were fed a maintenance diet of alfalfa hay cubes once a day. Hyperglycemic clamp (HGC) was carried out to examine glucose-induced insulin response from 48 to 53 h (fasting state) and from 3 to 8 h (meal-fed state) after feeding in Experiment 1 and 2 respectively. Total dose of 70 nmol/kg body weight of D-Lys3-GHRP6, a GH secretagogue receptor 1a (GHS-R1a) antagonist, was intravenously administered at 0, 60, and 120 min after the commencement of HGC. In the fasting state, the ghrelin antagonist significantly (P < 0.01) enhanced glucose-induced insulin secretion. In the meal-fed state, i.v. administration of synthetic ovine ghrelin (0.04 microg/kg body weight per min during HGC) significantly (P < 0.05) enhanced glucose-induced insulin secretion. d-Lys3-GHRP6 treatment suppressed ghrelin-induced enhancement of the insulin secretion. In conclusion, ghrelin has an inhibitory and stimulatory role in glucose-induced insulin secretion via GHS-R1a in fasting- and meal-fed state respectively.
    Journal of Endocrinology 10/2007; 194(3):621-5. DOI:10.1677/JOE-07-0206 · 3.59 Impact Factor
  • Shigeki Kobayashi, Yoshiaki Terashima, Hiroshi Itoh
    The Journal of Poultry Science 01/2006; 43(2):156-161. DOI:10.2141/jpsa.43.156 · 0.79 Impact Factor
  • Shigeki Kobayashi, Yoshiaki Terashima, Hiroshi Itoh
    The Journal of Poultry Science 01/2006; 43(2):162-166. DOI:10.2141/jpsa.43.162 · 0.79 Impact Factor