• Journal of the Korean Society of Food Science and Nutrition
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• v.35 no.3
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• pp.321-327
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• 2006

This study was performed to investigate the hypoglycemic effect of pine needle extract oil against type 2 diabetes. Six-week-old male C57BL/Ks(db/db) mice were divided into four groups : negative control, pine needle extract oil low dose, high dose and positive control groups, which fed daily for 6 weeks with corn oil, pine needle extract oil 112.5 mg/kg, 450 mg/kg or metformin (150 mg/kg ), respectively. The oral administration of the pine needle extract oil resulted in the significant and dose-dependent decreases of blood glucose levels in comparison with corn oil treatment. The levels of HbAlc showed a tendency of the decrease by the high dose treatment of the pine needle extract oil and were positively correlated with blood glucose levels (r=0.5046, p=0.0023) . However, the levels of serum insulin and C-peptide were not affected by pine needle extract oil or metformin treatments. The levels of serum leptin, which is related with the insulin sensitivity, showed a tendency of the increases by pine needle extract oil treatment and were negatively correlated to blood glucose levels (r=-0.4754, p=0.0052). In conclusion, these results suggest that the pine needle extract oil have a potential for the oral anti-hyperglycemic agent and the mode of action may be related with the improvement of the insulin sensitivity through blood leptin.

• Journal of Sasang Constitutional Medicine
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• v.12 no.1
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• pp.186-200
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• 2000

The purpose of this research was to investigate the effects of Indongdeungjikolpitang water extract(IJTE) on the complication of diabetes. IJTE did not affect the level of blood glucose in alloxan- or streptozotocin-induced hyperglycemic mice, but inhibited the motility of gastrointestine. IJTE inhibited the writhing syndrome induced by acetic acid, the permeability of evans blue into peritoneal cavity induced by acetic acid, the paw edema induced by histamine, and the formation of cotton pellet granuloma. IJTE increased the cell viability of thymocytes and splenocytes. IJTE decreased the release of ${\gamma}-interferone$(${\gamma}-IFN$) and interleukin-2(IL-2), but did not affect the release of interleukin-4(IL-4) from murine thymocytes. IJTE increased the release of IL-4 and decreased the release of tumor necrosis $factor-{\alpha}$($TNF-{\alpha}$) and $interleukin-1{\beta}$($IL-1{\beta}$), but did not affect of ${\gamma}-IFN$ and IL-2 from murine splenocytes. IJTE decreased the release of $TNF-{\alpha}$ and $IL-1{\beta}$ from murine peritoneal macrophages. IJTE decreased the production of niric oxide(NO) from murine peritioneal macrophages and increased the phagocytic activity of murine peritoneal macrophages. These results suggest that IJTE has an anti-inflammatory action via the inhibition of $TNF-{\alpha}$, $IL-1{\beta}$ and NO production from immune cells.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.1
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• pp.83-89
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• 2016

Sepsis is the life-threatening response to infection which can lead to tissue damage, organ failure, and death. In the current study, the effect of orally administered D-glucose on the mortality and the blood glucose level induced by D-Galactosamine (GaLN)/lipopolysaccharide (LPS)-induced sepsis was examined in ICR mice. After various amounts of D-glucose (from 1 to 8 g/kg) were orally fed, sepsis was induced by injecting intraperitoneally (i.p.) the mixture of GaLN /LPS. Oral pre-treatment with D-glucose dose-dependently increased the blood glucose level and caused a reduction of sepsis-induced mortality. The oral post-treatment with D-glucose (8 g/kg) up to 3 h caused an elevation of the blood glucose level and protected the mortality observed in sepsis model. However, D-glucose post-treated at 6, 9, or 12 h after sepsis induction did not affect the mortality and the blood glucose level induced by sepsis. Furthermore, the intrathecal (i.t.) pretreatment once with pertussis toxin (PTX; $0.1{\mu}g/5ml$) for 6 days caused a reduction of D-glucose-induced protection of mortality and hyperglycemia. Furthermore, once the hypoglycemic state is continued up to 6 h after sepsis initiated, sepsis-induced mortality could not be reversed by D-glucose fed orally. Based on these findings, it is assumed that the hypoglycemic duration between 3 and 6 h after the sepsis induction may be a critical time of period for the survival. D-glucose-induced protective effect against sepsis-induced mortality appears to be mediated via activating PTX-sensitive G-proteins in the spinal cord. Finally, the production of hyperglycemic state may be critical for the survival against the sepsis-induced mortality.