| Project/Area Number |
21700777
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Eating habits, studies on eating habits
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| Research Institution | Jin-ai University |
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Principal Investigator |
IKEDA Ryouko Jin-ai University, 人間生活学部, 講師 (80352805)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2010: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2009: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
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| Keywords | 食と栄養 / 鉄欠乏性貧血 / 糖尿病 / 基礎栄養学 / 耐糖能異常 / アディポカイン |
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| Research Abstract |
In the pilot study, blood glucose concentration of the iron-deficient rats rising at the same level with non-insulin-dependent diabetes mellitus (NIDDM) rats. Several investigations showed that the iron status altered energy metabolism. The purpose of this study is to examine the possibility that iron deficiency becomes the risk factor of through a change of serum adipocytokine.
Experiment 1: Male NIDDM model (GK) rats (n=12) were divided into the normal- diet group or the iron-deficient diet group. Every rat was trained to daily meal feeding (18:00-8:45) to measure blood glucose. In this study, acceleration of glucose intolerance was observed in the iron-deficient rats. It is known that iron deficiency impairs hepatic vitamin A release and induces the secondary vitamin A deficiency. Recently, it was also reported that both of vitamin A and its carrier protein affected energy metabolism by regulation of blood glucose. Therefore we compared serum adipocytokine in iron or vitamin A defici
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ent rats to clarify a cause of the glucose intolerance in the iron-deficient rats.
Experiment 2 : Male GK rats (n=18) were divided into the normal-diet group, the iron-deficient diet group and the vitamin A-deficient group. All breeding conditions were the same as experiment 1. After 6 weeks of these dietary regiments, serum glucose was higher in the iron deficient rats than the normal-diet rats. A tendency to high insulin concentration was shown in vitamin A deficiency. Serum RBP4 was significantly decreased against the increase of resistin, TNFα and visfatin in the iron-deficient rats. Serum leptin and adiponectin were decreased in iron-deficient rats. In the vitamin A-deficient rats, serum RBP4 and leptin were decreased. Other serum
adipocytokine concentrations did not changed in vitamin A deficiency.
These results suggested that glucose intolerance was induced by inflammatory adipocytokine which increased in iron-deficiency. It was also shown the possibility that vitamin A affected on expression or synthesis of leptin in the adipose tissue. In conclusion, this study indicated that nutritional management of iron and vitamin A is very important in NIDDM. Less
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