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論文
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佐藤, 江里 ; 田村, 綾女 ; 丹藤, 雄介 ; 須田, 俊宏 ; 中村, 光男 ; 山岸, 昌一
概要:
病歴の長い糖尿病患者において,アミラーゼ分泌の低下や障萎縮･線維化を呈する症例があることが報告されている.しかしこのような病態の動物モデルは現在確立されていない.また,終末糖化産物AGE,その受容体であるRAGEは糖尿病血管合併症に関与して
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いるとされているが,陣-の影響は不明である.糖尿病における障外分泌障害とその機序を明らかにするため,加齢により障ラ氏島の線維化を生じる自然発症2型糖尿病モデル,SpontaneouslyDiabeticTorii(SDT)ラットにcaerulein急性輝炎を発症させ,糖尿病の発症および程度,降の線維化に変化を生じるか否か,同時に,RAGEの発現をRT-PCRにより検討した.結果,障炎による糖尿病発症および降の線維化,糖尿病発症前後および輝炎の有無によるRAGEの発現に変化は認めず,糖尿病ラットモデルにおける障障害とRAGEの関連は明らかではなかった.
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| 2.
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論文
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Yoshida, Ikko ; Ishizaka, Hiroshi ; Hasegawa, Kazushi ; Satoh, Kiyohiko ; Osanai, Tomohiro ; Motomura, Shigeru ; Okumura, Ken
概要:
Objectives The purpose of this study was to test the hypothesis that adenosine-induced coronarymicrovascular dilation is
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blunted in the animals with diabetes mellitus（ DM） through the impairment of KATP channelfunction. Background Adenosine-induced coronary vasodilation is demonstrated to be mediated by activation of ATPsensitivepotassium（ KATP） channels and nitric oxide（ NO）. Methods The hearts of Otsuka Long-Evans Tokushima fatty rats （OLETF, type 2 DM rats）, and control Long-Evans Tokushima fatty rats（ LETO） at the ages of 32 and 8 weeks were perfused using a Langendorff system withconstant perfusion pressure （80 mmHg）. Changes in coronary fl ow to adenosine, pinacidil and sodium nitroprusside（SNP） were examined before and after administration of glibenclamide（ 10-7 M）, or NG-nitro-L-arginine methyl ester（L-NAME, 10-4 M）. Results At the age of 32 weeks, adenosine- and pinacidil-induced increases in coronary fl ow were blunted in OLETFas compared with those in LETO （both p<0.05）. Glibenclamide attenuated adenosine-induced increase in coronaryfl ow in LETO （p<0.05）, but not in OLETF. In contrast, L-NAME attenuated adenosine-induced increase in coronaryflow in OLETF （p<0.05）, but not in LETO. SNP-induced increases in coronary flow in LETO and OLETF werecomparable and were not aff ected by glibenclamide. In 8-week-old OLETF and LETO, no diff erence was observed inadenosine-, pinacidil- and SNP-induced increases in coronary fl ow between OLETF and LETO. Conclusions In this type 2 DM model, KATP channel function in coronary microcirculation is impaired. Adenosineinducedincrease in coronary fl ow is mediated mainly by NO mechanism.
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| 3.
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論文
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川原, 昌之
概要:
弘前医学会例会の一般演題抄録は、一部の演題のみリポジトリにて公開
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和田, 龍一
概要:
科学研究費補助金研究成果報告書 ; 研究種目:基盤研究(C) ; 研究期間：2007-2008 ; 課題番号:20260408 ; 研究代表者：和田龍一
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Hasan, Kazi N. ; Shoji, Masaru ; Sugimoto, Kazuhiro ; Tsutaya, Shoji ; Yasujima, Minoru
概要:
Arginine vasopressin (AVP), a peptide hormone released from the posterior pituitary, has been suggested to play important roles in cardiovascular regulation, glycogenolysis and platelet aggregation through its V1a receptor
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(V1aR). In this study, we investigated the association of 4 novel single nucleotide polymorphisms (SNPs) in V1aR gene (-6951G/A, -4112A/T, -3860T/C and -242C/T) with hypertension, diabetes mellitus (DM) and glycemic status, and platelet responsiveness to AVP. Genotypes were determined in 365 hypertensives and 255 healthy subjects, 186 patients with type 2 DM (T2DM) and 188 non-diabetic control subjects (CS), and 33 young healthy subjects in the Aomori prefecture. A significant association was found between the SNP -6951G/A and hypertension in nonobese individuals. Multiple logistic analysis demonstrated SNP -6951G/A as an independent risk factor for nonobese hypertension. One haplotype H3 (a-a-c-c) was characteristic to hypertension in nonobese. A significant association was found between the SNP -6951G/A and type 2 DM. Logistic regression also confirmed the significant association of the SNP -6951G/A with type 2 DM. There were a couple of characteristic distributions of heterozygous haplotype combinations in T2DM. In young healthy subjects, GA+AA carriers of SNP -6951 showed significantly higher HbAlc levels than in GG. Platelet aggregation responses to AVP were identical between wild types and variants of any SNPs. These results suggest that -6951G/A SNP and haplotypes created by 4 SNPs of V1aR gene might confer susceptibility to essential hypertension in nonobese individuals and type 2 DM. However, these SNPs might not be useful as genetic marker for platelet aggregation heterogeneity.
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