کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2023537 | 1069481 | 2006 | 5 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The elimination rates of intact GIP as well as its primary metabolite, GIP 3-42, are similar in type 2 diabetic patients and healthy subjects
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کلمات کلیدی
CmaxFPGGIPtmaxGLP-1DPP-IVAUC - AUCt1/2 - t1 / 2clearance - ترخیص کالا از گمرکElimination - حذفdipeptidyl peptidase IV - دیپپتیدیل پپتیداز IVtime to reach Cmax - زمان برای رسیدن به CmaxFasting plasma glucose - قند خون ناشتاHalf-life - نیمه عمرIncretin hormones - هورمونهای افزایش یافتهglucagon-like peptide-1 - پپتید 1-گلوکاگون-مانندPlasma glucose - گلوکز پلاسماglucose-dependent insulinotropic polypeptide - گلیکول وابسته به پلی پپتید انسولینوتروپیک
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
The incretin hormone, glucose-dependent insulinotropic polypeptide (GIP, previously known as gastric inhibitory polypeptide), is rapidly degraded to the biologically inactive metabolite GIP (3-42) in the circulation, but little is known about the kinetics of the intact hormone and the metabolite and whether differences exist between patients with type 2 diabetes mellitus and healthy subjects. We examined eight type 2 diabetic patients (six men, two women); mean (range) age: 59 (48-69) years; BMI: 31.6 (26.0-37.7) kg/m2; HbA1C: 9.0 (8.2-13.2) %; fasting plasma glucose (FPG): 10.0 (8.3-13.2) mmol/l and 8 healthy subjects matched for age, gender and BMI. An intravenous bolus injection of GIP (7.5 nmol) was given and venous blood samples were drawn the following 45 minutes. Peak concentrations of total GIP (intact + metabolite, mean ± SEM) and intact GIP (in brackets) were 920 ± 91 (442 ± 52) pmol/l in the type 2 diabetic patients and 775 ± 68 (424 ± 30) pmol/l in the healthy subjects (NS). GIP was eliminated rapidly with the clearance rate for intact GIP being 2.3 ± 0.2 l/min in the type 2 diabetic patients and 2.4 ± 0.2 l/min in the healthy subjects (NS). The volumes of distributions were similar in the two groups and ranged from 8 to 21 l per subject. The primary metabolite, GIP 3-42, generated through the action of dipeptidyl peptidase IV (DPP-IV), was eliminated with a mean half-life of 17.5 and 20.5 min in patients and healthy subjects (NS). Conclusion: Elimination of GIP is similar in obese type 2 diabetic patients and matched healthy subjects. Differences in elimination of GIP and its primary metabolite, therefore, do not seem to contribute to the defective insulinotropic effect of GIP in type 2 diabetes.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Regulatory Peptides - Volume 137, Issue 3, 10 December 2006, Pages 168-172
Journal: Regulatory Peptides - Volume 137, Issue 3, 10 December 2006, Pages 168-172
نویسندگان
Tina Vilsbøll, Henrik Agersø, Torsten Lauritsen, Carolyn F. Deacon, Kasper Aaboe, Sten Madsbad, Thure Krarup, Jens Juul Holst,