Metabolite Variation in Lean and Obese Streptozotocin (STZ)-Induced Diabetic Rats via 1H NMR-Based Metabolomics Approach

被引:21
|
作者
Sajak, Azliana Abu Bakar [1 ]
Mediani, Ahmed [2 ]
Maulidiani [1 ]
Ismail, Amin [3 ]
Abas, Faridah [1 ,2 ]
机构
[1] Univ Putra Malaysia, Lab Nat Prod, Inst Biosci, Upm Serdang 43400, Selangor, Malaysia
[2] Univ Putra Malaysia, Fac Food Sci & Technol, Dept Food Sci, Upm Serdang 43400, Selangor, Malaysia
[3] Univ Putra Malaysia, Fac Med & Hlth Sci, Dept Nutr & Dietet, Upm Serdang 43400, Selangor, Malaysia
关键词
Metabolomics; Diabetes; Nuclearmagnetic resonance; Metabolic pathways; INSULIN-RESISTANCE; ANIMAL-MODELS; BRANCHED-CHAIN; DIET; DECOCTION;
D O I
10.1007/s12010-016-2352-9
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Diabetes mellitus (DM) is considered as a complex metabolic disease because it affects the metabolism of glucose and other metabolites. Although many diabetes studies have been conducted in animal models throughout the years, the pathogenesis of this disease, especially between lean diabetes (ND + STZ) and obese diabetes (OB + STZ), is still not fully understood. In this study, the urine from ND + STZ, OB + STZ, lean/control (ND), and OB + STZ rats were collected and compared by using H-1 NMR metabolomics. The results from multivariate data analysis (MVDA) showed that the diabetic groups (ND + STZ and OB + STZ) have similarities and dissimilarities for a certain level of metabolites. Differences between ND + STZ and OB + STZ were particularly noticeable in the synthesis of ketone bodies, branched-chain amino acid (BCAA), and sensitivity towards the oral T2DM diabetes drug metformin. This finding suggests that the ND + STZ group was more similar to the T1DM model and OB + STZ to the T2DM model. In addition, we also managed to identify several pathways and metabolism aspects shared by obese (OB) and OB + STZ. The results from this study are useful in developing drug target-based research as they can increase understanding regarding the cause and effect of DM.
引用
收藏
页码:653 / 668
页数:16
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