A metabolomics approach to investigate the proceedings of mitochondrial dysfunction in rats from prediabetes to diabetes
| Autor: | Ming-Shi Shiao, Tso-Yen Mao, Mei-Ling Cheng, Ann Chen, Chun-Feng Huang, Siao-Yun Lin |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
0106 biological sciences
0301 basic medicine medicine.medical_specialty Normal diet QH301-705.5 STZ streptozotocin 01 natural sciences Methylation Excretion 03 medical and health sciences Insulin resistance KEGG kyoto encyclopedia of genes and genomes DM diabetes mellitus Internal medicine Diabetes mellitus medicine HF high-fructose Metabolomics HMDB human metabolome database Prediabetes Biology (General) GPT glutamate pyruvate transaminase CAN acetonitrile PCA principal component analysis business.industry Diabetes Tryptophan LC-MS liquid chromatography–mass spectrometry medicine.disease GOT glutamate oxaloacetate transaminase Metabolic syndrome TG triacylglycerol TC total cholesterol Metabolic pathway 030104 developmental biology Endocrinology Original Article HL high-fat General Agricultural and Biological Sciences business Mitochondrial dysfunction Dyslipidemia 010606 plant biology & botany |
| Zdroj: | Saudi Journal of Biological Sciences, Vol 28, Iss 8, Pp 4762-4769 (2021) Saudi Journal of Biological Sciences |
| Popis: | Background Diabetes mellitus (DM) is a leading cause of preventable cardiovascular disease, but the metabolic changes from prediabetes to diabetes have not been fully clarified. This study implemented a metabolomics profiling platform to investigate the variations of metabolites and to elucidate their global profiling from metabolic syndrome to DM. Methods: Male Sprague-Dawley rats (n = 44) were divided into four groups. Three groups were separately fed with a normal diet, a high-fructose diet (HF), or a high-fat (HL) diet while one group was treated with streptozotocin. The HF and HL diet were meant to induce insulin resistance, obesity, and dyslipidemia, which known to induce DM. Results: The most significant metabolic variations in the DM group’s urine samples were the reduced release of citric acid cycle intermediates, the increase in acylcarnitines, and the decrease in urea excretion, all of which indicated energy metabolism abnormalities and mitochondrial dysfunction. Overall, the metabolic analysis revealed tryptophan metabolic pathway variations in the prediabetic phase, even though the mitochondrial function remains unaffected. Conclusion: This study show that widespread methylations and impaired tryptophan metabolism occur in metabolic syndrome and are then followed by a decline in citric acid cycle intermediates, indicating mitochondrial dysfunction in diabetes. |
| Databáze: | OpenAIRE |
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