Sodium-Glucose Cotransporter 2 Inhibitor and a Low Carbohydrate Diet Affect Gluconeogenesis and Glycogen Content Differently in the Kidney and the Liver of Non-Diabetic Mice
| Autor: | Tsuyoshi Yanagimachi, Yasutaka Takeda, Yumi Takiyama, Kuralay Atageldiyeva, Yukihiro Fujita, Yuichi Makino, Masakazu Haneda, Atsuko Abiko, Katsutoshi Mizumoto, Jun Honjo |
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| Jazyk: | angličtina |
| Rok vydání: | 2016 |
| Předmět: |
Male
0301 basic medicine Glycogens Physiology medicine.medical_treatment Glycobiology lcsh:Medicine Gene Expression Kidney Biochemistry Fats Diet Carbohydrate-Restricted chemistry.chemical_compound Endocrinology 0302 clinical medicine Glucosides Medicine and Health Sciences Insulin lcsh:Science Cyclic AMP Response Element-Binding Protein Glucose tolerance test Multidisciplinary Glycogen medicine.diagnostic_test Organic Compounds Forkhead Box Protein O1 Monosaccharides Lipids Up-Regulation Chemistry Liver Sodium/Glucose Cotransporter 2 Physical Sciences 旭川医科大学：博士（医学）（甲第504号） 学位授与年月日:平成28年12月22日 Anatomy Research Article medicine.medical_specialty Carbohydrates 030209 endocrinology & metabolism Thiophenes Biology Diabetes Mellitus Experimental 03 medical and health sciences Insulin resistance Sodium-Glucose Transporter 2 Internal medicine Diabetes mellitus Genetics medicine Animals Obesity RNA Messenger Sodium-Glucose Transporter 2 Inhibitors Triglycerides Diabetic Endocrinology Endocrine Physiology lcsh:R Organic Chemistry Body Weight Chemical Compounds Gluconeogenesis Biology and Life Sciences Kidney metabolism Kidneys Renal System Glucose Tolerance Test Lipid Metabolism medicine.disease Hormones Mice Inbred C57BL Glucose 030104 developmental biology chemistry Hyperglycemia lcsh:Q Insulin Resistance Fatty Acid Synthases Energy Intake |
| Zdroj: | PLoS ONE PLoS ONE, Vol 11, Iss 6, p e0157672 (2016) |
| Popis: | A low carbohydrate diet (LCHD) as well as sodium glucose cotransporter 2 inhibitors (SGLT2i) may reduce glucose utilization and improve metabolic disorders. However, it is not clear how different or similar the effects of LCHD and SGLT2i are on metabolic parameters such as insulin sensitivity, fat accumulation, and especially gluconeogenesis in the kidney and the liver. We conducted an 8-week study using non-diabetic mice, which were fed ad-libitum with LCHD or a normal carbohydrate diet (NCHD) and treated with/without the SGLT-2 inhibitor, ipragliflozin. We compared metabolic parameters, gene expression for transcripts related to glucose and fat metabolism, and glycogen content in the kidney and the liver among the groups. SGLT2i but not LCHD improved glucose excursion after an oral glucose load compared to NCHD, although all groups presented comparable non-fasted glycemia. Both the LCHD and SGLT2i treatments increased calorie-intake, whereas only the LCHD increased body weight compared to the NCHD, epididimal fat mass and developed insulin resistance. Gene expression of certain gluconeogenic enzymes was simultaneously upregulated in the kidney of SGLT2i treated group, as well as in the liver of the LCHD treated group. The SGLT2i treated groups showed markedly lower glycogen content in the liver, but induced glycogen accumulation in the kidney. We conclude that LCHD induces deleterious metabolic changes in the non-diabetic mice. Our results suggest that SGLT2i induced gluconeogenesis mainly in the kidney, whereas for LCHD it was predominantly in the liver. |
| Databáze: | OpenAIRE |
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