Hepatic Gluconeogenesis and the Activity of PDH in Individual Tissues of GTG-Obese Mice Following Adrenalectomy
| Autor: | S C Blair, Jenny L. Phuyal, Gregory J. Cooney, Victoria R. Wensley, Ian D. Caterson, Timothy M. Greenaway, Janet M. Bryson |
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| Rok vydání: | 1996 |
| Předmět: |
Blood Glucose
Male medicine.medical_specialty Endocrinology Diabetes and Metabolism medicine.medical_treatment Mice Obese Medicine (miscellaneous) Pyruvate Dehydrogenase Complex Citrate (si)-Synthase Fatty Acids Nonesterified Carbohydrate metabolism Gold thioglucose Mice chemistry.chemical_compound Endocrinology Internal medicine medicine Animals Insulin Lactic Acid Obesity Triglycerides Aurothioglucose chemistry.chemical_classification Glycogen Adrenalectomy Gluconeogenesis Public Health Environmental and Occupational Health Fatty acid Organ Size Pyruvate dehydrogenase complex medicine.anatomical_structure Liver chemistry Hepatocyte Mice Inbred CBA hormones hormone substitutes and hormone antagonists Food Science |
| Zdroj: | Obesity Research. 4:367-375 |
| ISSN: | 1071-7323 |
| DOI: | 10.1002/j.1550-8528.1996.tb00244.x |
| Popis: | Adrenalectomy (ADX) lowers circulating glucose levels in animal models of non-insulin dependent diabetes (NIDDM) and obesity. To investigate the role of hepatic glucose production (HGP) and tissue glucose oxidation in the improvement in glucose tolerance, hepatocyte gluconeogenesis and the activity of pyruvate dehydrogenase (PDH) were examined in different tissues of gold thioglucose (GTG) obese mice 2 weeks after ADX or sham ADX. GTG-obese mice which had undergone ADX weighed significantly less than their adrenal intact counterparts (GTG ADX: 37.5 +/- 0.7 g; GTG: 44.1 +/- 0.4; p < 0.05), and demonstrated lower serum glucose (GTG ADX: 22.5 +/- 1.6 mmol/L; GTG: 29.4 +/- 1.9 mmol/L; p < 0.05) and serum insulin levels (GTG ADX: 76 +/- 10 microU/mL; GTG: 470 +/- 63 microU/mL; p < 0.05). Lactate conversion to glucose by hepatocytes isolated from ADX GTG mice was significantly reduced compared with that of hepatocytes from GTG mice (GTG ADX: 125 +/- 10 nmol glucose/10(6) cells; GTG: 403 +/- 65 nmol glucose/10(6) cells; p < 0.05). ADX also significantly reduced both the glycogen (GTG ADX: 165 +/- 27 mumol/liver; GTG: 614 +/- 60 mumol/liver; p < 0.05) and fatty acid content (GTG ADX: 101 +/- 9 mg fatty acid/g liver; GTG: 404 +/- 40 mg fatty acid/g liver; p < 0.05) of the liver of GTG-obese mice. ADX of GTG-obese mice reduced PDH activity by varying degrees in all tissues, except quadriceps muscle. These observations are consistent with an ADX induced decrease in hepatic lipid stores removing fatty acid-induced increases in gluconeogenesis and increased peripheral availability of fatty acids inhibiting PDH activity via the glucose/fatty acid cycle. It is also evident that the improvement in glucose tolerance which accompanies ADX of GTG-obese mice is not due to increased PDH activity resulting in enhanced peripheral glucose oxidation. Instead, it is more likely that reduced blood glucose levels after ADX of GTG-obese mice are the result of decreased gluconeogenesis in the liver. |
| Databáze: | OpenAIRE |
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