Diet, Not Aging, Causes Skeletal Muscle Insulin Resistance
| Autor: | R. J. Barnard, J. F. Youngren, Martin Da |
|---|---|
| Rok vydání: | 1995 |
| Předmět: |
Blood Glucose
Aging medicine.medical_specialty Sucrose medicine.medical_treatment Biological Transport Active Biology chemistry.chemical_compound Sarcolemma Insulin resistance Internal medicine Dietary Carbohydrates medicine Hyperinsulinemia Animals Insulin Muscle Skeletal Pancreatic hormone Glucose transporter Skeletal muscle Fasting medicine.disease Dietary Fats Rats Inbred F344 Diet Rats Glucose medicine.anatomical_structure Endocrinology chemistry Basal (medicine) Female Insulin Resistance Geriatrics and Gerontology |
| Zdroj: | Gerontology. 41:205-211 |
| ISSN: | 1423-0003 0304-324X |
| DOI: | 10.1159/000213683 |
| Popis: | The purpose of this study was to compare the effects of raising female Fischer rats on a low-fat, high-complex-carbohydrate diet (LFCC) versus a high-fat, sucrose diet (HFS) on serum glucose and insulin as well as skeletal muscle glucose transport. No significant differences were observed between 6- and 24-month-old rats raised on the LFCC diet for serum glucose (3.6 +/- 0.1 vs. 3.7 +/- 0.2 mM) and insulin (88 +/- 6 vs. 98 +/- 10 pM) or for basal (35 +/- 3 vs. 39 +/- 6 pmol/mg protein/15 s) or insulin-stimulated (74.2 +/- 7.6 vs. 69.4 +/- 3.8 pmol/mg protein/15 s) glucose transport. These data indicate that aging per se does not lead to insulin resistance. When the 24-month-old animals raised on the HFS diet were compared with those on the LFCC diet, major differences were observed. Fasting serum insulin was significantly higher in the HFS group (437 +/- 118 vs. 98 +/- 10 pM) and insulin-stimulated glucose transport was significantly reduced (52.5 +/- 3.7 vs. 69.4 +/- 3.8 pmol/mg protein/15 s). Fasting glucose (3.7 +/- 0.2 vs. 3.6 +/- 0.1 mM) and basal glucose transport (38 +/- 6 vs. 39 +/- 6 pmol/mg protein/15 s) were unchanged. These results indicate that diet and not aging per se caused insulin resistance. |
| Databáze: | OpenAIRE |
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