PPARalpha activation reverses adverse effects induced by high-saturated-fat feeding on pancreatic beta-cell function in late pregnancy
Autor: | Nicholas D. Smith, Mark J. Holness, Mary C. Sugden, Gemma K. Greenwood |
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Rok vydání: | 2006 |
Předmět: |
endocrine system
medicine.medical_specialty Time Factors Physiology Endocrinology Diabetes and Metabolism Saturated fat Peroxisome proliferator-activated receptor Biology In Vitro Techniques Insulin resistance Pregnancy Physiology (medical) Internal medicine Insulin-Secreting Cells Fatty Acids Omega-3 Insulin Secretion medicine Animals Insulin PPAR alpha Rats Wistar chemistry.chemical_classification Glucose tolerance test medicine.diagnostic_test Fatty Acids Glucose clamp technique Glucose Tolerance Test medicine.disease Dietary Fats Insulin oscillation Rats Endocrinology Glucose chemistry Hyperglycemia Saturated fatty acid Dietary Supplements Glucose Clamp Technique Pregnancy Animal Female Insulin Resistance |
Zdroj: | American journal of physiology. Endocrinology and metabolism. 292(4) |
ISSN: | 0193-1849 |
Popis: | We examined whether the additional demand for insulin secretion imposed by dietary saturated fat-induced insulin resistance during pregnancy is accommodated at late pregnancy, already characterized by insulin resistance. We also assessed whether effects of dietary saturated fat are influenced by PPARα activation or substitution of 7% of dietary fatty acids (FAs) with long-chain ω-3 FA, manipulations that improve insulin action in the nonpregnant state. Glucose tolerance at day 19 of pregnancy in the rat was impaired by high-saturated-fat feeding throughout pregnancy. Despite modestly enhanced glucose-stimulated insulin secretion (GSIS) in vivo, islet perifusions revealed an increased glucose threshold and decreased glucose responsiveness of GSIS in the saturated-fat-fed pregnant group. Thus, insulin resistance evoked by dietary saturated fat is partially countered by augmented insulin secretion, but compensation is compromised by impaired islet function. Substitution of 7% of saturated FA with long-chain ω-3 FA suppressed GSIS in vivo but did not modify the effect of saturated-fat feeding to impair GSIS by perifused islets. PPARα activation (24 h) rescued impaired islet function that was identified using perifused islets, but GSIS in vivo was suppressed such that glucose tolerance was not improved, suggesting modification of the feedback loop between insulin action and secretion. |
Databáze: | OpenAIRE |
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