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Islet dysfunction in rats fed a high fat diet (HFD): A structurefunction study
Author(s) -
Sweazea Karen L,
Brower Jeremy,
Faust James,
Malenica Ivana,
Herman Richard
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1113.3
Subject(s) - medicine , endocrinology , islet , glucagon , postprandial , insulin , insulin resistance , pancreas , biology
Sprague‐Dawley (SD) rats exposed to increased dietary fat are an important and relevant animal model simulating consequences of increased adiposity in humans. This model demonstrates mild fasting hyperglycemia, insulin resistance and modulation of postprandial glucose‐stimulated insulin responses and glucose tolerance, the latter implying insufficent islet cell compensation. In this study, two groups of male SD rats fed either chow (5% kcal from fat) or a high‐fat (60% kcal from fat) (HFD) diet for 6 weeks were investigated by determining: (1) post‐prandial insulin, glucose and glucagon concentrations; and (2) islet fractional area comprised of α‐ and β‐cells of isolated pancreata by immunofluorescence. Rats fed a HFD develop significantly increased post‐prandial plasma glucose and insulin concentrations. Preliminary studies suggest substantial disruption of the core:mantle arrangement of islet architecture in the pancreas of HFD rats. Further studies are being conducted to complete these analyses and quantify post‐prandial glucagon concentrations as well as pancreatic insulin and glucagon concentrations. Unquestionably, HFD‐fed rats demonstrated marked functional (‘pre‐diabetic” stage) and structural islet changes which may suggest intrinsic and extrinsic neurohormonal mechanisms of dysfunction.