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Phosphatidylcholine supplementation alleviates the impaired glucose response induced by acute methionine loading
Author(s) -
Lopez Annalee N,
GossellWilliams Maxine D,
Simon Oswald R,
Phillips Howard
Publication year - 2010
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.24.1_supplement.569.3
Subject(s) - medicine , endocrinology , methionine , homocysteine , hyperhomocysteinemia , insulin , carbohydrate metabolism , impaired glucose tolerance , phosphatidylcholine , nefa , chemistry , insulin resistance , biochemistry , phospholipid , amino acid , membrane
Methionine metabolism liberates homocysteine. Emerging evidence suggests acute hyperhomocysteinemia may play a critical role in impaired insulin secretion from pancreatic beta cells and thus could prevent the normal response to a glucose challenge. The aim of the study was to evaluate the benefits of supplemental phosphatidylcholine (PC) on the glucose response associated with an oral glucose tolerance test (OGTT) in rats subjected to acute methionine loading. Male Sprague‐Dawley rats were divided into groups for corn oil (n=4) and PC supplementation, 458mg/kg (n=4), by gavage 5 days weekly for 3 weeks. Animals were fed a standard pellet diet and tap water ad libitum. OGTT and methionine loading was conducted after supplementation. Fasting blood glucose concentration was unaffected by treatment with PC. Impaired glucose tolerance was observed in control group (7.48 ± 0.14) at 2hrs post methionine and glucose load. Conversely, PC supplementation resulted in a significant reduction in glucose levels at 1.5hrs and 2hrs when compared to controls (P<0.05 and P<0.001 respectively). Additionally, values approaching significance were also recorded at 1hr (P=0.055). PC supplementation may be very effective in preventing the impaired glucose tolerance associated with decreased insulin secretion that can occur with acute hyperhomocysteinemia. Source of funding: Office of Graduate Studies and Research, UWI Mona