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Selective amylin antagonist suppresses rise in plasma lactate after intravenous glucose in the rat
Author(s) -
Young Andrew A.,
Gedulin Bronislava,
Gaeta Laura S.L.,
Prickett Kathryn S.,
Beaumont Kevin,
Larson Erica,
Rink Timothy J.
Publication year - 1994
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(94)80563-6
Subject(s) - amylin , medicine , endocrinology , antagonist , chemistry , insulin , in vivo , carbohydrate metabolism , hormone , islet , biology , receptor , microbiology and biotechnology
Data presented here provide the first demonstration that circulating amylin regulates metabolism in vivo, and support an endocrine hormonal role that is distinct from its autocrine action at pancreatic islets. When rats were pre‐treated with the potent amylin antagonist AC187 ( n = 18), and then administered a 2 mmol glucose load, the rise in plasma lactate was less than in rats administered glucose only ( n = 27; P < 0.02). When rats were treated so that plasma glucose and insulin profiles were similar ( n = 8), the increase in plasma lactate in the presence of AC187 was only 50.3% as high as the increase when AC187 was absent ( P < 0.001). These experimental results fit with the view that some of the lactate appearing in plasma after a glucose load comes from insulin‐sensitive tissues. The experiments also support the view that an important fraction of the increase in lactate depends on processes inhibited by a selective amylin antagonist, most likely amylin action in muscle.