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ARS Home » Research » Publications at this Location » Publication #120983
Title: OXIDIZED FATTY ACIDS STIMULATE ALDOSTERONE SECRETION

Author
item GOODFRIEND, THEODORE - UNIV OF WI, MADISON, WI
item BALL, DENNIS - UNIV OF WI, MADISON, WI
item Gardner, Harold

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 6/6/2001
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: To explore a hypothesis about visceral obesity, the role of the liver, the adrenal, and the development of hypertension, we studied hepatic oxidation of fatty acids and the biological properties of the oxidation products. Isolated rat hepatocytes converted eighteen-carbon (C18) polyunsaturated fatty acids into a myriad of products in the presence of oxygen. Some of the oxidized derivatives of linolenic and linoleic acids stimulated production of aldosterone by suspensions of rat adrenal glomerulosa cells. The quantity of each oxidation product produced by hepatocytes was small and difficult to characterize; therefore, we produced larger quantities by autoxidation of C18 polyunsaturated fatty acids. Some of these products in microgram quantities stimulated production of aldosterone by rat adrenal cells. Two biologically-active products of linoleic acid oxidation were assigned tentative structures. In addition, one of these products stimulated vascular smooth muscle contraction, (rat aortic strips). The biological activities of the compounds are consistent with the hypothesis that fatty acid oxidation products can contribute to the hypertension of visceral obesity. In addition, they may mediate other phenomena subsumed under the term "oxidative stress."