Failing to Extend Life Via Altered Levels of Membrane Fatty Acid Unsaturation

The membrane pacemaker hypothesis suggests that composition of cell membranes, especially those of mitochondria, is an important determinant of longevity differences between species - and possibly between individuals within a species as well. One specific proposed mechanism is the degree to which membranes contain unsaturated fatty acids, as these are more vulnerable to oxidative damage. Oxidative damage is connected to aging, but its role is subtle and complex: look back in the archives for an outline of the mitochondrial free radical theory of aging, for example, in which oxidative damage inside cells is only the initiator for a long chain of consequences.

Here researchers make an attempt to demonstrate the relevance of the membrane pacemaker hypothesis by running a life span study in mice wherein membrane unsaturated fatty acid levels are lowered. They achieve the expected results in mouse biochemistry, changes that look a lot like slowing of aging, but without any resulting extension of life - an outcome that they blame on side-effects of the method used:

The membrane fatty acid unsaturation hypothesis of aging and longevity is experimentally tested for the first time in mammals. Lifelong treatment of mice with the β1-blocker atenolol increased the amount of the extracellular-signal-regulated kinase signaling protein and successfully decreased one of the two traits appropriately correlating with animal longevity, the membrane fatty acid unsaturation degree of cardiac a...

Source: Fight Aging! - March 17, 2014 Category: Health Medicine and Bioethics Commentators Authors: Reason Tags: Daily News Source Type: blogs