Wednesday, December 02, 2015

Stored fat fights against the body's attempts to lose weight

http://www.eurekalert.org/pub_releases/2015-11/uoc-sff112415.php

Public Release: 24-Nov-2015
Stored fat fights against the body's attempts to lose weight
University of Cambridge

The fatter we are, the more our body appears to produce a protein that inhibits our ability to burn fat, suggests new research published in the journal Nature Communication. The findings may have implications for the treatment of obesity and other metabolic diseases.

Most of the fat cells in the body act to store excess energy and release it when needed but some types of fat cells, known as brown adipocytes, function primarily for a process known as thermogenesis, which generates heat to keep us warm. However, an international team of researchers from the Wellcome Trust-Medical Research Council Institute of Metabolic Sciences at the University of Cambridge, UK, and Toho University, Japan, have shown that a protein found in the body, known as sLR11, acts to suppress this process.

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When the researchers examined levels of sLR11 in humans, they found that levels of the protein circulating in the blood correlated with total fat mass - in other words, the greater the levels of the protein, the higher the total fat mass. In addition, when obese patients underwent bariatric surgery, their degree of postoperative weight loss was directly proportional to the reduction in their sLR11 levels, suggesting that sLR11 is produced by fat cells.

In their paper the authors suggest that sLR11 helps fat cells resist burning too much fat during 'spikes' in other metabolic signals following large meals or short term drops in temperature. This in turn makes adipose tissue more effective at storing energy over long periods of time.

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Dr Andrew Whittle, joint first author, said: "Our discovery may help explain why overweight individuals find it incredibly hard to lose weight. Their stored fat is actively fighting against their efforts to burn it off at the molecular level."

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