Thick padding around the hip or on the bud. A horror for the surgeon, a risk for the internist threatening the cardiovascular system and for the orthopedist an arthrosis factor. Well enough, we owe the fat our round or edged body shapes, the distinctive figure and our facial features. In case of emergency, the fat pads retain strong bumps and are on top of it long-term energy stores for bad days. That’s the one we usually build up over the years, but hardly every get rid off again.
Leptin – Link to the immune system
Over the last few years, the fat research surprised not only with new findings regarding the handing down of BMI value and physique but also about new functions you would never have expected in the storage organ. The energy depot provides with a number of self-produced factors important control signals. In 1993, the work group of Bruce Spiegelman of the Boston Dana-Farber-Institute was able to show that the fat tissue of overweight rodents produces tumor-necrossi-factor-alpha (TNF-alpha), a relevant inflammation factor. TNF also contributes to an increasing insulin resistance.
Just one year later, Jeffrey Friedman and his colleagues at the Howard-Hughes-Medical Institute discovered one of the most important messengers of adipocytes, the leptin.
The leptin level supplies information regarding the energy stock in the fat storage and controls the feeling of hunger. But it seems that leptin does a lot more. Fro example obese mice with a leptin deficiency have a protection against auto-immune encephalitis or allergic reactions. The group of Britta Siegmund at the Berlin Charité found out that leptin also stimulates naïve t-cells of the immune system during reactions on inflammation. All cells of the immune system carry the leptin receptor on their surface, a clear sign of the strong alliance between energy depot and infection defence.
Immune cells in the fat tissue
The long list of the “adipokines” shows that adipocytes do more than just provide fuel. Adiponectine from fat tissue at the joints expedites inflammation processes of rheumatoid arthritis as shown by Andreas Schäffler in Regensburg. On the other hand this hormone appears to slake the immune response in other tissues. Further factors from fat tissue: Visfatin connects to the insulin receptor thus contributing to insulin resistance. Particularly high levels produce intestinal inflammations such as Morbus Crohn. Resistin or the retinol-bond proteine-4 also class among the important adipokines.
So it did not come as a surprise in 2003 when researchers at the New York Columbia University found macrophages in the middle of the fat tissue of overweight children and adults. It is getting more and more obvious, that overfull fat depots lead to inflammations. Thus the metabolic syndrome as a prestage of insulin resistance is a consequence of the nonequilibrium of adipokines. Carl Nathan writes in a review of the latest edition “Molecular Medicine“: Uninhibited intake of food leads to an overproduction of reactive oxygen- (ROI) and nitrogen (RNI)-molecules initially targeted at the microbial enemy in the own body, but now causing permanent stress with it.
Just how close the relations between immune system and adipocytes are, also show in the results provided by Caroline Pond from Milton Keynes in the UK. For example the signals of dentritic cells in fat cells fully targeted the transformation of the stored fat to fatty acids particularly customized for those specialized cells. In local centers of inflammation you will always find centers of adipocytes arranging for the energy to come from its storage and not from the depot of important muscle cells.
That little roly-poly, a pile of well-filled fat storage cells, seems to turn out to be a transhipment point for energy and control co-center for the immune system. The links between healthy food and functioning defence against intruders, but also cancer and autoimmune processes become clearer. A lack of fat due to a lack of food supply is just as dangerous as those spare tires around your hip.