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Interleukin-6: Exercise’s Fat-burning Hormone PDF Print E-mail
Written by Dan Gwartney, MD   
Saturday, 04 July 2009
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Of Most Interest to Guys Who Work Out

 Clearly, the immune system defies an easy understanding, even when it’s functioning properly. However, scientists are scrutinizing the immune system with great interest in the hopes of developing therapies to treat many of the diseases afflicting the world’s population. There’s hope that the cure for several diseases may be managed by stimulating a person’s own body to correct or eradicate cancerous tumors, viral infections such as hepatitis or HIV, autoimmune disorders and of most interest to those trying to get fit— obesity.
 Since their discovery, fat cells have been considered passive storage sites, existing merely to hold extra energy to allow our ancestors to withstand periods of famine. Yet clandestinely, fat cells have been communicating via a system of hormones and chemical signals to aid in the control or balance of whole body energy. Many great discoveries have been made in the last 25 years dealing with adipocytes (fat cells) as an endocrine organ. The most simple to understand have been the endocrine-like effects of hormones such as leptin. Leptin travels to the brain and signals to the body the amount of stored fat. When leptin is high due to a large fat mass, the brain responds by lowering appetite and increasing metabolism. When leptin drops due to low fat mass, the brain increases the appetite and lowers metabolism. This stimulates the low-leptin individual to eat more and preserve energy. This discovery excited scientists who hoped that injecting obese people with leptin would help them to lose weight. Unfortunately, it didn’t, as most obese Americans aren’t deficient in leptin, but rather resist the hormonal signal.
 With the dawn of the new century, several intriguing studies have been published, describing other messengers used by the fat cells to communicate with distant organs in the body (brain), nearby tissues and cells (other fat cells) and even self-regulation (same cell). These processes are referred to as endocrine, paracrine and autocrine functions. They all utilize chemical messengers to change the metabolism; the primary difference is the target cell, whether it be far, near or even the cell talking to itself. Many of the chemical messengers related to fat cell function have been implicated in a variety of diseases, including type 2 diabetes, cardiovascular disease and obesity. According to the published literature, IL-6 appears to hold a prominent position in these relationships.

A Potent Messenger

 The earliest data regarding cytokines (IL-6 specifically) and body fat were confusing and often contradictory. Researchers noted that relatively high IL-6 levels in the blood, a sign of chronic, low-level inflammation, is associated with insulin resistance, obesity and the development of type 2 diabetes. Further, IL-6 directly stimulates the production of C-reactive protein (CRP), a marker associated with the development of cardiovascular disease and type 2 diabetes.
 Yet, despite all this evidence showing elevated blood levels of IL-6 are associated with obesity, insulin resistance, type 2 diabetes and cardiovascular disease, other studies strongly support a lipolytic (fat reducing) effect of IL-6 on fat cells and whole body fat. Early animal studies demonstrated that mice injected with IL-6 had higher free fatty acid blood levels, indicative of lipolysis (fat release). Mice born without IL-6 develop obesity later in life, but this is corrected with IL-6 treatment, suggesting that IL-6 plays a role in energy balance for rodents.
 Studies using fat cells from humans demonstrated that IL-6 induces lipolysis by 26 percent to 79 percent; leptin production was increased when cortisol was present; and the effect of insulin on the enzyme lipoprotein lipase, which is necessary to transport fat from the blood into the fat cell, was reduced. When infused (injected slowly via an IV) into healthy adults, IL-6 increased lipolysis by 50 percent and increased cortisol and GH.
 Though the evidence isn’t considered conclusive by scientists, there’s strong evidence suggesting that IL-6 may be one of the more potent messengers signaling for fat loss on an autocrine or paracrine level (affecting the same or nearby cells). The level of impact on fat loss or gain may not be as potent as insulin or norepinephrine (a nerve signal similar to adrenaline), but it’s significant.



 
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