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IL6 is known to cause some effects that on the face of things would seem to be obesigenic (promoting obesity). When IL6 interacts with receptors on liver cells, it stimulates enzymatic reactions that increase insulin resistance.3,5,14 During periods of fasting (not eating), the liver creates sugar by breaking down glycogen or from fatty acids or Amino Acids in a process called gluconeogenesis. When a person begins eating, one of the first responses of the body is for this process to be shut down in the liver, as the first phase of insulin is released during a meal. The shutdown of gluconeogenesis occurs because the constant efflux (outpouring) of sugar from the liver would strain sugar control mechanisms and force the body to maintain higher insulin levels longer, resulting in a pre-diabetic state. In fact, several of the latest diabetes drugs function by restoring this first phase response and result in significant weight loss for many people.15 The constant bombardment of the liver with TNF and IL6 from visceral fat likely creates a state of hepatic (liver) insulin resistance that accounts for some of the negative consequences seen in states with chronic low-level inflammation, such as obesity.
IL6 also produces insulin resistance in adipocytes (fat cells).4 Though this sounds bad, in regard to fat loss, it may be a good thing. Fat cells are necessary for long-term health, as they buffer the concentration of fatty acids in the bloodstream— during periods of starvation (which is associated with low insulin levels), fats are broken down and released; following a meal, when insulin is high, fats are stored. Recall that when the liver suffers from insulin resistance, it continues to pump out sugar, forcing insulin to rise. This increases the fat storage signal, which increases the fat mass, the source of TNF, which stimulates IL6 production. It is a vicious cycle, like metabolic poverty. When IL6 creates a state of insulin resistance in the fat cell, it prevents it from storing fat to the same degree, so it would seem that there would be a balance— a give and take. However, remember that the IL6 affecting the liver comes primarily from the visceral fat, whose blood supply drains directly into the liver; whereas the circulating IL6 in the bloodstream that interacts with all other depots of fat is diluted by the greater volume of blood or generated by other tissue, such as skeletal muscle or by the fat cell itself.
This brings to the forefront one of the areas of confusion in the field of IL6 research, acute versus chronic effects. IL6 does indeed have some effects that can lead to insulin resistance and pre-diabetes, therefore promoting obesity if IL6 levels are mildly elevated long-term. However, in normal-weight people who do not have large depots of visceral fat, acute (short-term) spikes in IL6 actually appear to be beneficial. To better understand this, it is important to realize the impact of lifestyle— active versus sedentary.
Aside from fat cells and cells involved in immunity and inflammation, there is one other major source of IL6— contracting muscle.9,16,17 When skeletal muscle contracts, such as during exercise, IL6 is released in huge quantities. This IL6 acts on the tissue immediately surrounding the area as well as getting into the bloodstream. By the time it reaches the liver (through the hepatic circulation rather than the portal circulation which is the route taken by visceral fat-originated IL6), the IL6 is diluted. However, the levels reaching subcutaneous fat are considerable. Why would the body want to put out loads of IL6, especially during exercise when it needs to absorb energy, when IL6 has been shown to increase insulin resistance in the liver and fat cell?
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Research and Review 
