Different fats and inflammation

Let me just start off by saying that fat gain happens mostly in the presence of caloric excess (when more calories are consumed than is being burned). For healthy adipose tissue expansion, there needs to be acute inflammation, collagen remodeling and growth of new blood vessels (angiogenesis). Without these factors, healthy fat gain cannot take place; fat cells become hypoxic and chronic inflammation occurs.

An impaired local proinflammatory response in the adipocyte leads to increased ectopic lipid accumulation (places where you don’t want it), glucose intolerance, and systemic inflammation.

In white adipose tissue, chronic inflammation is associated with an increase in macrophage (immune cells) infiltration. Surgically induced weight loss, diet and exercise, and improving insulin sensitivity all reduce macrophage infiltration in white adipose tissue (AT), and decrease the expression of proinflammatory markers in white AT and plasma.

In obese subjects, adipose tissue macrophages content is higher in visceral than subcutaneous adipose tissue, consistent with the hypothesis that visceral fat plays a more prominent role in insulin resistance (1). ATMs (AT macrophages) are a prominent source of proinflammatory cytokines such as TNF-α and IL-6 that can block insulin action in adipocytes, providing a potential link between inflammation and insulin resistance.

In my previous article, I showed that SFAs make a cell more insulin resistant and can thus protect against nutrient overload in the cell. But white adipose tissue, which is where fat is stored, contains much less mitochondria than brown adipose tissue, and WAT doesn’t oxidize fats the same as BAT.

In this article we are going to look at TLR4, TNFα, and IKKβ in the context of gaining healthy fat while being in a caloric surplus. TLR4 is needed for angiogenesis, TNFα is needed for collagen remodeling, and IKKβ is needed for new fat cell synthesis.


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