When obese adults lose 10% of their body weight, their fat tissue becomes more responsive to insulin, with a 26% improvement in a key measure of insulin resistance, even though levels of immune...

After losing weight, fat tissue becomes more responsive to insulin without changes in the number of immune cells or inflammatory signals. In some cases, higher levels of inflammation markers are linked to lower insulin resistance, suggesting immune cells may play a supportive role in tissue adaptation.

In people with obesity, the link between inflammation in fat tissue and insulin resistance is explained by the size of fat cells; when researchers account for fat cell size, the connection between inflammation and insulin resistance no longer remains.

In people with obesity, larger fat cells in the subcutaneous layer are more closely linked to insulin resistance in fat tissue than the presence of immune cells, aging cells, or inflammatory molecules, suggesting that fat cell enlargement, not inflammation, is the main factor disrupting fat breakdown.

Even when obese mice lose weight by eating less on a high-fat diet, their belly fat stays inflamed — unlike mice that eat a healthy low-fat diet, whose inflammation goes away.

In humans, larger fat cells in the abdomen and thighs are linked to reduced effectiveness of insulin in stopping fat breakdown, which is measured by a specific marker called IC50.