Key result
Visceral fat is closely related to the risk of Type 2 diabetes and its macrovascular complications, with inflammation serving as a major pathway linking insulin resistance to obesity.
Visceral fat and its associated inflammatory pathways are key drivers of insulin resistance and macrovascular complications in Type 2 diabetes.
Should not yet change T2D practice; hypothesis-generating for inflammation-targeted visceral fat interventions, pending RCTs.
SUMMARY Macrovascular complications of Type 2 diabetes account for the majority of mortality in this condition and are related to insulin resistance. Abdominal obesity, and especially visceral fat, has proven to be particularly important in these associations. Indeed the risk for Type 2 diabetes and its complications is more closely related to visceral fat than overall obesity. Whether visceral fat by itself is pathogenic or a marker for ectopic accumulation of fat or a combination of both remains unresolved. Inflammation has now been established as a major pathway linking insulin resistance to obesity. Adipose tissue macrophage infiltration has been implicated in the activation of inflammatory pathways and development of insulin resistance. However, the mechanisms leading to these events are not clearly identified and remain active areas of investigation.
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Sam et al. (2011) conducted a review in Type 2 diabetes. Visceral fat was evaluated. Visceral fat is closely related to the risk of Type 2 diabetes and its macrovascular complications, with inflammation serving as a major pathway linking insulin resistance to obesity.
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