The Concept of CMR
Intra-abdominal Adipose Tissue: the Culprit?
Type 2 Diabetes: the Ultimate Manifestation
It is firmly established that insulin resistance is a powerful risk factor for the development of type 2 diabetes. To maintain euglycemia (normal blood sugar levels), insulin secretion must increase as a function of the degree of insulin resistance. However, if pancreatic beta cells are vulnerable, these cells may become exhausted, leading to a progressive deficit in insulin secretion. This causes hyperglycemia and the clustering metabolic abnormalities of type 2 diabetes. As excess intra-abdominal (visceral) fat is closely related to insulin resistance, at least 75% (if not more) of type 2 diabetic patients have excess intra-abdominal adipose tissue. Abdominal obesity associated with excess intra-abdominal adiposity is therefore one of the key features of type 2 diabetes. The excess intra-abdominal fat found in type 2 diabetic patients is also linked to excess liver fat and ectopic fat deposition (accumulation of fat at undesirable locations such as the skeletal muscles, heart, etc.). This accumulation of fat is closely linked to the insulin resistance state found in patients with type 2 diabetes. Insulin resistance has also been found to be a central component of a constellation of athero-thrombotic, inflammatory abnormalities that have often been referred to as the insulin resistance or metabolic syndrome. These abnormalities seen in type 2 diabetic patients with excess intra-abdominal/ectopic fat are also found in non-diabetic patients with excess intra-abdominal fat and insulin resistance and therefore increase the risk of cardiovascular disease/coronary heart disease beyond the risk associated with hyperglycemia.
These results emphasize the notion that in addition to the well-documented importance of improving the glycemic control of patients with type 2 diabetes, special focus should also be placed on managing their insulin resistant state. Because insulin resistance in type 2 diabetic patients is closely linked to their excess intra-abdominal/ectopic fat, losing intra-abdominal fat will improve most features of the metabolic syndrome. On that basis, type 2 diabetes should be considered as the end of a continuum linking excess intra-abdominal/ectopic fat to insulin resistance among genetically susceptible individuals with inadequate β-cell response. Type 2 diabetes can therefore be considered as the ultimate manifestation of excess intra-abdominal/ectopic fat deposition.