Visceral Adipose Tissue: the Culprit?

Visceral obesity (excess fat in the abdominal cavity) is closely linked to blood sugar and lipid problems that increase the risk of type 2 diabetes and coronary heart disease. Compared to normal weight individuals or obese subjects with low levels of visceral fat, obese patients with large amounts of visceral fat are characterized by high blood pressure, atherogenic dyslipidemia (elevated triglycerides and low levels of good HDL cholesterol), impaired glucose-insulin homeostasis (elevated blood glucose and a state of insulin resistance), and an inflammatory and pro-thrombotic (tendency to form clots in the blood, impeding blood flow) profile. Several studies have shown that a selective excess of visceral fat increases the risk of type 2 diabetes. The development of sophisticated imaging techniques has made it possible to accurately measure and distinguish visceral from subcutaneous fat (the fat located just under the skin). These non-invasive imaging techniques have also enabled researchers to conclude that, unlike visceral fat, subcutaneous fat is seldom associated with metabolic complications. It is unclear which factors influence whether dietary fat is stored under the skin or in the abdominal cavity. Variables such as age, gender, menopause, and ethnicity all influence where fat is stored.

It has been proposed that excess visceral fat may indicate that an individual’s subcutaneous adipose tissue is unable to serve as an “energy sink” for a calorie surplus resulting from excess energy intake and/or reduced energy expenditure. This inability may cause fat to accumulate at undesired locations, a phenomenon that has been described as ectopic fat deposition. Excess visceral fat may therefore be a “red light” or warning sign that excess energy is being stored as fat in unusual places, increasing the risk of diabetes and cardiovascular disease.

Obesity increases the risk of chronic complications. There is also compelling evidence that a high-risk form of overweight/obesity—visceral obesity—is linked to the most severe metabolic abnormalities. With its peculiar metabolism, hyperlipolytic activity, and anatomic location, excess visceral fat plays a key role in insulin resistance, especially in the liver. This can cause glucose intolerance and type 2 diabetes in genetically susceptible individuals. High amounts of visceral fat are also closely tied to the typical atherogenic dyslipidemia found in individuals with abdominal obesity. High blood pressure, a pro-thrombotic state, and—more recently—a pro-inflammatory profile are other abnormalities seen mainly in individuals with excess visceral fat, irrespective of body weight. In addition to its possible role in causing insulin resistance and related metabolic abnormalities, excess visceral fat may also be a marker of ectopic fat deposition. This means that visceral obesity may indicate that an obese individual has too much fat at undesirable locations—such as the liver, skeletal muscle, and the pancreas—which can cause serious problems with carbohydrate and lipid metabolism.

Read more on Complications of Visceral Obesity.

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 visceral fat is closely related to insulin resistance, at least 75% (if not more) of type 2 diabetic patients have excess visceral adipose tissue. Abdominal obesity associated with excess visceral adiposity is therefore one of the key features of type 2 diabetes. The excess visceral 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 visceral /ectopic fat are also found in non-diabetic patients with excess visceral 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 visceral /ectopic fat, losing visceral 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 visceral /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 visceral /ectopic fat deposition.

Read more on Type 2 Diabetes: The Ultimate Manifestation.

Obesity is an acknowledged health hazard and risk factor for cardiovascular disease (CVD) and type 2 diabetes, yet physicians have been perplexed by the remarkable heterogeneity of obese patients in clinical practice. Some obese patients display no CVD risk factors whereas others have type 2 diabetes, clinical signs of coronary heart disease, and are characterized by insulin resistance, atherogenic dyslipidemia, and a whole constellation of risk factors. Though we know that obesity is a health hazard, it is still unclear why this condition is so heterogeneous in its clinical manifestations.

The fact that obesity is so multifaceted means it must be redefined as a clinical entity. Evidence published over the last 25 years has proven that the subgroup of overweight or obese patients with excess abdominal fat—visceral fat in particular—has the highest risk of developing type 2 diabetes and CVD. Many factors influence the accumulation of visceral fat.

Read more on Causes and Correlates of Visceral Obesity.

Individuals vary in terms of how they store fat in response to a positive energy balance. However, the factors underpinning these differences are poorly understood. Excess visceral fat may be a marker of the inability of subcutaneous adipose tissue to act as an ‘energy sink’ for surplus calories resulting from excess energy intake and/or reduced energy expenditure. The inability of subcutaneous fat to store excess energy may cause fat to accumulate at undesirable locations such as the liver, skeletal muscle, heart, and even in pancreatic beta cells. This phenomenon has been described as ectopic fat deposition. In this regard, many of the metabolic complications found in individuals with excess visceral fat have also been found in those with a fatty liver and ectopic fat. Although liver fat has been frequently linked to excess visceral fat, several studies have shown that liver fat and visceral fat each contribute independently to the metabolic complications of abdominal obesity.

Read more on A Marker of Ectopic Fat Deposition.