Abdominal Obesity and Type 2 Diabetes

• The fast, simultaneous growth of obesity and type 2 diabetes has led to the coining of the term “diabesity” to illustrate the close relationship between these two diseases.
• A preferential accumulation of abdominal adipose tissue has been linked to glucose intolerance, hyperinsulinemia, and insulin resistance, which are metabolic complications predictive of increased type 2 diabetes risk.
• Using simple tools such as waist circumference to measure visceral adiposity can help assess type 2 diabetes risk independent of relative weight (BMI).
• These findings underscore the need to go beyond simple measurement of total body weight and BMI when evaluating type 2 diabetes risk in patients.

As a health hazard, obesity has been linked to numerous metabolic complications such as dyslipidemia, type 2 diabetes, and cardiovascular disease (CVD) [1,2]. The number of overweight or obese individuals is fast increasing worldwide, and this increase has meant a concomitant rise in the prevalence of type 2 diabetes [2,3]. With type 2 diabetes reaching epidemic proportions, the International Diabetes Federation (IDF) has predicted that the number of individuals with diabetes may rise to 700 million by 2045 [4]. The term “diabesity” has been coined [5,6] to emphasize the close relationship between these two diseases. Indeed, obesity and type 2 diabetes frequently occur together, and the vast majority of type 2 diabetic individuals are or have been obese [7,8]. Along with genetic susceptibility, obesity is the most important risk factor for type 2 diabetes [9,10]. The term “diabesity” singles out excess body weight as the major cause of type 2 diabetes [5].

The strong relationship between obesity and type 2 diabetes does not mean that being overweight or obese will inevitably cause type 2 diabetes. For example, some normal weight individuals may be at high risk of developing type 2 diabetes, whereas many very obese individuals are not insulin resistant [11] and may never develop the disease. Some etiological factors linking excess body fat and type 2 diabetes could explain this phenomenon. Obesity and type 2 diabetes share a number of causative lifestyle factors such as excessive energy intake, a diet high in saturated fat, and a sedentary lifestyle. However, the risk of developing type 2 diabetes may also depend on genetic susceptibility and the distribution of adipose tissue [12].

The possibility of a relationship between body fat distribution and type 2 diabetes was first raised in the mid-forties by French physician Jean Vague [13]. He reported that the complications generally found in obese patients depended more on the location of the excess fat rather than obesity per se [13]. Following this observation, he described the high-risk form of obesity as “android obesity,” a condition commonly found in men and in which adipose tissue accumulates in the trunk. In opposition, he described the accumulation of body fat in the gluteo-femoral region—the common fat pattern of premenopausal women—as “gynoid obesity.” This type of fat distribution rarely leads to common obesity-related complications [14,15]. Since these pioneering observations, many cross-sectional and prospective studies have linked type 2 diabetes to body fat distribution.

Evidence is mounting in support of the notion that it is not excess body fat but rather high visceral adiposity that increases the risk of type 2 diabetes and CVD [30]. For a given amount of total body fat, individuals with more visceral adipose tissue are at substantially greater risk of being insulin resistant and developing atherogenic and diabetogenic complications [30,31]. It has been shown that visceral adipose tissue is more metabolically active and more closely tied to metabolic abnormalities than subcutaneous adipose tissue [32,33]. In 1987, Fujioka et al. [34] were the first to propose that a preferential accumulation of visceral adipose tissue could explain the deterioration in glucose and lipid metabolism observed in obese patients. They found that subjects with large amounts of visceral adipose tissue had higher fasting plasma triglyceride levels and higher plasma glucose responses following an oral glucose challenge than subjects who had the same total body fat mass (as measured by BMI) but a preferential accumulation of abdominal subcutaneous adipose tissue. Pouliot et al. [35] later quantified the respective contributions of subcutaneous and visceral fat to glucose intolerance and hyperinsulinemia in obese individuals. Two groups of obese patients were carefully matched for the same amount of total body fat but had either low or high amounts of visceral adipose tissue. The authors found that obese individuals with low levels of visceral adipose tissue had normal glucose tolerance when compared to lean controls. However, obese subjects with high levels of visceral adipose tissue showed an increase in their glycemic and insulinemic responses to an oral glucose challenge. Additional studies by Ross et al. [36,37] further explored the relationship between visceral adipose tissue and metabolic risk in men and women. When individuals who were matched for similar abdominal subcutaneous adipose tissue but had different levels of visceral adipose tissue were compared, it was revealed that subjects with high visceral adipose tissue had higher glucose values following an OGTT and lower glucose disposal values compared to subjects with low visceral adipose tissue. These results lend weight to the idea that obese individuals with excess visceral adipose tissue display alterations in indices of plasma glucose-insulin homeostasis and are therefore at increased risk of developing type 2 diabetes.

Similarly, the Insulin Resistance Atherosclerosis Study (IRAS) showed that waist circumference—which is the best anthropometric parameter to crudely assess the absolute amount of visceral fat—was a strong predictor of reduced peripheral insulin action in non-diabetic lean individuals [38]. Wang et al. [29] have also confirmed that waist circumference is a better predictor of type 2 diabetes than WHR or BMI.

In addition, a prospective study by Boyko et al. [39] conducted among Japanese Americans followed for 6 to 10 years examined the relationship between direct measurement of visceral fat via computed tomography and incidence of type 2 diabetes. They found that excess visceral adiposity preceded the disease’s development in Japanese Americans. Visceral adipose tissue was predictive of type 2 diabetes independent of fasting insulin, insulin secretion, glycemia, total and regional adiposity, and family history of diabetes. This study confirms that visceral adipose tissue plays a key role in the development of type 2 diabetes.

In summary, measuring waist circumference makes it easier to identify patients with visceral obesity, insulin resistance, and metabolic complications leading to type 2 diabetes [40]. Unlike overall obesity per se—which can cause moderate metabolic complications—excess visceral adipose tissue has a significant negative effect on indices of plasma glucose-insulin homeostasis that predict an increased risk of type 2 diabetes [41]. Measuring visceral adipose tissue using simple tools such as waist circumference should therefore be a crucial step in assessing type 2 diabetes risk among patients.