A dangerous alliance between obesity and insulin resistance
According to the statistics of World Health Organization, in 2008, 34% of men and 35% of women aged 20+ were overweight (BMI ≥ 25 kg/m2). The worldwide prevalence of obesity has nearly doubled between 1980 and 2008. In 2008, 10% of men and 14% of women in the world were obese (BMI ≥30 kg/m2), compared with 5% for men and 8% for women in 1980. Since obesity is linked with insulin resistance, the current trends of obesity will correspondingly increase the prevalence of insulin resistance worldwide. Undoubtedly, an epidemic of obesity-insulin resistance-type-2diabtes has taken over the world. Surprisingly, the statistics indicate that worldwide at least 2.8 million people die each year as a result of being overweight or obese.
It has been well established that there exists an association between body weight and development of insulin resistance. The persons, who are overweight or obese, are more likely to develop insulin resistance, which is precursor to type-2 diabetes. Central obesity, commonly called potbelly, is also known to predispose the individuals to insulin resistance even if they have normal weight. Central obesity may, therefore, lead to type-2 diabetes.
Underlying mechanism –
In obese individuals, fat primarily white adipose tissue (WAT) releases increased amounts of hormones, pro-inflammatory cytokines and other factors that are involved in the development of insulin resistance. When insulin resistance is accompanied by dysfunction of pancreatic islet β-cells that release insulin, blood glucose levels rise. Therefore, abnormalities in pancreatic β-cell function are critical in defining the risk and development of type 2 diabetes.
A study in 1993 showed a link between obesity and inflammation, demonstrating that the pro-inflammatory cytokine tumor-necrosis factor (TNF)-α was expressed in adipose tissue of obese mice and linked to insulin resistance (IR).
White adipose tissue (WAT) is primarily associated with insulin resistance in humans. Obesity-associated inflammation starts in adipose tissue and liver with elevated macrophage infiltration and expression of pro-inflammatory cytokines. The pro-inflammatory cytokines enter the blood stream to cause systemic inflammation. In obesity, chronic inflammation has many detrimental effects in the body. And one of its detrimental effects is development of insulin resistance.
It has been found that central obesity raises serum resistin levels in the body, which directly co-relates to insulin resistance. Studies also validate a direct co-relation between resistin levels and type-2 diabetes. Central obesity seems to be the foremost type of fat deposits contributing to rising levels of serum resistin. Conversely, serum resistin levels have been found to decline with decreased adiposity following its management.
Worldwide statistics reveal that prevalence of obesity is steadily increasing all over the world. And since obesity undoubtedly causes insulin resistance, which is turn may lead to type-2 diabetes.
According to reliable projections of the prevalence of type-2 diabetes, it is assumed that total diabetes cases, diagnosed and undiagnosed, will increase from 14% in 2010 to 21% of the US adult population by 2050. These projections are largely attributable to aging population that has a higher risk of insulin resistance. And, moreover, older people are living longer these days. The scenario of prevalence of type-2 diabetes is more or less the same in the developed and in some of the developing nations.
It will not be an exaggeration to say that the nexus of obesity, insulin resistance and type-2 diabetes is epidemically prevalent worldwide. If this nexus is not broken in time, notwithstanding other harmful effects of obesity, there will a big surge in the prevalence type-2 diabetes and its associated co-morbidities.