Obesity and type 2 diabetes (T2D) often go hand in hand. In fact their seeming inseparability has led to the convenient catch phrase diabesity. However since not all type-2 diabetics are obese and not all overweight people are diabetic the natural question is: which comes first obesity or diabetes?  As our understanding of the metabolic disturbances underlying the two conditions expands and evolves it is clear that cases can be made for both: the deranged glucose metabolism and insulin signaling that underlie diabetes can cause obesity but obesity itself whatever the initial cause can interfere with proper glucose and insulin regulation.

A fundamental concept here is that excess body fat is more than just something visually unappealing in light of our modern aesthetic ideal. Adipose tissue itself is a complex endocrine organ whose products have far-reaching effects throughout the body. Hundreds of secretory products have been identified in adipose tissue and researchers have barely scratched the surface regarding the possible effects these have locally and systemically.

Whatever initially causes the accumulation of excess body fat be it impaired carbohydrate metabolism overeating across all macronutrients or some other trigger once the adipose tissue is established its secretions can instigate changes to the pancreas and skeletal muscles that may lead to T2D.

Expanding adipose tissue particularly when that expansion is due to hypertrophy rather than hyperplasia (that is enlargement of existing fat cells rather than the generation of new ones) seems to move toward a more inflammatory secretory profile than adipose cells that stay closer to physiological norms. Larger cells exhibit increased secretion of pro-inflammatory signaling molecules including interleukin-1² interleukin-6 interleukin-8 and tumor necrosis factor. To make matters worse these larger fat cells show a reduced secretion of adiponectin a protein positively correlated with insulin sensitivity as well as being anti-inflammatory and having specific beneficial and anti-apoptotic effects on the insulin-producing pancreatic beta cells. It is also noteworthy that visceral abdominal fat tissue commonly referred to as the apple shape somatotype that seems to bring with it detrimental metabolic consequences shows markedly reduced adiponectin secretion compared to subcutaneous fat or fat stored in the lower body which we currently understand to be less metabolically threatening. 

If we think of adipose tissue in general as an endocrine organ then just like any other organ it may undergo changes from metabolic and environmental insults that result in dysfunction. And in obese patients with metabolic complications specifically this seems to be one of the factors that leads to a vicious circle in which systemic inflammation induces negative changes to the adipose tissue and the adipose tissue itself secretes increased amounts of inflammatory signaling molecules that negatively affect beta cell function and skeletal muscle insulin sensitivity.

If this dysfunctional fat tissue is largely the result of systemic inflammation and oxidative stress caused by overnutrition or unbalanced macronutrient intake (specifically excessive carbohydrate intake); then a reduced-carbohydrate anti-inflammatory diet combined with appropriate cardiovascular and muscle-building exercise in conjunction with a targeted supplementation program would likely go a long way toward protecting the entire body from the long-term adverse effects of fat tissue that has seemingly turned against its host.

As always a diet of whole unprocessed foods should be the foundation to restore and maintain optimum health but supplemental nutrients that could potentially be beneficial in therapeutic doses include those that support healthy glucose metabolism and insulin regulation such as chromium picolinate and vanadium cinnamon gymnema sylvestre magnesium and B vitamins.