The considerable commonalities between patients with obesity and type 2 diabetes (T2D) can be useful for clinicians as they develop treatment plans for these serious diseases. The risk for developing prediabetes and T2D increases as BMI increases. An increase in visceral adipose tissue increases diabetes risk, in part because visceral fat itself responds weakly to insulin. Less susceptible to the anti-lipolytic property of insulin than other tissues, this fat becomes a source of lipotoxic circulating free fatty acids, which in turn further reduces insulin sensitivity in muscle and liver tissue, limiting glucose disposal after meals. Another contribution of excess weight to diabetes risk is related to inflammation.


There is a powerful feedback loop at work here: overweight leads to hyperinsulinemia, which leads to further overweight, which leads to further hyperinsulinemia and insulin resistance. The scope of the problem is daunting, but our understanding of the treatment of obesity and diabetes has been refined to a point that we may address both at once. Clinicians who focus on obesity treatment and arm themselves with the tools and principles of obesity medicine to prevent and care for T2D can help their patients lead healthier lives.

The Diabetes Prevention Program found that even a 7% decrease in body weight is associated with a 58% reduction in the risk of developing T2D. A weight loss of 5% to 10% improves glycemic control, and a 20% weight loss can potentially reverse T2D. By treating diabetes with an obesity focus, clinicians can control glucose levels while also treating the underlying pathophysiology of T2D—insulin resistance. Thus, treating diabetes with medications that benefit weight, like metformin, GLP-1 receptor agonists, and SGLT-2 inhibitors rather than using medications that promote weight gain, like insulin and sulfonylureas, can have a dual benefit.