There are many types of diabetes. All are unified by elevated levels of blood sugar. Type 1 diabetes accounts for less than 10% of cases and results from autoimmune destruction of the beta cells in the pancreas, which produce and release insulin. (In an autoimmune process, antibodies that normally target and fight infection instead target one’s own cells). Type 3c (secondary) diabetes can occur when there has been destruction of the pancreatic beta cells through some other process, such as excessive alcohol, inflammation or surgical resection.
There are also many genetic forms of diabetes, each usually resulting from a single gene mutation that affects pancreatic function in some way. Finally, there is type 2 diabetes (T2D), which accounts for more than 90% of cases globally. Media reports of diabetes, particularly in the context of obesity, usually relate to T2D, the two terms often being used interchangeably.
Only T2D appears to be associated with obesity. Epidemiological studies across the world have shown that the greater one’s body mass index (BMI), the greater the chance of developing T2D. However, this is not the same as saying that obesity causes T2D. The majority of people who are obese will never develop T2D – a fact that exposes the statement “obesity causes diabetes” as absurd. Rather than referring to obesity as a cause of diabetes, it is more accurate to frame the issue as one of association between obesity and T2D (which is incontrovertibly true). As we gain weight, the sensitivity of our tissues to the effects of insulin diminishes (so-called “insulin resistance”). In response, our pancreatic beta cells, which produce insulin, need to work harder to produce more of it.
Our genetic makeup determines the strength of our pancreatic beta cells, and therefore influences which of us will make it up the hill and which of us will halt and roll back down. This is why T2D is in fact a genetic condition, and weight gain or obesity often contribute to its manifestation.
Why does insulin resistance occur with weight gain? To answer this, it is important to understand that abdominal (visceral) fat confers the greatest risk. Blood from visceral fat, laden with fatty acids, drains directly into the liver. Some of these fatty acids can spill over into the general circulation, where they can compete with glucose (sugar) uptake into more peripheral tissues, such as muscle. Given that glucose uptake is an insulin-mediated process, this competition promotes insulin resistance. Visceral fat also produces hormones called adipokines, some of which can further dampen the sensitivity of the insulin receptor to the effects of insulin.
The development of T2D is complex. There are many processes implicated, ranging from excretion of glucose in the urine, appetite regulation, control of pancreatic hormonal function and the role of gut bacteria. However, weight gain and insulin resistance appear to be associated with many of these processes.