Understanding the role metabolic inflammation plays in obesity and diabesity
Obesity is a disease that has plagued the modern day man in recent time. Access to highly processed foods and decrease in physical activity are key contributors to this ailment. Researchers are hard at work looking into what other underlying factors lead to obesity, especially given its relationship with the onset of Type 2 Diabetes, Cardiovascular diseases, and liver disease. We will take an in-depth look at metabolic inflammation and its role in the onset of obesity. Let’s dive in.
Obesity is a state in which there is an over-accumulation of subcutaneous and/or abdominal fat (adipose tissue) characterized by a low grade chronic state of inflammation in which the level of pro inflammatory cytokines are increased. This adipose tissue is no longer considered inert and mainly devoted to storing energy; it is emerging as an active tissue in the regulation of physiological and pathological processes including immunity and inflammation.
| Weight (Pounds) x 703 OR Weight (Kilograms)
|Height (Inches) x Height (Inches) Height (Meters) x Height (Meters)|
Obesity is diagnosed when your body mass index (BMI) is 30 or higher. To determine your body mass index, use one of these formulas:
|30.0 and higher||Obesity|
For most people, BMI provides a reasonable estimate of body fat. Because BMI doesn’t directly measure body fat, some people such as muscular athletes may have a BMI in the obesity category even though they don’t have excess body fat.
‘Diabesity’ is the term for diabetes occurring in the context of obesity. This form of obesity-dependent diabetes has emerged as a major public health problem in recent times. Though it is basically explained by insulin resistance and pancreatic beta cell dysfunction, new patterns have evolved to explain these modifications in the context of the modern rates of obesity and diabetes.
The connection between obesity and inflammation has been in debate in the recent past. Unbeknownst to many, the link between these conditions was made decades ago. Over a century ago, high doses of a class of anti-inflammatory compounds including aspirin (salicylates) were used to treat Type 2 diabetes. In some cases, the symptoms of diabetes totally disappeared. Unfortunately, this treatment was discontinued due to the serious side effects caused by the high doses of salicylates.
We will now look at the questions of our topic today in-depth; does obesity cause inflammation, or is inflammation caused by something secondary to obesity such as high blood sugar or triglycerides levels? How about diabesity? Does diabesity cause inflammation, or does inflammation cause diabesity? How and why does the body initiate an inflammatory response to diabesity? Let us tackle each item separately.
Listed are some lines of evidence that show inflammation directly causes obesity and diabesity.
In the past, fat was considered an inactive tissue with no biological action. It wasn’t considered for much other than storing energy. It has now emerged that fat tissue is a metabolically active endocrine organ that secretes hormones and inflammatory cytokines such as IL-6 and TNF-α. This metabolic activity of fat is the key to understanding its role in diabesity.
The first theory is that obesity-induced inflammation is a protective mechanism that prevents the body from losing mobility or fitness. Fat storage is an anabolic process, which means it builds up the organs and tissues. Inflammation, on the other hand, is a catabolic process which breaks down organs and tissues. It’s possible that the activation of catabolism via inflammation is the body’s attempt to keep weight within acceptable bounds. Evidence that experimentally induced local inflammation in fat tissue improves insulin resistance and causes weight loss supports this theory.
The second theory is that, obesity-induced inflammation is simply a malfunction that was never selected against in human evolution. Obesity and its related disorders have been extremely rare throughout human history, and have only become common in the past 40 years. The surplus of modern, processed foods that accompanies diabesity is also a relatively new phenomenon. It’s possible that the stresses of obesity are similar enough to the stresses of an infection that the body reacts to obesity in the same way it would to an infection: via inflammation. Supporting this theory is evidence that the same intracellular, inflammatory stress pathways are activated in both obesity and infection.
We can therefore conclude that inflammation is both the cause and the result of diabesity. Once obesity and/or insulin resistance have been established, each can further stimulate the production of inflammatory cytokines, forming a vicious cycle of inflammation and diabesity.
Reduction of inflammation is a major key in preventing and treating diabesity. Focusing exclusively on regulating blood sugar and fat hormones without addressing other potential causes of inflammation is bound to produce inferior results.