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What is Diabesity?

Understanding diabesity, or obesity-dependent diabetes.

diabesity wordss

Diabesity is a common cause of chronic inflammation, so it’s important for fit pros to have a basic understanding of what it is and how it can affect clients. Here, Len Kravitz, PhD, Gabriella Bellissimo, MA and Jessica Smith, MS, CSCS, explain this relatively new term.

Diabesity is defined as diabetes caused by or highly associated with obesity. Diabesity is sometimes referred to as obesity-dependent diabetes (Farag & Gaballa 2011).

The Science Behind Diabesity

In diabesity, chronic overnutrition induces a “glucolypotoxic” state (Keane et al. 2015). In other words, if a diet is constantly full of high carbohydrates (gluco) and fats (lypo), a toxic physiologic state may result. Glucolypotoxicity negatively influences the function of mitochondria (the energy factories of cells) (Keane et al. 2015).

See also: More Evidence That Ultraprocessed Foods Lead to Obesity and Diabetes

In a glucolypotoxic state, the energy-producing capacity of mitochondria becomes impaired. That leads to a buildup of potentially damaging mitochondrial byproducts called reactive oxygen species molecules (also known as free radicals). Free radicals are unstable, highly reactive molecules that can damage RNA, DNA and proteins.

The buildup of free radicals stimulates low-grade inflammation throughout peripheral tissues in the body, as well as in beta cells (the cells that synthesize and secrete insulin) in the pancreas (Keane et al. 2015). Eventually, this leads to desensitization and blocking of the insulin signaling pathway and dysfunction of beta cells (Keane et al. 2015). Continual exposure to elevated glucose and lipids will impede the pancreatic beta cell secretion of insulin.

See also: Inflammation: Obesity, Diabetes, Aging and Exercise

The Pathway to Type 2 Diabetes

In a state of diabesity, the insulin signaling pathway becomes blocked by inflammatory cytokines inhibiting the muscle, fat and liver cells from using glucose. Skeletal-muscle mitochondrial cells are especially affected by this, as skeletal muscle is the principal tissue responsible for insulin-stimulated glucose disposal, accounting for up to 75% of glucose uptake (Zierath, Krook & Wallberg-Henriksson 2000). Eventually, insulin resistance and chronically elevated blood glucose levels will lead to type 2 diabetes.

Farag & Gaballa also cite research indicating that chronic stress may promote the development of diabesity through activation of inflammatory, autonomic, hormonal and immunological systems. They suggest that targeting stress management should be a cornerstone in the treatment of diabesity.

See also: How Exercise Helps Inflammation



Diabesity Chart

References

Farag, Y.M.K., & Gaballa, M.R. 2011. Diabesity: An overview of a rising epidemic. Nephrology Dialysis Transplantation, 26 (1), 28–35.

Keane, K.N., et al. 2015. Molecular events linking oxidative stress and inflammation to insulin resistance and b-cell dysfunction. Oxidative Medicine and Cellular Longevity, doi:10.1155/2015/181643.

Zierath, J.R., Krook, A., & Wallberg-Henriksson, H. 2000. Insulin action and insulin resistance in human skeletal muscle. Diabetologia, 43 (7), 821–35.

 

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