Abstract
Background Type 2 diabetes (T2D) is a chronic metabolic disease potentially leading to serious widespread tissue damage. Human organism develops T2D when the glucose-insulin control is broken for reasons that are not fully understood but have been demonstrated to be linked to the emergence of a chronic inflammation. Indeed such low-level chronic inflammation affects the pancreatic production of insulin and triggers the development of insulin resistance, eventually leading to an impaired control of the blood glucose concentration. On the contrary, it is well-known that obesity and inflammation are strongly correlated. Aim In this study, we investigate in silico the effect of overfeeding on the adipose tissue and the consequent set up of an inflammatory state. We model the emergence of the inflammation as the result of adipose mass increase which, in turn, is a direct consequence of a prolonged excess of high calorie intake. Results The model reproduces the fat accumulation due to excessive caloric intake observed in two clinical studies. Moreover, while showing consistent weight gains over long periods of time, it reveals a drift of the macrophage population toward the proinflammatory phenotype, thus confirming its association with fatness.
Highlights
Diabetes is a chronic disease characterized by a decreased production of insulin and by a reduced efficacy of the insulin produced. is impaired condition is differently caused by both type 1 and type 2 diabetes
We employed computational modeling and simulation to describe the effects of high calorie diets on the pathology of type 2 diabetes limiting our observation to the process of weight gain leading to the onset of an inflammation state
It is worth to note that, overall, body weight (BW)(t) in Figure 4 is nonlinear and has two phases: the first one due to the swelling of the adipocytes present at the initial time, and the second due to the enlargement of the newly recruited adipocytes. is result suggests that the weight gain dynamics has the characteristics of a nonlinear process with a quicker phase followed by a slower progression due to, respectively, swelling and recruitment of new cells; a peculiar dynamics which certainly depends on the individual characteristics such as the distribution and/or metabolic characteristics of the adipocytes in the adipose tissue
Summary
Type 2 diabetes (T2D) is a chronic metabolic disease potentially leading to serious widespread tissue damage. Human organism develops T2D when the glucose-insulin control is broken for reasons that are not fully understood but have been demonstrated to be linked to the emergence of a chronic inflammation. Such low-level chronic inflammation affects the pancreatic production of insulin and triggers the development of insulin resistance, eventually leading to an impaired control of the blood glucose concentration. We model the emergence of the inflammation as the result of adipose mass increase which, in turn, is a direct consequence of a prolonged excess of high calorie intake. While showing consistent weight gains over long periods of time, it reveals a drift of the macrophage population toward the proinflammatory phenotype, confirming its association with fatness
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