Changes

This pathophysiology can be linked as follows:  

This pathophysiology can be linked as follows:  

Excess nutrition leads to the expansion of fat mass and an increase in the size of adipocytes (hypertrophy).  This leads to obesity. In the fat cells of obese individuals, there is increased production of metabolism modulators, such as glycerol, hormones, macrophage stimulating chemokines, and pro-inflammatory cytokines, leading to the development of insulin resistance.</ref>Kahn SE, Hull RL, Utzschneider KM (December 2006). "Mechanisms linking obesity to insulin resistance and type 2 diabetes". Nature. 444 (7121): 840-6. doi:10.1038/nature05482. PMID 17167471</ref> Insulin plays a major role in fat production in adipocytes, synthesis of unsaturated fatty acids, and stimulating lipogenesis. It also plays a role in the uptake of glucose by muscles.  The malfunctioning of insulin in turn leads to diabetes.

Excess nutrition leads to the expansion of fat mass and an increase in the size of adipocytes (hypertrophy).  This leads to obesity. In the fat cells of obese individuals, there is increased production of metabolism modulators, such as glycerol, hormones, macrophage stimulating chemokines, and pro-inflammatory cytokines, leading to the development of insulin resistance.<ref>Kahn SE, Hull RL, Utzschneider KM (December 2006). "Mechanisms linking obesity to insulin resistance and type 2 diabetes". Nature. 444 (7121): 840-6. doi:10.1038/nature05482. PMID 17167471</ref> Insulin plays a major role in fat production in adipocytes, synthesis of unsaturated fatty acids, and stimulating lipogenesis. It also plays a role in the uptake of glucose by muscles.  The malfunctioning of insulin in turn leads to diabetes.

==Current researches: ==

==Current researches: ==