Steroids and diabetes mechanism

The immediate effects of AAS in the brain are mediated by their binding to androgen (male sex hormone) and estrogen (female sex hormone) receptors on the surface of a cell. This AAS–receptor complex can then shuttle into the cell nucleus to influence patterns of gene expression. Because of this, the acute effects of AAS in the brain are substantially different from those of other drugs of abuse. The most important difference is that AAS are not euphorigenic, meaning they do not trigger rapid increases in the neurotransmitter dopamine , which is responsible for the “high” that often drives substance abuse behaviors. However, long-term use of AAS can eventually have an impact on some of the same brain pathways and chemicals—such as dopamine, serotonin, and opioid systems—that are affected by other drugs of abuse. Considering the combined effect of their complex direct and indirect actions, it is not surprising that AAS can affect mood and behavior in significant ways.

Steroid diabetes must be distinguished from stress hyperglycemia , hyperglycemia due to excessive intravenous glucose, or new-onset diabetes of another type. Because it is not unusual for steroid treatment to precipitate type 1 or type 2 diabetes in a person who is already in the process of developing it, it is not always possible to determine whether apparent steroid diabetes will be permanent or will go away when the steroids are finished. More commonly undiagnosed cases of type 2 diabetes are brought to clinical attention with corticosteroid treatment because subclinical hyperglycemia worsens and becomes symptomatic. Generally, steroid diabetes without preexisting type 2 diabetes will resolve upon termination of corticosteroid administration.

Steroids and diabetes mechanism

steroids and diabetes mechanism


steroids and diabetes mechanismsteroids and diabetes mechanismsteroids and diabetes mechanismsteroids and diabetes mechanismsteroids and diabetes mechanism