Biology Forums - Study Force

How do all the systems in the body work together to maintain homeostasis?

An advantage of homeostatic regulation is that it allows an organism to function effectively in a broad range of environmental conditions. For example, ectotherms tend to become sluggish at low temperatures, whereas a co-located endotherm may be fully active. That thermal stability comes at a price since an automatic regulation system requires additional energy. One reason snakes may eat only once a week is that they use much less energy to maintain homeostasis.

Most homeostatic regulation is controlled by the release of hormones into the bloodstream. However other regulatory processes rely on simple diffusion to maintain a balance.

Homeostatic regulation extends far beyond the control of temperature. All animals also regulate their blood glucose, as well as the concentration of their blood. Mammals regulate their blood glucose with insulin and glucagon. These hormones are released by the pancreas, the inadequate production of the two for any reason, would result in diabetes. The kidneys are used to remove excess water and ions from the blood. These are then expelled as urine. The kidneys perform a vital role in homeostatic regulation in mammals, removing excess water, salt, and urea from the blood. These are the body's main waste products.

Another homeostatic regulation occurs in the gut. Homeostasis of the gut is not fully understood but it is believed that Toll-like receptor (TLR) expression profiles contribute to it. Intestinal epithelial cells exhibit important factors that contribute to homeostasis: 1)They have different cellular distribution of TLR?s compared to the normal gut mucosa. An example of this is how TLR5 (activated by flagellin) can redistribute to the basolateral membrane which is the perfect place where flagellin can be detected.[1] 2)The enterocytes express high levels of TLR inhibitor Toll-interacting protein (Tollip). Tollip is a human gene that is a part of innate immune system and is highest in a healthy gut, it correlates to luminal bacterial load.[1] 3)Surface enterocytes also express high levels of Interleukin-1 receptor (IL-1R) -containing inhibitory molecule. IL-1R are also referred to as single immunoglobulin IL-1R (SIGIRR). Animals deficient of this are more susceptible to induced colitis, implying that SIGIRR might possibly play a role in tuning mucosal tolerance towards commensal flora.[1] Nucleotide-binding Oligomerization Domain containing 2 (NOD2) is suggested to have an affect on suppressing inflammatory cascades based on recent evidence.[1] It is believed to modulate signals transmitted through TLRs, TLR3, 4, and 9 specifically. Mutation of it has resulted in Crohn's disease. Excessive T-helper 1 responses to resident flora in the gut are controlled by inhibiting the controlling influence of regulatory T cells and tolerance-inducing dendritic cells.