Homeostasis Model Assessment

Nagasaka S, Aiso Y, Yoshiwaza K, Ishibashi S. Comparison of pioglitazone and metformin efficacy using homeostasis model assessment. Diabetic Med 2004 21 136 1. 

The homeostasis model assessment-insulin resistance (HOMA-IR) can be calculated with the following formula ... 

HOMA-IR Homeostasis model assessment of insulin resistance... 

Homeopathic medicine, 1507 Homeostasis, 3670 Homeostasis model assessment of... 

Tonalin 22.6% tran5- 0,cis-l2, 23.6%cis-, tram- 3, 17.6% cis-9,tram-, 16.6% trans-S,cis-lO, 7.7% tram-9,transAl and tram-l0,tram- 2, and 11.9% otiier CLA isomers. HOMA homeostasis model assessment QUICKI quantitative insulin sensitivity check index. 

Matthews, D.R., Hosker, J.P., Rudenski, A.S., Naylor, B.A., Treacher, D.F., and Turner, R.C. 1985 Homeostasis model assessment insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 28, 412-419. 

Endocrine In addition to peripheral insulin resistance and an impaired incretin effect, type 2 diabetes is associated with increased plasma levels of tumour necrosis factor alpha (TNFa). In a cross-over study on 10 healthy male volunteers, systemic inflammation induced by TNFa was used to examine any resultant alteration in the incretin hormone response to intravenous glucose. TNFa levels that induced symptoms of systemic inflammation increased plasma levels of this cytokine as well as levels of cortisol and IL-6 and increased the homeostasis model assessment of insulin resistance. By contrast, secretion of incretin hormones and the incretin effect remained unchanged [69 ]. 

Modulation of the SR Ca2+ ATPase by PLB perhaps provides the clearest evidence of the significance of the SR to smooth muscle Ca2+ homeostasis and contractility. It also offers some cautions since the effects of modulation of SR function were clearly dependent on the smooth muscle tissue studied. In summary, genetically altered mouse models provide a new approach for assessing the physiological significance of the SR to smooth muscle function in vivo. 

Compared to efficacy, safety is typically more multifactorial, as it is dependent on homeostasis of virtually all cellular processes. A wider number and diversity of potential molecular and cellular effects of compound interactions may affect safety than may affect efficacy or bioavailability. Accordingly, cytotoxicity assessment is less specific, more multi parametric and extrapolatable with less certainty, unless there are specific safety signals indicated by the chemical structure or by its precedents. Extrapolation of safety biomarker data needs a greater foundation of mechanistic understanding of both in vitro and in vivo pathogenesis of toxicities, as well as rigorous, empirical validation of models. 

In the absence of definitive human data, risk assessment may have to depend on the results of cancer bioassays in laboratory animals, short-term tests, or other experimental methods. Hence the following issues must be addressed under such circumstances the ability of the test system to predict risks for man (quantitatively as well as qualitatively) the reproducibility of test results the influence of species differences in pharmacokinetics, metabolism, homeostasis, repair rates, life span, organ sensitivity, and baseline cancer rates extrapolation across dose and dose rates, and routes of exposure the significance of benign tumors fitting models to the data in order to characterize dose-incidence relationships and the significance of negative results. 

Recently, Lautenschlager et al. (2010) described a multiparameter model in isolated rat intestinal segments to allow perfusion through the mesenteric artery and the gut lumen. In this model, blood vessels, lymphatics, interstitial space, and lumen are maintained, allowing the assessment of potential effects of drugs on fluid homeostasis, barrier functions, transport mechanisms, immtme responses, and gut motility in situ. 

Garcia J, Torres N (2011) Mathematical modeling and assessment of the pH homeostasis mechanisms in Aspergillus niger while in citric acid producing conditions. J Theor Biol 282 23-35... 

---