Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Heavy-breed (HB) chicks differed from light-breed (LB) ones in their propensity to be overfed. Whereas in the LB chicks the amount by which they could be overfed reached 70% more than the food consumed daily by the ad lib.-fed chicks, in the HB chicks the maximal excess was only 13%. 2. Overfeeding caused a slight but statistically significant increase in the linear growth rate (shank length) of the LB chicks, with an opposite effect in the HB chicks. 3. Overfeeding increased the weight of the crop, proventriculus, small intestine, pancreas, liver and adipose tissue but had no such effect on the heart, cerebrum or cerebellum. 4. Overfeeding had no effect on the specific activities of the pancreatic digestive enzymes, liver xanthine dehydrogenase, or tryptophan oxygenase (EC 1.13.1.12). The increase in the total activities was due entirely to organ hypertrophy. 5. Obesity induced in young chicks had no residual effects on the adult LB chicks, but reduced the linear growth of the adult HB chicks. 6. An explanation for the difference between breeds in response to overfeeding at an early age is discussed.
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PMID:Influence of overfeeding on growth, obesity and intestinal tract in young chicks of light and heavy breeds. 61 76

Kynurenine pathway (KP) is the primary path of tryptophan (Trp) catabolism in most mammalian cells. The KP generates several bioactive catabolites, such as kynurenine (Kyn), kynurenic acid (KA), 3-hydroxykynurenine (3-HK), xanthurenic acid (XA), and 3-hydroxyanthranilic acid (3-HAA). Increased catabolite concentrations in serum are associated with several cardiovascular diseases (CVD), including heart disease, atherosclerosis, and endothelial dysfunction, as well as their risk factors, including hypertension, diabetes, obesity, and aging. The first catabolic step in KP is primarily controlled by indoleamine 2,3-dioxygenase (IDO) and tryptophan 2,3-dioxygenase (TDO). Following this first step, the KP has two major branches, one branch is mediated by kynurenine 3-monooxygenase (KMO) and kynureninase (KYNU) and is responsible for the formation of 3-HK, 3-HAA, and quinolinic acid (QA); and another branch is controlled by kynurenine amino-transferase (KAT), which generates KA. Uncontrolled Trp catabolism has been demonstrated in distinct CVD, thus, understanding the underlying mechanisms by which regulates KP enzyme expression and activity is paramount. This review highlights the recent advances on the effect of KP enzyme expression and activity in different tissues on the pathological mechanisms of specific CVD, KP is an inflammatory sensor and modulator in the cardiovascular system, and KP catabolites act as the potential biomarkers for CVD initiation and progression. Moreover, the biochemical features of critical KP enzymes and principles of enzyme inhibitor development are briefly summarized, as well as the therapeutic potential of KP enzyme inhibitors against CVD is briefly discussed.
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PMID:Abnormal kynurenine pathway of tryptophan catabolism in cardiovascular diseases. 2831 92

Several enzymes and metabolites of the kynurenine pathway (KP) have immunomodulatory effects. Modulation of the activities and levels of these molecules might be of particular importance under disease conditions when the amelioration of overreacting immune responses is desired. Results obtained by the use of animal and tissue culture models indicate that by eliminating or decreasing activities of key enzymes of the KP, a beneficial shift in disease outcome can be attained. This review summarizes experimental data of models in which IDO, TDO, or KMO activity modulation was achieved by interventions affecting enzyme production at a genomic level. Elimination of IDO activity was found to improve the outcome of sepsis, certain viral infections, chronic inflammation linked to diabetes, obesity, aorta aneurysm formation, and in anti-tumoral processes. Similarly, lack of TDO activity was advantageous in the case of anti-tumoral immunity, while KMO inhibition was found to be beneficial against microorganisms and in the combat against tumors, as well. On the other hand, the complex interplay among KP metabolites and immune function in some cases requires an increase in a particular enzyme activity for the desired immune response modulation, as was shown by the exacerbation of liver fibrosis due to the elimination of IDO activity and the detrimental effects of TDO inhibition in a mouse model of autoimmune gastritis. The relevance of these studies concerning possible human applications are discussed and highlighted. Finally, a brief overview is presented on naturally occurring genetic variants affecting immune functions via modulation of KP enzyme activity.
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PMID:Immunomodulatory Effects of Genetic Alterations Affecting the Kynurenine Pathway. 3178 Oct 97