Plasma-free amino acid profiles are predictors of cancer and diabetes development.

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Term Occurence Count Dictionary
hyperglycemia 4 endocrinologydiseases
hyperinsulinemia 10 endocrinologydiseases
metabolic syndrome 1 endocrinologydiseases
obesity 15 endocrinologydiseases
Insulin 4 endocrinologydiseasesdrugs
diabetes mellitus 1 endocrinologydiseases

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Select Drug Character Offset Drug Term Instance
Insulin 2298 links between these two diseases are yet incompletely understood but may involve insulin resistance.[3] Insulin resistance, intertwined with hyperinsulinemia, has been suggested as one of the possible underlying
Insulin 3612 was reported.[9] Hyperaminoacidemia in obesity may be a manifestation of increased insulin resistance. Insulin has long been recognized as the regulator of branched-chain alpha-keto acid dehydrogenase complex, an
Insulin 3770 branched-chain alpha-keto acid dehydrogenase complex, an enzyme complex involved in BCAA catabolism.[10] Insulin resistance has been found to reduce the enzymatic activity of branched-chain alpha-keto acid dehydrogenase
Insulin 26663 needed to maintain normal (or near-normal) glucose tolerance are at increased risk of cancers. IGF-1, Insulin -like growth factor 1; IRS, insulin receptor substrate; mTORC1, mammalian target of rapamycin complex
Select Disease Character Offset Disease Term Instance
diabetes mellitus 17035 the significance of PFAA alterations in cancers development and management.Altered PFAA profiles in diabetes mellitus T2D is characterized by insulin resistance and/or impaired insulin secretion from beta cells. The prevalence
hyperglycemia 634 colon, liver and pancreas. Many observational studies suggest that certain medications used to treat hyperglycemia (or T2D) may affect cancer cells directly or indirectly. The potential mechanisms of the direct T2D
hyperglycemia 808 potential mechanisms of the direct T2D cancer links have been hypothesized to be hyperinsulinemia, hyperglycemia and chronic inflammation; however, the metabolic pathways that lead to T2D and cancers still remain
hyperglycemia 24638 progression or T2D and its complications because the roles of insulin resistance or hyperinsulinemia or hyperglycemia in regulating the enzymes utilizing amino acids are still incompletely understood. Although our understanding
hyperglycemia 36611 dyslipidemia.Wurtz et al.[88]2012Finnish cohorts1873 (58% women)Alterations in BCAAs and AAAs metabolism precede hyperglycemia in the general population.Abbreviations: AAA, aromatic amino acid; BCAA, branched-chain amino acid;
hyperinsulinemia 790 or indirectly. The potential mechanisms of the direct T2D cancer links have been hypothesized to be hyperinsulinemia , hyperglycemia and chronic inflammation; however, the metabolic pathways that lead to T2D and cancers
hyperinsulinemia 2335 incompletely understood but may involve insulin resistance.[3]Insulin resistance, intertwined with hyperinsulinemia , has been suggested as one of the possible underlying mechanisms for the direct connection between T2D
hyperinsulinemia 2500 underlying mechanisms for the direct connection between T2D and cancers.[3] T2D is typically preceded by hyperinsulinemia to maintain glucose homeostasis.[4] Additionally, convincing evidence have suggested that hyperinsulinemia
hyperinsulinemia 2607 hyperinsulinemia to maintain glucose homeostasis.[4] Additionally, convincing evidence have suggested that hyperinsulinemia may affect the signaling pathways of insulin and insulin-like growth factor 1 (IGF-1) and thus facilitate
hyperinsulinemia 18856 cardiovascular diseases.[78] One of the possible mechanisms by which hyperaminoacidemia could promote DM is via hyperinsulinemia leading to pancreatic beta cell exhaustion. The association between insulin resistance and increased
hyperinsulinemia 23349 several cancers. The underlying link between obesity, T2D, and cancer is related to insulin resistance, hyperinsulinemia , and disturbances in IGF signaling systems (Figure 1). The insulin resistant state is correlated with
hyperinsulinemia 24618 cancer risk and progression or T2D and its complications because the roles of insulin resistance or hyperinsulinemia or hyperglycemia in regulating the enzymes utilizing amino acids are still incompletely understood.
hyperinsulinemia 26544 of T2D. On the other hand, some insulin resistant individuals who are able to maintain the degree of hyperinsulinemia needed to maintain normal (or near-normal) glucose tolerance are at increased risk of cancers. IGF-1,
hyperinsulinemia 34956 al.[81]2014T2D patients51 (23 men and 28 women)Ala, Tyr, Glu and Pro were strongly associated with hyperinsulinemia , while Ala, Glu, Trp and BCAAs were associated with hypoadiponectinemia.Martin et al.[82]2013Healthy
hyperinsulinemia 37259 insulin resistance.AAAsAAAs are metabolized to catecholamines, which alter the liver function leading to hyperinsulinemia and dyslipidemia.MetMet metabolism may intersect with Phe/Tyr catabolism and stimulate insulin secretion.
metabolic syndrome 36392 the development of DM; Ile, Leu, Tyr, Ala and Ser were significantly related to the development of metabolic syndrome ; Ile, Leu, Tyr, Val, Ala, Pro, Ser and Gly significantly related to the development of dyslipidemia.Wurtz
obesity 1117 with the risks of developing T2D and cancers in individuals with different ethnic groups and degree of obesity . The alterations of PFAAs might be predominately caused by the metabolic shift resulted from insulin
obesity 2163 T2D) and cancers share many common risk factors, for example, aging, physical inactivity, diet and obesity . The potential biologic links between these two diseases are yet incompletely understood but may involve
obesity 2882 of insulin resistance has been either focused on lipid-mediated mechanisms[6] or the interplay with obesity , which induces metabolic abnormalities.[7] The latter is partly reflected in the abnormal circulating
obesity 3549 is, tyrosine (Tyr) and phenylalanine (Phe) in obese subjects, was reported.[9] Hyperaminoacidemia in obesity may be a manifestation of increased insulin resistance.Insulin has long been recognized as the regulator
obesity 4002 suppress BCAA catabolism. This is considered as the plausible etiology of increased BCAA levels in obesity and/or diabetes.[11] Indeed, evidence is accumulating that there is positive association between insulin
obesity 19082 circulating BCAAs levels were supported by several other studies with different ethnic groups and degree of obesity .[12], [13], [14], [16], [79], [80]Table 3 summarizes 16 recent studies reporting the associations between
obesity 20431 towards the development of atherosclerosis.[78] The plausible etiology of elevated BCAAs levels in obesity is through the suppression of BCAA catabolism by insulin resistance.[11] It should be noted that, besides
obesity 20545 through the suppression of BCAA catabolism by insulin resistance.[11] It should be noted that, besides obesity -associated insulin resistance, BCAAs levels were also positively correlated with HOMA-IR in individuals
obesity 23176 tool to access the risk of cancers and T2D. Results from epidemiological studies have suggested that obesity and T2D are positively correlated with the increased risk of several cancers. The underlying link between
obesity 23290 T2D are positively correlated with the increased risk of several cancers. The underlying link between obesity , T2D, and cancer is related to insulin resistance, hyperinsulinemia, and disturbances in IGF signaling
obesity 24014 the variations in participant characteristics, for example, age, gender, ethnic background, degree of obesity , diet, different techniques for amino acids measurement, different types and stages of cancers and limited
obesity 25075 evident that Asian populations are more insulin resistant than other ethnic groups, in spite of less obesity , it is necessary to better identify the factors underlying the interethnic differences. As mentioned
obesity 33380 African-American, 36 White and 12 others)Elevated circulating BCAAs levels were significantly associated with obesity in children and adolescents, and may predict future insulin resistance independently.Wurtz et al.[15]2013Finnish
obesity 34377 al.[79]2012Finnish cohorts7098 (3433 men and 3665 women)Circulating amino acids displayed sex- and obesity -dependent interactions with HOMA-IR. The associations of HOMA-IR with Ile, Leu, Val, Phe, Tyr and Ala
obesity 35381 peripheral amino acid profile; A multivariate logistic regression model of PFAAs could distinguish visceral obesity .Wang-Sattler et al.[84]2012Cooperative Health Research in the Region of Augsburg (KORA) cohort1297 (cross-sectional

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