Effects of Dietary Fatty Acids in Pancreatic Beta Cell Metabolism, Implications in Homeostasis.

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Annotation Summary

Term Occurence Count Dictionary
obesity 6 endocrinologydiseases
Insulin 1 endocrinologydiseasesdrugs
glucose intolerance 1 endocrinologydiseases
hyperinsulinemia 2 endocrinologydiseases
hypertriglyceridemia 1 endocrinologydiseases
hypogonadism 1 endocrinologydiseases

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Select Drug Character Offset Drug Term Instance
Insulin 737 high-caloric diet rich in dietary saturated fats have been broadly characterized as triggers of T2D. Insulin resistance resulting from a high saturated fat diet leads to alterations in lipid cellular intake and
Select Disease Character Offset Disease Term Instance
glucose intolerance 15207 for FFAs in the amplification of insulin secretion; these mice did not develop hyperinsulinemia nor glucose intolerance when given a high-fat diet, since this deficiency protected from the harmful metabolic effects of high-fat
hyperinsulinemia 5529 synthesis in β-cells due to hyperglycemic conditions can result in β-cell expansion and generate hyperinsulinemia as a compensatory mechanism. However, this process gradually leads to β-cell mass loss, generating
hyperinsulinemia 15186 mice confirmed a role for FFAs in the amplification of insulin secretion; these mice did not develop hyperinsulinemia nor glucose intolerance when given a high-fat diet, since this deficiency protected from the harmful
hypertriglyceridemia 15511 FA augmentation of insulin secretion [[46]]. FFAR1 deficiency protected from hepatic steatosis and hypertriglyceridemia and FFAR1 overexpression led to liver steatosis and, subsequently, impairment of islet function and
hypogonadism 21028 an exome sequencing of morbidly obese women with intellectual disability, T2D and hypogonadotrophic hypogonadism led to the discovery of a new monogenic obesity syndrome with CPE deficiency [[74]]. An obesity-diabetes
obesity 16162 chain length, in addition to being considered a contributing factor for T2D evolution in patients with obesity [[51]]. In β-cells, prolonged exposure to high concentrations of long chain FFAs leads to the inhibition
obesity 21081 intellectual disability, T2D and hypogonadotrophic hypogonadism led to the discovery of a new monogenic obesity syndrome with CPE deficiency [[74]]. An obesity-diabetes syndrome is elicited by a genetic defect in
obesity 21129 hypogonadism led to the discovery of a new monogenic obesity syndrome with CPE deficiency [[74]]. An obesity -diabetes syndrome is elicited by a genetic defect in CPE previously described in fat/fat and Cpe knockout
obesity 27175 consuming a high n-3/n-6 PUFA ratio diet (1:1, PUFA1:1), when compared to SFA-fed rats, had alleviated obesity and lipid stores, as well as decreased serum triglycerides and total cholesterol levels. However, non-significant
obesity 27994 found. Collectively, a PUFA1:1 diet alleviates insulin resistance and contributes to improvement of obesity in rats by suppressing TLR4 activation [[88]]. Nevertheless, the effect of TLR-4 activation and insulin
obesity 31837 and PUFA1:1 to counteract the effects of a high SFA diet, which is a signature condition in T2D and obesity patients. This enhances insulin sensitivity, diminishes inflammation and, overall, improves β-cell

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